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33 results on '"Rocio, Aller"'

2. Copy number variation and expression of exportin-4 associates with severity of fibrosis in metabolic associated fatty liver disease

Author

Mayada Metwally, Ali Bayoumi, Anis Khan, Leon A. Adams, Rocio Aller, Carmelo García-Monzón, María Teresa Arias-Loste, Elisabetta Bugianesi, Luca Miele, Alisi Anna, Olivier Latchoumanin, Shuanglin Han, Shafi Alenizi, Rasha EL Sharkawy, Afaf Elattar, Rocio Gallego-Durán, Janett Fischer, Thomas Berg, Christopher Liddle, Manuel Romero-Gomez, Jacob George, and Mohammed Eslam

Subjects
MAFLD, XPO4, Fibrosis, TGFβ, Medicine, Medicine (General), R5-920
Abstract

Background: Liver fibrosis risk is a heritable trait, the outcome of which is the net deposition of extracellular matrix by hepatic stellate cell-derived myofibroblasts. Whereas nucleotide sequence variations have been extensively studied in liver fibrosis, the role of copy number variations (CNV) in which genes exist in abnormal numbers of copies (mostly due to duplication or deletion) has had limited exploration. Methods: The impact of the XPO4 CNV on histological liver damage was examined in a cohort comprised 646 Caucasian patients with biopsy-proven MAFLD and 170 healthy controls. XPO4 expression was modulated and function was examined in human and animal models. Findings: Here we demonstrate in a cohort of 816 subjects, 646 with biopsy-proven metabolic associated liver disease (MAFLD) and 170 controls, that duplication in the exportin 4 (XPO4) CNV is associated with the severity of liver fibrosis. Functionally, this occurs via reduced expression of hepatic XPO4 that maintains sustained activation of SMAD3/SMAD4 and promotes TGF-β1-mediated HSC activation and fibrosis. This effect was mediated through termination of nuclear SMAD3 signalling. XPO4 demonstrated preferential binding to SMAD3 compared to other SMADs and led to reduced SMAD3-mediated responses as shown by attenuation of TGFβ1 induced SMAD transcriptional activity, reductions in the recruitment of SMAD3 to target gene promoters following TGF-β1, as well as attenuation of SMAD3 phosphorylation and disturbed SMAD3/SMAD4 complex formation. Interpretation: We conclude that a CNV in XPO4 is a critical mediator of fibrosis severity and can be exploited as a therapeutic target for liver fibrosis. Funding: ME and JG are supported by the Robert W. Storr Bequest to the Sydney Medical Foundation, University of Sydney; a National Health and Medical Research Council of Australia (NHMRC) Program Grant (APP1053206) and Project and ideas grants (APP2001692, APP1107178 and APP1108422). AB is supported by an Australian Government Research Training Program (RTP) scholarship. EB is supported by Horizon 2020 under grant 634413 for the project EPoS.

Published
2021
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3. Mistranslation Drives Alterations in Protein Levels and the Effects of a Synonymous Variant at the Fibroblast Growth Factor 21 Locus

Author

Ali Bayoumi, Asmaa Elsayed, Shuanglin Han, Salvatore Petta, Leon A. Adams, Rocio Aller, Anis Khan, Carmelo García‐Monzón, María Teresa Arias‐Loste, Luca Miele, Olivier Latchoumanin, Shafi Alenizi, Rocio Gallego‐Durán, Janett Fischer, Thomas Berg, Antonio Craxì, Mayada Metwally, Liang Qiao, Christopher Liddle, Hannele Yki‐Järvinen, Elisabetta Bugianesi, Manuel Romero‐Gomez, Jacob George, and Mohammed Eslam

Subjects
fibroblast growth factor 21, genetics, metabolic, metabolic associated fatty liver disease, Science
Abstract

Abstract Fibroblast growth factor 21 (FGF21) is a liver‐derived hormone with pleiotropic beneficial effects on metabolism. Paradoxically, FGF21 levels are elevated in metabolic diseases. Interventions that restore metabolic homeostasis reduce FGF21. Whether abnormalities in FGF21 secretion or resistance in peripheral tissues is the initiating factor in altering FGF21 levels and function in humans is unknown. A genetic approach is used to help resolve this paradox. The authors demonstrate that the primary event in dysmetabolic phenotypes is the elevation of FGF21 secretion. The latter is regulated by translational reprogramming in a genotype‐ and context‐dependent manner. To relate the findings to tissues outcomes, the minor (A) allele of rs838133 is shown to be associated with increased hepatic inflammation in patients with metabolic associated fatty liver disease. The results here highlight a dominant role for translation of the FGF21 protein to explain variations in blood levels that is at least partially inherited. These results provide a framework for translational reprogramming of FGF21 to treat metabolic diseases.

Published
2021
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5. Genetic variation in the TLL1 gene is not associated with fibrosis in patients with metabolic associated fatty liver disease.

Author

Ali Bayoumi, Ismail Jalil, Mayada Metwally, Leon A Adams, Rocio Aller, Carmelo García-Monzón, María Teresa Arias-Loste, Luca Miele, Salvatore Petta, Antonio Craxì, Rocio Gallego-Durán, Janett Fischer, Thomas Berg, Liang Qiao, Christopher Liddle, Elisabetta Bugianesi, Manuel Romero-Gomez, Jacob George, and Mohammed Eslam

Subjects
Medicine, Science
Abstract

Metabolic associated fatty liver disease (MAFLD) is the most prevalent liver disease in Western nations, with high heritability. A recent study of Japanese patients with the disease suggested that TLL1 rs17047200 is associated with fibrosis; whether a similar association is observed in Caucasian patients with MAFLD is unknown. We investigated the association of the TLL1 rs17047200 polymorphism with liver fibrosis in a cohort of Caucasian patients with MAFLD (n = 728). We also investigated whether TLL1 expression is altered during liver injury in humans, in murine models of fibrosis, and in in-vitro. While TLL1 expression is upregulated in the liver of humans with MAFLD and in mice, the rs17047200 variant was not associated with fibrosis or any other histological features, or with hepatic TLL1 expression. In conclusion, the TLL1 rs17047200 variant is not a risk variant for fibrosis in Caucasian patients with MAFLD. However, TLL1 could be involved in the pathogenesis of liver fibrosis.

Published
2020
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6. Predicting liver-related events in NAFLD: A predictive model

Author

Luis Calzadilla-Bertot, Gary P. Jeffrey, Zhengyi Wang, Yi Huang, George Garas, Michael Wallace, Bastiaan de Boer, Jacob George, Mohammed Eslam, Amy Phu, Javier Ampuero, Ana Lucena Valera, Manuel Romero-Gómez, Rocio Aller de la Fuente, and Leon A. Adams

Subjects
Hepatology
Published
2023
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8. ABIDE: An Accurate Predictive Model of Liver Decompensation in Patients With Nonalcoholic Fatty Liver‐Related Cirrhosis

Author

Naga Chalasani, Luis Calzadilla-Bertot, Archita P. Desai, Mohammed Eslam, Manuel Romero-Gómez, Rocio Aller-de la Fuente, Eduardo Vilar-Gomez, Jacob George, Leon A. Adams, Vincent Wai-Sun Wong, Grace Lai-Hung Wong, Marlen Castellanos, and Gary P. Jeffrey

Subjects
0301 basic medicine, medicine.medical_specialty, Cirrhosis, Hepatology, business.industry, Fatty liver, medicine.disease, Gastroenterology, Confidence interval, 03 medical and health sciences, Liver disease, 030104 developmental biology, 0302 clinical medicine, Internal medicine, Nonalcoholic fatty liver disease, medicine, 030211 gastroenterology & hepatology, Cumulative incidence, Decompensation, business, Hepatic encephalopathy
Abstract

BACKGROUND AND AIMS Nonalcoholic fatty liver disease (NAFLD) is an increasingly important cause of liver cirrhosis and subsequent complications. We retrospectively developed and validated a model to predict hepatic decompensation in patients with NAFLD and cirrhosis and compared this with currently available models. APPROACH AND RESULTS Baseline variables from an international cohort of 299 patients with biopsy-proven NAFLD with compensated cirrhosis were examined to construct a model using competing risk multivariate regression and Akaike/Bayesian information criteria. Validation was performed in 244 patients with biopsy-proven NAFLD cirrhosis from the United States. Prognostic accuracy was compared with the NAFLD fibrosis score (NFS), fibrosis-4 (FIB-4), Model for End-Stage Liver Disease (MELD), Child-Turcotte-Pugh (CTP), and albumin-bilirubin (ALBI)-FIB-4 score using time-dependent area under the curve (tAUC) analysis. During a median follow-up of 5.6 years (range 2.4-14.1) and 5.4 years (range 1.5-13.8), hepatic decompensation occurred in 81 and 132 patients in the derivation and validation cohorts, respectively. In the derivation cohort, independent predictors of hepatic decompensation (Aspartate aminotransferase/alanine aminotransferase ratio, Bilirubin, International normalized ratio, type 2 Diabetes, and Esophageal varices) were combined into the ABIDE model. Patients with a score ≥4.1 compared with those with a score

Published
2021
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9. The metabolic dysfunction-associated fatty liver disease definition, regardless of its clinical subclassification, identifies patients at high risk for liver disease progression

Author

Del Barrio Azaceta, María, primary, Iruzubieta, Paula, additional, de la Fuente, Rocio Aller, additional, Banales, Jesus Maria, additional, Santos-Laso, Álvaro, additional, Calleja Panero, José Luis, additional, Ibañez, Luis, additional, Arias Loste, María Teresa, additional, Gomez, Manuel Romero, additional, García-Monzón, Carmelo, additional, Gómez-Camarero, Judith, additional, Ginès, Pere, additional, Morillas, Rosa M, additional, Pericàs, Juan Manuel, additional, Aspichueta, Patricia, additional, Martin-Mateos, Rosa, additional, Gallego-Durán, Rocío, additional, De La Torre Sanchez, Mercedes, additional, Escudero-García, Desamparados, additional, Monterde, Vanesa Bernal, additional, Benlloch, Salvador, additional, Turnes, Juan, additional, and Crespo, Javier, additional

Published
2022
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10. Metabolic dysfunction-associated fatty liver disease increases cardiovascular risk regardless of classical risk factors

Author

Del Barrio Azaceta, María, primary, Iruzubieta, Paula, additional, De La Fuente, Rocio Aller, additional, Banales, Jesus Maria, additional, Santos-Laso, Álvaro, additional, Calleja Panero, José Luis, additional, Ibañez, Luis, additional, Arias Loste, María Teresa, additional, Gomez, Manuel Romero, additional, García-Monzón, Carmelo, additional, Gómez-Camarero, Judith, additional, Ginès, Pere, additional, Morillas, Rosa M, additional, Pericàs, Juan Manuel, additional, Aspichueta, Patricia, additional, Martin-Mateos, Rosa, additional, Gallego-Durán, Rocío, additional, De La Torre Sanchez, Mercedes, additional, Escudero-García, Desamparados, additional, Monterde, Vanesa Bernal, additional, Benlloch, Salvador, additional, Turnes, Juan, additional, and Crespo, Javier, additional

Published
2022
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11. Association of the APOA-5 Genetic Variant rs662799 with Metabolic Changes after an Intervention for 9 Months with a Low-Calorie Diet with a Mediterranean Profile

Author

Daniel de Luis Roman, David Primo, Olatz Izaola, and Rocio Aller

Subjects
Leptin, Nutrition and Dietetics, Diet, Reducing, Genotype, Polymorphism, Single Nucleotide, ApoA5 gene, rs662799, low-calorie diet, triglycerides, Cross-Sectional Studies, Humans, Insulin, Adiponectin, Obesity, Insulin Resistance, Apolipoproteins A, Triglycerides, Food Science, Caloric Restriction
Abstract

In cross-sectional studies, the genetic variant rs662799 of the APOA5 gene is associated with high serum triglyceride concentrations, and in some studies, the effect of short-term dietary interventions has been evaluated. The aim of the present investigation was to evaluate the role of this genetic variant in metabolic changes after the consumption of a low-calorie diet with a Mediterranean pattern for 9 months. A population of 269 Caucasian obese patients was recruited. Adiposity and biochemical parameters were measured at the beginning (basal level) and after 3 and 9 months of the dietary intervention. The rs662799 genotype was assessed with a dominant analysis (TT vs. CT + CC). The APOA5 variant distribution was: 88.1% (n = 237) (TT), 11.5% (n = 31) (TC) and 0.4% (n = 1) (CC). There were significant differences only in triglyceride levels at all times of the study between the genotype groups. After 3 and 9 months of dietary intervention, the following parameters improved in both genotype groups: adiposity parameters, systolic pressure, total cholesterol, LDL cholesterol, leptin, adiponectin and the leptin/adiponectin ratio. The intervention significantly decreased insulin levels, HOMA-IR and triglyceride levels in non-C allele carriers (Delta 9 months TT vs. TC + CC). i.e., insulin levels (delta: −3.8 + 0.3 UI/L vs. −1.2 + 0.2 UI/L; p = 0.02), HOMA-IR levels (delta: −1.2 + 0.2 units vs. −0.3 + 0.1 units; p = 0.02), triglyceride levels (delta: −19.3 + 4.2 mg/dL vs. −4.2 + 3.0 mg/dL; p = 0.02). In conclusion, non-C allele carriers of rs662799 of the APOA5 gene showed a decrease of triglyceride, insulin and HOMA-IR levels after consuming a low-calorie diet with a Mediterranean pattern; we did not observe this effect in C allele carriers, despite a significant weight loss.

Published
2022

12. Relation of osteocalcin with insulin resistance and histopathological changes of non alcoholic fatty liver disease

Author

Rocio Aller, Jose Luis Perez Castrillon, Daniel Antonio de Luis, Rocio Conde, Olatz Izaola, Manuel González Sagrado, María Concepción Velasco, Tomas Alvarez, and David Pacheco

Subjects
Adipose Tissue, Non Alcoholic Fatty Liver Disease, Obesity, Osteocalcin, Specialties of internal medicine, RC581-951
Abstract

Background. Osteocalcin is a hormone with a complex cross-talk between adipose tissue and the skeleton. The aim of the present study was to explore the relation of osteocalcin with histopathological changes of NALFD patients.Subjects. A population of 69 NAFLD patients was analyzed. A liver biopsy was realized. Weight, fat mass, body mass index, basal glucose, insulin, insulin resistance (HOMA), total cholesterol, LDL-cholesterol, HDL-cholesterol, triglycerides and osteocalcin levels were measured.Results. Patients were divided in two groups by median osteocalcin value (11.34 ng/mL), group I (patients with the low values) and group II (patients with the high values). Only liver fibrosis frequencies were different between groups (group I: 22.9% vs group II: 9.4%; p < 0.05). Patients in group I had higher levels of glucose (115.6 ± 28.1 mg/ dL vs. 103.7 ± 24.3 mg/dL; p < 0.04), HOMA (4.6 ± 3.1 units vs. 3.6 ± 1.8 units; p < 0.04), weight (102.9 ± 32.4 kg vs. 85.9 ± 16.8 kg; p = 0.002) and body mass index (38.3 ± 11.4 kg/m2 vs. 30.1 ± 5.7 kg/m2; p = 0.001)) than patients in group II. Osteocalcin was inverse correlated with glucose (r =-0.4; p = 0.002) and HOMA (r = -0.3:p = 0.01).Conclusion. Osteocalcin is associated with liver fibrosis. However, this association disappeared in a multivariate analysis, and HOMA remained as an independent factor.

Published
2011
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13. Global multi-stakeholder endorsement of the MAFLD definition

Author

Nahum Méndez-Sánchez, Elisabetta Bugianesi, Robert G Gish, Frank Lammert, Herbert Tilg, Mindie H Nguyen, Shiv K Sarin, Núria Fabrellas, Shira Zelber-Sagi, Jian-Gao Fan, Gamal Shiha, Giovanni Targher, Ming-Hua Zheng, Wah-Kheong Chan, Shlomo Vinker, Takumi Kawaguchi, Laurent Castera, Yusuf Yilmaz, Marko Korenjak, C Wendy Spearman, Mehmet Ungan, Melissa Palmer, Mortada El-Shabrawi, Hans-Juergen Gruss, Jean-François Dufour, Anil Dhawan, Heiner Wedemeyer, Jacob George, Luca Valenti, Yasser Fouad, Manuel Romero‐Gomez, Mohammed Eslam, Maria Lorena Abate, Bahaa Abbas, Ahmed Amr Abbassy, Waleed Abd El Ghany, Amira Abd Elkhalek, Emad Abd ElMajeed, Mohammad Abdalgaber, Mohamed AbdAllah, Marwa Abdallah, Nourhan Abdallah, Shereen Abdelaleem, Yasser Abdelghani, Wael Abdelghany, Safaa Mohamed Abdelhalim, Wafaa Abdelhamid, Nehal Abdelhamid, Nadia A. Abdelkader, Elsayed Abdelkreem, Aly Mohamed Abdelmohsen, Awny Ali Abdelrahman, Sherief M Abd-elsalam, Doaa Abdeltawab, Abdulbaset Abduh, Nada Abdulhakam, Maheeba Abdulla, Navid Abedpoor, Ludovico Abenavoli, Fredrik Åberg, Omala Ablack, Mostafa Abo elftouh, Yousry Esam-Eldin Abo-Amer, Ashraf Aboubkr, Alaa Aboud, Amr M. Abouelnaga, Galal A. Aboufarrag, Ashraf Aboutaleb, Leticia Abundis, Gupse Adalı, Enrique Adames, Leon Adams, Danjuma Adda, Noor Adel, Nada Adel, Muhammad Adel Sayed, Taiba Jibril Afaa, Nawal Afredj, Gulnara Aghayeva, Alessio Aghemo, Carlos A. Aguilar-Salinas, Golo Ahlenstiel, Walid Ahmady, Wafaa Ahmed, Amira Ahmed, Samah Nasser Ahmed, Heba Mostafa Ahmed, Rasha Ahmed, Elmar Aigner, Mesut Akarsu, Maisam Akroush, Umit Akyuz, Mamun Al Mahtab, Tahani Al Qadiri, Yusriya Al Rawahi, Razzaq AL rubaee, Muna Al Saffar, Shahinul Alam, Zaid Al-Ani, Agustín Albillos, Mohamed Alboraie, Said Al-Busafi, Mohamed Al-Emam, Jawaher Alharthi, Kareem Ali, Basma Abdelmoez Ali, Mohammad Ali, Raja Affendi Raja Ali, Anna Alisi, Ali Raad AL-Khafaji, Maryam Alkhatry, Rocio Aller, Yahya Almansoury, Khalid Al-Naamani, Alaa Alnakeeb, Anna Alonso, Saleh A. Alqahtani, Leina Alrabadi, Khalid Alswat, Mahir Altaher, Turki Altamimi, Jose Altamirano, Mario R. Alvares-da-Silva, Elsragy Adel M. Aly, Amgad Alzahaby, Ahmed Alzamzamy, Keisuke Amano, Maysa A. Amer, Mona A. Amin, Sayed A. Amin, Ashraf A. Amir, Javier Ampuero, Noha Anas, Pietro Andreone, Soa Fy Andriamandimby, Mahmoud Anees, Peltec Angela, Manal Antonios, Wael Arafat, Jose Moreno Araya, Juan Armendariz-Borunda, Matthew J. Armstrong, Hassan Ashktorab, Patricia Aspichueta, Fathia Assal, Mira Atef, Dina Attia, Hoda Atwa, Reham Awad, Mohyeldeen Abd Elaziz Awad, Sally Awny, Obafemi Awolowo, Yaw Asante Awuku, Ibrahim Ayada, Than Than Aye, Sherif Ayman, Hedy Ayman, Hesham Ayoub, Hosny M. Azmy, Romiro P. Babaran, Omneya Badreldin, Ahmed Badry, İbrahim Halil Bahçecioğlu, Amira Bahour, Jiajia Bai, Yasemin Balaban, Muthuswamy Balasubramanyam, Khaled Bamakhrama, Jesus M Banales, Babu Bangaru, Jianfeng Bao, Jorge Suazo Barahona, Salma Barakat, Sandra Maria Barbalho, Bikwa Barbra, Beatriz Barranco, Francisco Barrera, Ulrich Baumann, Shamardan Bazeed, Eva Bech, Aourarh Benayad, Andreas Benesic, David Bernstein, Fernando Bessone, Susie Birney, Cyrille Bisseye, Martin Blake, Bilal Bobat, Leonilde Bonfrate, Dmitry S Bordin, Francisco Bosques-Padilla, Jerome Boursier, Boushab Mohamed Boushab, David Bowen, Patricia Medina Bravo, Paul N Brennan, Bisi Bright, Ilse Broekaert, Xabier Buque, Diego Burgos-Santamaría, Julio Burman, Luca Busetto, Chris D. Byrne, Patricia Anne I. Cabral-Prodigalidad, Guillermo Cabrera-Alvarez, Wei Cai, Francesca Cainelli, Ali Riza Caliskan, Ali Canbay, Ana Cano-Contreras, Hai-Xia Cao, Zhujun Cao, Andres Carrion, Francesca Carubbi, Teresa Casanovas, Marlen Ivón Castellanos Fernández, Jin Chai, Siew Pheng Chan, Phunchai Charatcharoenwitthaya, Norberto Chavez-Tapia, Kazuaki Chayama, Jinjun Chen, Lin Chen, Zhong-Wei Chen, Huiting Chen, Sui-Dan Chen, Qiang Chen, Yaxi Chen, Gang Chen, En-Quang Chen, Fei Chen, Pei-Jer Chen, Robert Cheng, Wendy Cheng, Jack Tan Wei Chieh, Imad Chokr, Evangelos Cholongitas, Ashok Choudhury, Abhijit Chowdhury, Evaristus Sunday Chukwudike, Stefano Ciardullo, Michelle Clayton, Karine Clement, Marie Michelle Cloa, Cecilia Coccia, Cristina Collazos, Massimo Colombo, Arif Mansur Cosar, Helma Pinchemel Cotrim, Joris Couillerot, Alioune Coulibaly, Gonzalo Crespo, Javier Crespo, Maria Cruells, Ian Homer Y. Cua, Hesham K. Dabbous, George N Dalekos, Patricia D'Alia, Li Dan, Viet Hang Dao, Mostafa Darwish, Christian Datz, Milagros B Davalos-Moscol, Heba Dawoud, Blanca Olaechea de Careaga, Robert de Knegt, Victor de Ledinghen, Janaka de Silva, Nabil Debzi, Marie Decraecker, Elvira Del Pozo, Teresa C Delgado, Manuel Delgado-Blanco, Łukasz Dembiński, Adilson Depina, Moutaz Derbala, Hailemichael Desalegn, Christèle Desbois-Mouthon, Mahmoud Desoky, Anouk Dev, Agostino Di Ciaula, Moisés Diago, Ibrahima Diallo, Luis Antonio Díaz, Melisa Dirchwolf, Paola Dongiovanni, Andrriy Dorofeyev, Xiaoguang Dou, Mark W. Douglas, Michael Doulberis, Cecil K. Dovia, Adam Doyle, Ivana Dragojević, Joost PH Drenth, Xuefei Duan, Audrius Dulskas, Dan L Dumitrascu, Oliver Duncan, Vincent Dusabejambo, Rev. Shem N.A. Dwawhi, Sho Eiketsu, Doaa El Amrousy, Ahmed El Deeb, Ghada El Deriny, Hesham Salah El Din, Salwa El Kamshishy, Mohamed El Kassas, Maissa El Raziky, Osama A Elagamy, Wafaa Elakel, Dina Elalfy, Hanaa Elaraby, Heba ElAwady, Reda Elbadawy, Hanaa Hassan Eldash, Manal S. Eldefrawy, Carol Lezama Elecharri, Amel Elfaramawy, Mohammed Elfatih, Mahmoud Elfiky, Mohamed Elgamsy, Mohamed Elgendy, Mohamed A. El-Guindi, Nagi Elhussieny, Ahmed Maher Eliwa, Zeineb Elkabbany, Hesham El-Khayat, Nehal M. El-Koofy, Alaa Elmetwalli, Amr Elrabat, Fathiya El-Raey, Fatma Elrashdy, Medhat Elsahhar, Esraa M. Elsaid, Shimaa Elsayed, Hany Elsayed, Aly Elsayed, Amr M. Elsayed, Hamdy Elsayed, Magdy El-Serafy, Ahmed M. Elsharkawy, Reem Yehia Elsheemy, Eman Elsayed Elshemy, Sara Elsherbini, Naglaa Eltoukhy, Reda Elwakil, Ola Emad, Shaimaa Emad, Mohamed Embabi, Ilkay Ergenç, Tatiana Ermolova, Gamal Esmat, Doaa M. Esmat, Enrique Carrera Estupiñan, Said Ettair, Tcaciuc Eugen, Mohammed Ezz-Eldin, Lidia Patricia Valdivieso Falcón, Yu-Chen Fan, Samah Fandari, Mahmoud Farag, Taghreed Mohamed Farahat, Eman M. Fares, Michael Fares, Eduardo Fassio, Hayam Fathy, Dina Fathy, Wael Fathy, Soheir Fayed, Dan Feng, Gong Feng, Miguel Fernández-Bermejo, Cristina Targa Ferreira, Javier Díaz Ferrer, Alastair Forbes, Rabab Fouad, Hanan M. Fouad, Tove Frisch, Hideki Fujii, Shuhei Fukunaga, Shinya Fukunishi, Hacer Fulya, Masato Furuhashi, Yasmine Gaber, Augusto Jose G. Galang, Jacqueline Cordova Gallardo, Rocío Galloso, Mahmoud Gamal, Reham Gamal, Hadeel Gamal, Jian Gan, Anar Ganbold, Xin Gao, George Garas, Tony Garba, Miren García-Cortes, Carmelo García-Monzón, Javier García-Samaniego, Amalia Gastaldelli, Manuel Gatica, Elizabeth Gatley, Tamar Gegeshidze, Bin Geng, Hasmik Ghazinyan, Salma Ghoneem, Luca Giacomelli, Gianluigi Giannelli, Edoardo G. Giannini, Matthew Giefer, Pere Ginès, Marcos Girala, Pablo J Giraudi, George Boon-Bee Goh, Ahmed Ali Gomaa, Benbingdi Gong, Dina Hilda C. Gonzales, Humberto C. Gonzalez, Maria Saraí Gonzalez-Huezo, Isabel Graupera, Ivica Grgurevic, Henning Grønbæk, Xuelian Gu, Lin Guan, Ibrahima Gueye, Alice Nanelin Guingané, Ozen Oz Gul, Cuma Bulent Gul, Qing Guo, Pramendra Prasad Gupta, Ahmet Gurakar, Juan Carlos Restrepo Gutierrez, Ghada Habib, Azaa Hafez, Emilia Hagman, Eman Halawa, Osama Hamdy, Abd Elkhalek Hamed, Dina H. Hamed, Saeed Hamid, Waseem Hamoudi, Yu Han, James Haridy, Hanan Haridy, David C H Harris Harris, Michael Hart, Fuad Hasan, Almoutaz Hashim, Israa Hassan, Ayman Hassan, Essam Ali Hassan, Adel Ahmed Hassan, Magda Shehata Hassan, Fetouh Hassanin, Alshymaa Hassnine, John Willy Haukeland, Amr Ismael M. Hawal, Jinfan He, Qiong He, Yong He, Fang-Ping He, Mona Hegazy, Adham Hegazy, Osama Henegil, Nelia Hernández, Manuel Hernández-Guerra, Fatima Higuera-de-la-Tijera, Ibrahim Hindy, Keisuke Hirota, Lee Chi Ho, Alexander Hodge, Mohamed Hosny, Xin Hou, Jiao-Feng Huang, Yan Huang, Zhifeng Huang, Yuan Huang, Ang Huang, Xiao-Ping Huang, Sheng Hui-ping, Bela Hunyady, Mennatallah A. Hussein, Osama Hussein, Shahinaz Mahmoud Hussien, Luis Ibáñez-Samaniego, Jamal Ibdah, Luqman Ibrahim, Miada Ibrahim, Ibrahim Ibrahim, Maria E. Icaza-Chávez, Sahar Idelbi, Ramazan Idilman Idilman, Mayumi Ikeda, Giuseppe Indolfi, Federica Invernizzi, Iram Irshad, Hasan Mohamed Ali Isa, Natacha Jreige Iskandar, Abdulrahman Ismaiel, Mariam Ismail, Zulkifli Ismail, Faisal Ismail, Hideki Iwamoto, Kathryn Jack, Rachael Jacob, Fuad Jafarov, Wasim Jafri, Helen Jahshan, Prasun K Jalal, Ligita Jancoriene, Martin Janicko, Hiruni Jayasena, Meryem Jefferies, Vivekanand Jha, Fanpu Ji, Yaqiu Ji, Jidong Jia, Changtao Jiang, Ni Jiang, Zong-zhe Jiang, Xing Jin, Yi Jin, Xu Jing, Qian Jingyu, Maia Jinjolava, FX Himawan Haryanto Jong, Alina Jucov, Ibecheole Julius, Mona Kaddah, Yoshihiro Kamada, Abobakr kamal, Enas Mohamed Kamal, Ashraf Sayed Kamel, Jia-Horng Kao, Maja Karin, Thomas Karlas, Mohammad Kashwaa, Leolin Katsidzira, Eda Kaya, M.Azzam Kayasseh, Bernadette Keenan, Caglayan Keklikkiran, William Keml, Deia K. Khalaf, Rofida Khalefa, Sherin Khamis, Doaa Khater, Hamed khattab, Anatoly Khavkin, Olga Khlynova, Nabil Khmis, Nazarii Kobyliak, Apostolos Koffas, Kazuhiko Koike, Kenneth Y.Y. Kok, Tomas Koller, Narcisse Patrice Komas, Nataliya V. Korochanskaya, Yannoula Koulla, Shunji Koya, Colleen Kraft, Bledar Kraja, Marcin Krawczyk, Mohammad Shafi Kuchay, Anand V Kulkarni, Ashish Kumar, Manoj Kumar, Sulaiman Lakoh, Philip Lam, Ling Lan, Naomi F. Lange, Kamran Bagheri Lankarani, Nicolas Lanthier, Kateryna Lapshyna, Sameh A. Lashen, Konang Nguieguia Justine Laure, Leonid Lazebnik, Didier Lebrec, Samuel S. Lee, Way Seah Lee, Yeong Yeh Lee, Diana Julie Leeming, Nathalie Carvalho Leite, Roberto Leon, Cosmas Rinaldi Adithya Lesmana, Junfeng Li, Qiong Li, Jun Li, Yang-Yang Li, Yufang Li, Lei Li, Min Li, Yiling li, Huiqing Liang, Tang Lijuan, Seng Gee Lim, Lee-Ling Lim, Shumei Lin, Han-Chieh Lin, Rita Lin, Rania Lithy, Yaru Liu, Yuanyuan Liu, Xin Liu, Wen-Yue Liu, Shourong Liu, Ken Liu, Tian Liu, Amedeo Lonardo, Mariana Bravo López, Eva López-Benages, Patricio Lopez-Jaramillo, Huimin Lu, Lun Gen Lu, Yan Lu, John Lubel, Rashid Lui, Iulianna Lupasco, Elena Luzina, Xiao-Hui Lv, Kate Lynch, Hong-Lei Ma, Mariana Verdelho Machado, Nonso Maduka, Katerina Madzharova, Russellini Magdaong, Sanjiv Mahadeva, Amel Mahfouz, Nik Ritza Kosai Nik Mahmood, Eman Mahmoud, Mohamed Mahrous, Rakhi Maiwall, Ammar Majeed, Avik Majumdar, Loey Mak, Madiha M Maklouf, Reza Malekzadeh, Claudia Mandato, Alessandra Mangia, Jake Mann, Hala Hussien Mansour, Abdellah Mansouri, Alessandro Mantovani, Jun qian Mao, Flor Maramag, Giulio Marchesini, Claude Marcus, Rui António Rocha Tato Marinho, Maria L Martinez-Chantar, Antonieta A. 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Neuman, M, Ng'Wanasayi, M, Ni, Y, Nicoll, A, Niizeki, T, Nikolova, D, Ningning, W, Niriella, M, Nogoibaeva, K, Nordien, R, O Sullivan, C, O'Beirne, J, Obekpa, S, Ocama, P, Ochwoto, M, Ogolodom, M, Ojo, O, Okrostsvaridze, N, Oliveira, C, Omana, R, Omar, O, Omar, H, Omar, M, Omran, S, Omran, R, Osman, M, Owise, N, Owusu-Ansah, T, Padilla- Machaca, P, Palle, S, Pan, Z, Pan, X, Pan, Q, Papaefthymiou, A, Paquissi, F, Par, G, Parkash, A, Payawal, D, Peltekian, K, Peng, X, Peng, L, Peng, Y, Pengoria, R, Perez, M, Perez, J, Perez, N, Persico, M, Pessoa, M, Petta, S, Philip, M, Plaz Torres, M, Polavarapu, N, Poniachik, J, Portincasa, P, Pu, C, Purnak, T, Purwanto, E, Qi, X, Qian, Z, Qiang, Z, Qiao, Z, Qiao, L, Queiroz, A, Rabiee, A, Radwan, M, Rahetilahy, A, Ramadan, Y, Ramadan, D, Ramli, A, Ramm, G, Ran, A, Rankovic, I, Rao, H, Raouf, S, Ray, S, Reau, N, Refaat, A, Reiberger, T, Remes-Troche, J, Reyes, E, Richardson, B, Ridruejo, E, Riestra Jimenez, S, Rizk, I, Roberts, S, Roblero, J, Robles, J, Rockey, D, Rodriguez, M, Rodriguez Hernandez, H, Roman, E, Romeiro, F, Romeo, S, Rosales-Zabal, J, Roshdi, G, Rosso, N, Ruf, A, Ruiz, P, Runes, N, Ruzzenente, A, Ryan, M, Saad, A, Sabbagh, E, Sabbah, M, Saber, S, Sabrey, R, Sabry, R, Saeed, M, Said, D, Said, E, Sakr, M, Salah, Y, Salama, R, Salama, A, Saleh, H, Saleh, A, Salem, A, Salifou, A, Salih, A, Salman, A, Samouda, H, Sanai, F, Sanchez-Avila, J, Sanker, L, Sano, T, Sanz, M, Saparbu, T, Sawhney, R, Sayed, F, Sayed, S, Sayed, A, Sayed, M, Sebastiani, G, Secadas, L, Sediqi, K, Seif, S, Semida, N, Senates, E, Serban, E, Serfaty, L, Seto, W, Sghaier, I, Sha, M, Shabaan, H, Shalaby, L, Shaltout, I, Sharara, A, Sharma, V, Shawa, I, Shawkat, A, Shawky, N, Shehata, O, Sheils, S, Shewaye, A, Shi, G, Shi, J, Shimose, S, Shirono, T, Shou, L, Shrestha, A, Shui, G, Sievert, W, Sigurdardottir, S, Sira, M, Siradj, R, Sison, C, Smyth, L, Soliman, R, Sollano, J, Sombie, R, Sonderup, M, Sood, S, Soriano, G, Stedman, C, Stefanyuk, O, Stimac, D, Strasser, S, Strnad, P, Stuart, K, Su, W, Su, M, Sumida, Y, Sumie, S, Sun, D, Sun, J, Suzuki, H, Svegliati-Baroni, G, Swar, M, Taharboucht, S, Taher, Z, Takamura, S, Tan, L, Tan, S, Tanwandee, T, Tarek, S, Tatiana, G, Tavaglione, F, Tecson, G, Tee, H, Teschke, R, Tharwat, M, Thong, V, Thursz, M, Tine, T, Tiribelli, C, Tolmane, I, Tong, J, Tongo, M, Torkie, M, Torre, A, Torres, E, Trajkovska, M, Treeprasertsuk, S, Tsutsumi, T, Tu, T, Tur, J, Turan, D, Turcan, S, Turkina, S, Tutar, E, Tzeuton, C, Ugiagbe, R, Uygun, A, Vacca, M, Vajro, P, Van der Poorten, D, Van Kleef, L, Vashakidze, E, Velazquez, C, Velazquez, M, Vento, S, Verhoeven, V, Vespasiani-Gentilucci, U, Vethakkan, S, Vilaseca, J, Vitek, L, Volkanovska, A, Wallace, M, Wan, W, Wang, Y, Wang, X, Wang, C, Wang, M, Wangchuk, P, Weltman, M, White, M, Wiegand, J, Wifi, M, Wigg, A, Wilhelmi, M, William, R, Wittenburg, H, Wu, S, Wubeneh, A, Xia, H, Xiao, J, Xiao, X, Xiaofeng, W, Xiong, W, Xu, L, Xu, J, Xu, W, Xu, K, Xu, Y, Xu, S, Xu, M, Xu, A, Xu, C, Yan, H, Yang, J, Yang, R, Yang, Y, Yang, Q, Yang, N, Yao, J, Yara, J, Yaras, S, Yilmaz, N, Younes, R, Younes, H, Young, S, Youssef, F, Yu, Y, Yu, M, Yuan, J, Yue, Z, Yuen, M, Yun, W, Yurukova, N, Zakaria, S, Zaky, S, Zaldastanishvili, M, Zapata, R, Zare, N, Zerem, E, Zeriban, N, Zeshuai, X, Zhang, H, Zhang, X, Zhang, Y, Zhang, W, Zhang, Z, Zhao, J, Zhao, R, Zhao, H, Zheng, C, Zheng, Y, Zheng, R, Zheng, T, Zheng, K, Zhou, X, Zhou, Y, Zhou, H, Zhou, L, Zhu, L, Zhu, Y, Zhu, P, Ziada, E, Ziring, D, Ziyi, L, Zou, S, Zou, Z, Zou, H, Zuart Ruiz, R, and Global Multi-Stakeholder Consensus on the Redefinition of Fatty Liver Disease

Subjects
Renal disorders Radboud Institute for Molecular Life Sciences [Radboudumc 11], Hepatology, Non-alcoholic Fatty Liver Disease, NAFLD, consensu, Gastroenterology, MAFLD, definition, Humans, MAFLD, NAFLD, Human medicine
Abstract

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Published
2022
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14. A Randomized Trial with Two Hypocaloric Diets with Different Lipid Profiles and Effects on Serum Omentin-1 Levels in Obese Subjects

Author

Daniel de Luis, Olatz Izaola, David Primo, and Rocio Aller

Subjects
Male, Article Subject, Diet, Reducing, Biochemistry (medical), Clinical Biochemistry, General Medicine, Middle Aged, Diet, High-Fat, GPI-Linked Proteins, Body Mass Index, Adipokines, Lectins, Weight Loss, Genetics, Cytokines, Humans, Insulin, Female, Obesity, Molecular Biology
Abstract

Background. The effects of weight loss therapies on omentin-1 levels have been unclear, showing both elevations and decreases in circulating levels. The role of dietary fat might have an important role. The aim of our investigation was to evaluate the influence of weight decrease on omentin-1 levels after two different high-fat hypocaloric diets. Methods. 319 Caucasian obese subjects were randomly allocated during 12 weeks (Diet M (high monounsaturated fat diet) vs. Diet P (high polyunsaturated fat diet)). The mean age was 47.2 ± 5.0 years (range: 26-64), and the mean body mass index (BMI) was 37.9 ± 4.1 kg/m2 (range: 30.6-39.8). Sex distribution was 237 females (74.7%) and 72 males (25.3%). Anthropometric and biochemical parameters were evaluated at basal and after both diets. SPSS 23.0 has been used to realize univariant and multivariant statistical analysis. Results. After both diets, BMI, weight, fat mass, waist circumference, systolic blood, LDL-cholesterol, insulin levels, and HOMA-IR decreased in a statistical way from basal values. These improvements were similar in both diets. After Diet P, omentin-1 levels increase ( 21.2 ± 9.1 ng/ml: P = 0.02 ), and after Diet M, this adipokine increases ( 47.1 ± 11.2 ng/ml: P = 0.02 ), too. The increase of omentin-1 with Diet M was statistically significantly higher than that after Diet P ( P = 0.01 ). A multiple regression analyses adjusted by age and sex reported a statistical relation between BMI (kg/m2) and insulin (UI/L) with omentin-1 levels. Conclusions. Our study demonstrated a significant improvement on serum omentin-1 levels after weight loss secondary to both diets; in contrast, omentin-1 improvement was higher with Diet M than with Diet P.

Published
2021

15. Type 2 Diabetes and Metformin Use Associate With Outcomes of Patients With Nonalcoholic Steatohepatitis-Related, Child-Pugh A Cirrhosis

Author

Mohammed Eslam, Luis Calzadilla-Bertot, Rocio Aller-de la Fuente, Eduardo Vilar-Gomez, Leon A. Adams, Vincent Wai-Sun Wong, Manuel Romero-Gómez, Marlen Castellanos, Grace Lai-Hung Wong, and Jacob George

Subjects
Liver Cirrhosis, medicine.medical_specialty, Cirrhosis, Carcinoma, Hepatocellular, Type 2 diabetes, Encephalopathy, Chronic liver disease, Gastroenterology, Chemoprevention, 03 medical and health sciences, 0302 clinical medicine, Non-alcoholic Fatty Liver Disease, Internal medicine, Diabetes mellitus, Nonalcoholic fatty liver disease, Glucose Intolerance, medicine, Humans, Decompensation, Hepatology, business.industry, Hazard ratio, Liver Neoplasms, Type 2 Diabetes Mellitus, Ascites, medicine.disease, Metformin, Fatty Liver, Diabetes Mellitus, Type 2, 030220 oncology & carcinogenesis, 030211 gastroenterology & hepatology, business
Abstract

Background & Aims Factors that affect outcomes of patients with nonalcoholic steatohepatitis (NASH)-related cirrhosis are unclear. We studied associations of type 2 diabetes, levels of hemoglobin A1c (HbA1c), and use of antidiabetic medications with survival and liver-related events in patients with NASH and compensated cirrhosis. Methods We collected data from 299 patients with biopsy-proven NASH with Child–Pugh A cirrhosis from tertiary hospitals in Spain, Australia, Hong Kong, and Cuba, from April 1995 through December 2016. We obtained information on the presence of type 2 diabetes, level of HbA1c, and use of antidiabetic medications. Cox proportional and competing risk models were used to estimate and compare rates of transplant-free survival, hepatic decompensation, and hepatocellular carcinoma (HCC). Results A total of 212 patients had type 2 diabetes at baseline and 8 of 87 patients developed diabetes during a median follow-up time of 5.1 years (range, 0.5–10.0 y). A lower proportion of patients with diabetes survived the entire follow-up period (38%) than of patients with no diabetes (81%) (adjusted hazard ratio [aHR], 4.23; 95% CI, 1.93–9.29). Higher proportions of patients with diabetes also had hepatic decompensation (51% vs 26% of patients with no diabetes; aHR, 2.03; 95% CI, 1.005–4.11) and HCC (25% vs 7% of patients with no diabetes; aHR, 5.42; 95% CI, 1.74–16.80). Averaged annual HbA1c levels over time were not associated with outcomes. Metformin use over time was associated with a significant reduction in risk of death or liver transplantation (aHR, 0.41; 95% CI, 0.26–0.45), hepatic decompensation (aHR, 0.80; 95% CI, 0.74–0.97), and HCC (aHR, 0.78; 95% CI, 0.69–0.96). Metformin significantly reduced the risk of hepatic decompensation and HCC only in subjects with HbA1c levels greater than 7.0% (aHR, 0.97; 95% CI, 0.95–0.99 and aHR, 0.67; 95% CI, 0.43–0.94, respectively). Conclusions In an international cohort of patients with biopsy-proven NASH and Child–Pugh A cirrhosis, type 2 diabetes increased the risk of death and liver-related outcomes, including HCC. Patients who took metformin had higher rates of survival and lower rates of decompensation and HCC.

Published
2020

16. [Multidisciplinary methodology and ketogenic diet in real clinical practice: efficacy and rapidity in weight loss. Survival Analysis PROMET Lipoinflammation study]

Author

Germán, Guzmán, Ignacio, Sajoux, Rocio, Aller, Olatz, Izaola, and Daniel, de Luis

Subjects
Adult, Male, Adolescent, Diet, Reducing, Body Weight, Age Factors, Guidelines as Topic, Kaplan-Meier Estimate, Middle Aged, Overweight, Survival Analysis, Young Adult, Sex Factors, Treatment Outcome, Weight Loss, Humans, Female, Obesity, Diet, Ketogenic, Exercise, Aged
Abstract

Objective: the aim of the current work was to evaluate the response time to a method of weight loss that includes dietary guidelines, physical exercise and emotional support. The response was defined as a loss of 10% of the baseline weight. Methods: data was obtained from the patients' record recruited in Promet Lipoinflamación, an observational study of real world data in obese or overweight patients treated with a multidisciplinary method and based initially on a very-low-calorie ketogenic (VLCK) diet. Weight loss rate was evaluated through a survival analysis Kaplan-Meier and related factors through Cox regression). Results: 6,369 subjects were included and 74.4% managed to reach a weight loss of 10% in a mean time of 57.64 days (IC 95%: 56.95-58.33). The factors associated with a greater probability of reaching a loss of 10% or more were male gender (RR: 1.37, p0.001), obesity types I, II and III vs. overweight (RR: 1.24, p0.001, 1.26, p0.001 and 1.22, p0.001, respectively) and young age vs. more than 55 years old (RR: 2.17, p0.001). Conclusion: Results obtained through real clinical practice show that the method produces fast and intense weight loss. Three out of four patients lost at least 10% of body weight in an average of 58 days.Objetivo: el objetivo del estudio fue evaluar el tiempo de respuesta, definido como pérdida del 10% del peso, al tratamiento con un método multidisciplinar de pérdida de peso que incluye dieta (inicialmente cetogénica), ejercicio físico y soporte emocional. Métodos: los datos se obtuvieron a partir del registro de pacientes reclutados en el estudio Promet Lipoinflamación, un estudio observacional de práctica clínica real en pacientes obesos o con sobrepeso tratados con el método multidisciplinar, basado inicialmente en una dieta cetogénica de muy bajas calorías. La velocidad se valoró mediante un análisis de supervivencia Kaplan-Meier y los factores asociados mediante regresión de Cox. Resultados: la muestra estudiada fue de 6369 sujetos. El 74,4% consiguió alcanzar una pérdida de peso del 10% en una media de tiempo de 57,64 días (IC 95%: 56,95-58,33]. Los factores asociados a mayor probabilidad de alcanzar pérdida del 10% o más fueron género masculino (RR: 1,37; p0,001), obesidad de tipos I, II y III frente a sobrepeso (RR: 1,24; p0,001; 1,26; p0,001 y 1,22; p0,001, respectivamente) y edad joven frente a mayor de 55 años (RR: 2,17; p0,001). Conclusiones: los resultados obtenidos a través de la práctica clínica real muestran que el método produce una pérdida de peso rápida e intensa. Tres de cada cuatro pacientes perdieron, como mínimo, el 10% del peso corporal en una media de 58 días.

Published
2020

18. Association of the rs10830963 polymorphism in MTNR1B with fasting glucose, serum adipokine levels and components of metabolic syndrome in adult obese subjects

Author

Daniel Antonio, de Luis Román, David, Primo, Rocio, Aller, and Olatz, Izaola

Subjects
Adult, Blood Glucose, Male, Metabolic Syndrome, Polymorphism, Genetic, Anthropometry, Genotype, Receptor, Melatonin, MT2, Blood Pressure, Middle Aged, Lipids, C-Reactive Protein, Adipokines, Diabetes Mellitus, Type 2, Humans, Insulin, Female, Obesity, Insulin Resistance, Aged
Abstract

Background and objectives: the aim of the present investigation was to describe the association of this single nucleotide polymorphism (SNP) with fasting glucose levels, serum adipokine levels and diabetes mellitus. Methods: the study involved a population of 1,002 adult obese subjects. Measurements of anthropometric parameters, blood pressure, fasting blood glucose, C-reactive protein (CRP), insulin concentration, insulin resistance (HOMA-IR), HOMA-B, lipid profi le and adipocytokines levels were performed. Genotype of MTNR1B gene polymorphism (rs10830963) was evaluated. Results: fasting glucose levels (GG: 101.5 ± 19.1 mg/dl vs GT: 103.5 ± 8.1 units vs TT: 107.2 ± 8.0 mg/dl; p = 0.01) and HOMA-IR (GG: 3.1 ± 1.6 units vs GT: 3.4 ± 1.1 units vs TT: 3.7 ± 1.0 units; p = 0.02) were higher in subjects with GG genotype than in other genotypes. Total adiponectin levels (CC: 20.5 ± 8.4 ng/dl vs CG: 21.8 ± 5.4 ng/dl vs GG: 15.4 ± 1.4 ng/dl; p = 0.02) and HOMA-B (CC: 2.3 ± 0.8 units vs CG: 2.2 ± 1.1 units vs GG: 1.9 ± 0.9 units; p = 0.01) were lower in subjects with GG genotype than GC or CC genotypes. Logistic regression analysis showed an increased risk of hyperglicemia (OR = 1.31, 95% CI = 1.12-2.78, p = 0.03) and diabetes mellitus (OR = 1.37, 95% CI = 1.14-2.86, p = 0.04). Conclusions: this study showed that the MTNR1B rs10830963 polymorphism was associated with increased fasting glucose levels, HOMA-IR, and risk of DM2. This SNP was associated with decreased adiponectin levels and HOMA-B.Introducción y objetivos: el objetivo de la presente investigación fue describir la asociación del polimorfi smo del gen MTNR1B (rs10830963) con los niveles de glucosa en ayunas, los niveles séricos de adipocitoquinas y la diabetes mellitus. Métodos: el estudio incluyó una población de 1.002 adultos obesos. Se realizó la determinación de parámetros antropométricos, presión arterial, glucosa en sangre en ayunas, proteína C reactiva (CRP), concentración de insulina, resistencia a la insulina (HOMA-IR), HOMA-B, perfil lipídico y niveles de adipocitoquinas. Se evaluó el genotipo del polimorfi smo del gen MTNR1B (rs10830963). Resultados: los niveles de glucosa en ayunas (GG: 101,5 ± 19,1 mg/dl vs. GT: 103,5 ± 8,1 unidades vs. TT: 107,2 ± 8,0 mg/dl; p = 0,01) y HOMA-IR (GG: 3,1 ± 1,6 unidades vs. GT: 3,4 ± 1,1 unidades vs. TT: 3,7 ± 1,0 unidades, p = 0,02) fueron más altos en sujetos con genotipo GG que en otros genotipos. Los niveles totales de adiponectina (CC: 20,5 ± 8,4 ng/dl vs. CG: 21,8 ± 5,4 ng/dl vs. GG: 15,4 ± 1,4 ng/dl, p = 0,02) y HOMA-B (CC: 2,3 ± 0,8 unidades vs. CG: 2,2 ± 1,1 unidades frente a GG: 1,9 ± 0,9 unidades, p = 0,01) fueron menores en sujetos con genotipo GG que en genotipos GC o CC. El análisis de regresión logística mostró un mayor riesgo de hiperglicemia (OR = 1,31, IC 95% = 1,12-2,78, p = 0,03) y diabetes mellitus (OR = 1,37, IC 95% = 1,14-2,86, p = 0,04). Conclusiones: este estudio mostró que el polimorfi smo MTNR1B rs10830963 se asoció con un aumento de los niveles de glucosa en ayunas, HOMA-IR y riesgo de DM2. Este SNP se asoció con niveles de adiponectina disminuidos y HOMA-B.

Published
2019

19. THU076 - The metabolic dysfunction-associated fatty liver disease definition, regardless of its clinical subclassification, identifies patients at high risk for liver disease progression

Author

Del Barrio Azaceta, María, Iruzubieta, Paula, de la Fuente, Rocio Aller, Banales, Jesus Maria, Santos-Laso, Álvaro, Calleja Panero, José Luis, Ibañez, Luis, Arias Loste, María Teresa, Gomez, Manuel Romero, García-Monzón, Carmelo, Gómez-Camarero, Judith, Ginès, Pere, Morillas, Rosa M, Pericàs, Juan Manuel, Aspichueta, Patricia, Martin-Mateos, Rosa, Gallego-Durán, Rocío, De La Torre Sanchez, Mercedes, Escudero-García, Desamparados, Monterde, Vanesa Bernal, Benlloch, Salvador, Turnes, Juan, and Crespo, Javier

Published
2022
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20. THU074 - Metabolic dysfunction-associated fatty liver disease increases cardiovascular risk regardless of classical risk factors

Author

Del Barrio Azaceta, María, Iruzubieta, Paula, De La Fuente, Rocio Aller, Banales, Jesus Maria, Santos-Laso, Álvaro, Calleja Panero, José Luis, Ibañez, Luis, Arias Loste, María Teresa, Gomez, Manuel Romero, García-Monzón, Carmelo, Gómez-Camarero, Judith, Ginès, Pere, Morillas, Rosa M, Pericàs, Juan Manuel, Aspichueta, Patricia, Martin-Mateos, Rosa, Gallego-Durán, Rocío, De La Torre Sanchez, Mercedes, Escudero-García, Desamparados, Monterde, Vanesa Bernal, Benlloch, Salvador, Turnes, Juan, and Crespo, Javier

Published
2022
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21. Metabolomic-based noninvasive serum test to diagnose nonalcoholic steatohepatitis: Results from discovery and validation cohorts

Author

Arun J. Sanyal, Jan Stritesky, Antonio Martín-Duce, Shelly C. Lu, Manuel Romero-Gómez, Mayte Arias, Javier Crespo, M. Luz Martínez-Chantar, Itziar Mincholé, Pablo Ortiz, Rocio Aller-de la Fuente, Joan Caballería, Cristina Alonso, José M. Mato, Michael O. Idowu, Radan Bruha, Rebeca Mayo, José Ignacio Busteros‐Moraza, D.A. de Luis, Jesus M. Banales, Raul Jimenez-Agüero, Jose Maria Mugüerza Huguet, Ibon Martínez-Arranz, Pierre Bedossa, Mazen Noureddin, A. Castro, and Libor Vítek

Subjects
0301 basic medicine, obesity, medicine.medical_specialty, Chronic Liver Disease and Cirrhosis, Chronic liver disease, Gastroenterology, digestive system, Oral and gastrointestinal, Hepatitis, histology, 03 medical and health sciences, 0302 clinical medicine, Clinical Research, Internal medicine, Nonalcoholic fatty liver disease, medicine, biopsy, Hepatology, medicine.diagnostic_test, Receiver operating characteristic, business.industry, hepatic steatosis, Liver Disease, fibrosis, Fatty liver, association, nutritional and metabolic diseases, Original Articles, Gold standard (test), medicine.disease, digestive system diseases, 3. Good health, 030104 developmental biology, fatty liver-disease, Liver biopsy, epidemiology, Original Article, 030211 gastroenterology & hepatology, Steatosis, Digestive Diseases, business, performance, magnetic-resonance elastography
Abstract

Nonalcoholic fatty liver disease (NAFLD) is the most common type of chronic liver disease worldwide and includes a broad spectrum of histologic phenotypes, ranging from simple hepatic steatosis or nonalcoholic fatty liver (NAFL) to nonalcoholic steatohepatitis (NASH). While liver biopsy is the reference gold standard for NAFLD diagnosis and staging, it has limitations due to its sampling variability, invasive nature, and high cost. Thus, there is a need for noninvasive biomarkers that are robust, reliable, and cost effective. In this study, we measured 540 lipids and amino acids in serum samples from biopsy-proven subjects with normal liver (NL), NAFL, and NASH. Using logistic regression analysis, we identified two panels of triglycerides that could first discriminate between NAFLD and NL and second between NASH and NAFL. These noninvasive tests were compared to blinded histology as a reference standard. We performed these tests in an original cohort of 467 patients with NAFLD (90 NL, 246 NAFL, and 131 NASH) that was subsequently validated in a separate cohort of 192 patients (7 NL, 109 NAFL, 76 NASH). The diagnostic performances of the validated tests showed an area under the receiver operating characteristic curve, sensitivity, and specificity of 0.88 +/- 0.05, 0.94, and 0.57, respectively, for the discrimination between NAFLD and NL and 0.79 +/- 0.04, 0.70, and 0.81, respectively, for the discrimination between NASH and NAFL. When the analysis was performed excluding patients with glucose levels >136 mg/dL, the area under the receiver operating characteristic curve for the discrimination between NASH and NAFL increased to 0.81 +/- 0.04 with sensitivity and specificity of 0.73 and 0.80, respectively. Conclusion: The assessed noninvasive lipidomic serum tests distinguish between NAFLD and NL and between NASH and NAFL with high accuracy. Supported by the National Institutes of Health Blueprint for Neuroscience Research (R01AT001576 to S.C.L., J.M.M.), Agencia Estatal de Investigacion of the Ministerio de Economia, Industria y Competitividad (SAF2014-52097R to J.M.M.), CIBER Hepatic and Digestive Diseases and Instituto de Salud Carlos III (PIE14/0003 to J.M.M.), Etorgai 2015-Gobierno Vasco (ER-2015/00015 to R.M., I.M.A., C.A., A.C.), Plan de Promocion de la Innovacion 2015-Diputacion Foral de Bizkaia (6/12/IN/2015/00131 to A.C., C.A.), National Institute of Diabetes and Digestive and Kidney Diseases (RO1DK81410 to A.J.S.), and Czech Ministry of Health (RVO VFN64165 to L.V.).

Published
2018

22. Polymorphism rs16147 of the Neuropeptide Y Gene Modifies the Response of Cardiovascular Risk Biomarkers and Adipokines to Two Hypocaloric Diets

Author

Daniel Antonio, de Luis, Olatz, Izaola, David, Primo, and Rocio, Aller

Subjects
Adult, Genetic Markers, Male, Diet, Reducing, Middle Aged, Polymorphism, Single Nucleotide, Diet, Carbohydrate-Restricted, Nutrigenomics, Adipokines, Cardiovascular Diseases, Risk Factors, Weight Loss, Humans, Insulin, Female, Neuropeptide Y, Obesity, Prospective Studies, Insulin Resistance, Diet, Fat-Restricted
Abstract

Our aim was to evaluate the relationship of weight loss and changes in adipokine levels after two hypocaloric diets in obese subjects with polymorphism rs16147 of the neuropeptide Y gene.A population of 283 obese patients was analyzed. At the basal visit, patients were randomly allocated to one of two diets for a period of 3 months (diet I, low in carbohydrates; diet II, low in fat).With diet I and in both genotype groups (major versus minor allele), body mass index (BMI), weight, fat mass, waist circumference, and leptin decreased. With diet II and in all genotypes, BMI, weight, fat mass, waist circumference, and leptin decreased. With both diets and in subjects with the minor allele, insulin levels (diet I: major allele -1.7 ± 7.8 IU/L versus minor allele -4.2 ± 6.1 IU/L, p = 0.01; diet II: major allele -2.3 ± 6.1 IU/L versus minor allele -4.0 ± 5.2 IU/L, p = 0.02) and insulin resistance (diet I: major allele -0.2 ± 3.1 units versus minor allele -1.7 ± 3.0 units, p = 0.03; diet II: major allele -0.9 ± 2.0 units versus minor allele -1.7 ± 1.3 units, p = 0.01) decreased.The rs16147 genotype affected the reduction in insulin resistance and insulin levels in response to two different hypocaloric diets in obese subjects, with a lack of response in subjects with the major allele.

Published
2017

23. Fibrosis Severity as a Determinant of Cause-Specific Mortality in Patients With Advanced Nonalcoholic Fatty Liver Disease: A Multi-National Cohort Study

Author

Anthony W.H. Chan, Mayada Metwally, Mohammed Eslam, Luis Calzadilla-Bertot, María Alvarez-Quiñones Sanz, Naga Chalasani, Duncan McLeod, Antonio Felix Conde-Martin, Bastiaan De Boer, Rocio Aller-de la Fuente, Jacob George, Licet Gonzalez-Fabian, Eduardo Vilar-Gomez, Manuel Romero-Gómez, Marlen Castellanos, Vincent Wai-Sun Wong, and Leon A. Adams

Subjects
Liver Cirrhosis, Male, 0301 basic medicine, medicine.medical_specialty, Carcinoma, Hepatocellular, Cirrhosis, Biopsy, medicine.medical_treatment, Nonalcoholic Steatohepatitis, Liver transplantation, Severity of Illness Index, Gastroenterology, 03 medical and health sciences, 0302 clinical medicine, Model for End-Stage Liver Disease, Non-alcoholic Fatty Liver Disease, Internal medicine, Nonalcoholic fatty liver disease, Humans, Medicine, Decompensation, Cumulative incidence, Competing Risk Analysis, Aged, Hepatology, medicine.diagnostic_test, business.industry, Incidence, Liver Neoplasms, Middle Aged, Gastroesophageal Varices, medicine.disease, Liver Transplantation, Transplantation, Editorial, 030104 developmental biology, Liver, Cryptogenic Cirrhosis, Cardiovascular Diseases, Liver biopsy, Disease Progression, Female, 030211 gastroenterology & hepatology, business, Follow-Up Studies
Abstract

Little is known about the natural course of nonalcoholic fatty liver disease (NAFLD) with advanced fibrosis. We describe long-term outcomes and evaluate the effects of clinical and histologic parameters on disease progression in patients with advanced NAFLD.We conducted a multi-national study of 458 patients with biopsy-confirmed NAFLD with bridging fibrosis (F3, n = 159) or compensated cirrhosis (222 patients with Child-Turcotte-Pugh scores of A5 and 77 patients with scores of A6), evaluated from April 1995 through November 2013 and followed until December 2016, death, or liver transplantation at hepatology centers in Spain, Australia, Hong Kong, and Cuba. Biopsies were re-evaluated and scored; demographic, clinical, laboratory, and pathology data for each patient were collected from the time of liver biopsy collection. Cox proportional and competing risk models were used to estimate rates of transplantation-free survival and major clinical events and to identify factors associated with outcomes.During a mean follow-up time of 5.5 years (range, 2.7-8.2 years), 37 patients died, 37 received liver transplants, 88 had initial hepatic decompensation events, 41 developed hepatocellular carcinoma, 14 had vascular events, and 30 developed nonhepatic cancers. A higher proportion of patients with F3 fibrosis survived transplantation-free for 10 years (94%; 95% confidence interval [CI], 86%-99%) than of patients with cirrhosis and Child-Turcotte-Pugh A5 (74%; 95% CI, 61%-89%) or Child-Turcotte-Pugh A6 (17%; 95% CI, 6%-29%). Patients with cirrhosis were more likely than patients with F3 fibrosis to have hepatic decompensation (44%; 95% CI, 32%-60% vs 6%, 95% CI, 2%-13%) or hepatocellular carcinoma (17%; 95% CI, 8%-31% vs 2.3%, 95% CI, 1%-12%). The cumulative incidence of vascular events was higher in patients with F3 fibrosis (7%; 95% CI, 3%-18%) than cirrhosis (2%; 95% CI, 0%-6%). The cumulative incidence of nonhepatic malignancies was higher in patients with F3 fibrosis (14%; 95% CI, 7%-23%) than cirrhosis (6%; 95% CI, 2%-15%). Death or transplantation, decompensation, and hepatocellular carcinoma were independently associated with baseline cirrhosis and mild (33%) steatosis, whereas moderate alcohol consumption was associated with these outcomes only in patients with cirrhosis.Patients with NAFLD cirrhosis have predominantly liver-related events, whereas those with bridging fibrosis have predominantly nonhepatic cancers and vascular events.

Published
2018
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24. [ASSESSMENT OF THE GENETIC MODIFICATION INDUCING DIET THROUGH BLOOD MONONUCLEAR CELLS]

Author

Daniel Antonio, de Luis Román, Olatz, Izaola, and Rocio, Aller

Subjects
Nutrigenomics, Animals, Gene Expression, Humans, Nutritional Status, Nutritional Physiological Phenomena, Monocytes, Diet
Abstract

The term nutrigenomics was created to describe how nutrition affects genes and the functions of the protein, at the transcriptional level, proteomic, and metabolic. Using changes in gene expression in blood mononuclear cells could be a model to assess the dietary intervention studies in order to understand the underlying mechanisms and impact of diet and nutrients in atherosclerosis, resistance insulin, obesity and diabetes mellitus. There are studies that have changed the dietary intake of cholesterol, polyunsaturated fat, monounsaturated, antioxidants and decreased caloric intake showing a variety of effects on the expression of mRNA in blood mononuclear cells related to inflammation, immunity, lipid metabolism genes, etc. These molecular findings entrench awareness of our body's response to diet and open up the possibility of rapid analysis of new diagnostic pathways in this area of knowledge and even new therapeutic tools.El término nutrigenómica fue creado para describir cómo la nutrición afecta a los genes y a las funciones de la proteínas, a nivel transcripcional, proteómico y metabólico. El uso de las modificaciones en la expresión génica en las células mononucleares sanguíneas (CMNS) podría ser un modelo que permita evaluar los estudios de intervención dietética con el objetivo de comprender los mecanismos subyacentes y la influencia de la dieta y los nutrientes en la aterosclerosis, la resistencia a la insulina, la obesidad y la diabetes mellitus. Existen trabajos que han modificado el aporte dietético de colesterol, grasas poliinsaturadas, grasas monoinsaturadas y antioxidantes, y disminuido el aporte calórico, mostrando una gran variedad de efectos sobre la expresión de RNAm en CMNS de genes relacionados con la inflamación, la inmunidad, el metabolismo lípidico, etc. Estos hallazgos moleculares afianzan el conocimiento sobre la respuesta de nuestro organismo a la dieta y abren la posibilidad del análisis rápido de nuevas vías diagnósticas e incluso de nuevas herramientas terapéuticas.

Published
2015

25. Surgical infection and malnutrition

Author

Daniel A, de Luis, Jesus M, Culebras, Rocio, Aller, and Jose María, Eiros-Bouza

Subjects
Postoperative Complications, Nutritional Support, Malnutrition, Humans, Bacterial Infections, Protein-Energy Malnutrition
Abstract

Malnutrition in surgical patients is associated with delayed recovery, higher rates of morbidity and mortality, prolonged hospital stay, increased healthcare costs and a higher early re-admission rate.Data synthesis after review of pertinent literature.The aetiology of malnutrition is multifactorial. In cancer patients, there is an abnormal peripheral glucose disposal, gluconeogenesis, and whole-body glucose turnover. Malnourished cancer patients undergoing major operations are at significant risk from perioperative complications such as infectious complications. Surgical aggression generates an inflammatory response which worsens intermediary metabolism.Nutritional evaluation and nutritional support must be performed in all surgical patients, in order to minimize infectious complications. Enteral nutrition early in the postoperative period is effective and well tolerated reducing infectious complications, improving wound healing and reducing length of hospital stay. Pharmaconutrition is indicated in those patients, who benefit from enteral administration of arginine, omega 3 and RNA, as well as parenteral glutamine supplementation. When proximal sutures are used, tubes allowing early jejunal feeding should be used.La malnutrición en pacientes quirúrgicos está relacionada con un retraso en la recuperación, tasas más elevadas de morbilidad y mortalidad, estancia hospitalaria prolongada, mayores costes de atención sanitaria y una tasa más elevada de re-hospitalización temprana.Síntesis de datos tras la revisión de la bibliografía pertinente.La etiología de la malnutrición es multifactorial. En pacientes con cáncer, existe una alteración en la utilización de la glucosa periférica, en la gluconeogénesis, y en la producción de glucosa en todo el cuerpo. Los pacientes con cáncer que se someten a operaciones mayores tienen un riesgo significativo de complicaciones perioperativas, como es el caso de las complicaciones de tipo infeccioso. La agresión quirúrgica genera una respuesta inflamatoria que empeora el metabolismo intermediario.Es necesario realizar una evaluación nutricional y llevar a cabo un soporte nutricional en todos los pacientes quirúrgicos con el fin de minimizar las posibles complicaciones infecciosas. La nutrición enteral justo al inicio del periodo postoperatorio es bien tolerada y resulta eficaz a la hora de reducir complicaciones infecciosas, mejorando el proceso de curación de la herida y la duración de la estancia hospitalaria. La nutrición farmacológica está indicada en pacientes que reciben administración enteral de arginina, omega 3 y ARN, además de suplementación por vía parenteral. Cuando se utilizan suturas proximales, se deben emplear sondas que permitan una alimentación yeyunal temprana.

Published
2014

26. Surgical infection and malnutrition

Author

Daniel A. de Luis, Jesus M. Culebras, Rocio Aller, and Jose Maria Eiros-Bouza

Subjects
Infection disease, lcsh:Nutritional diseases. Deficiency diseases, Suergery, Nutrición, Cirugía, Complicación infecciosa, lcsh:RC620-627, Nutrition
Abstract

Background: Malnutrition in surgical patients is associated with delayed recovery, higher rates of morbidity and mortality, prolonged hospital stay, increased healthcare costs and a higher early re-admission rate. Methods: Data synthesis after review of pertinent literature. Results: The aetiology of malnutrition is multifactorial. In cancer patients, there is an abnormal peripheral glucose disposal, gluconeogenesis, and whole-body glucose turnover. Malnourished cancer patients undergoing major operations are at significant risk from perioperative complications such as infectious complications. Surgical aggression generates an inflammatory response which worsens intermediary metabolism. Conclusions: Nutritional evaluation and nutritional support must be performed in all surgical patients, in order to minimize infectious complications. Enteral nutrition early in the postoperative period is effective and well tolerated reducing infectious complications, improving wound healing and reducing length of hospital stay. Pharmaconutrition is indicated in those patients, who benefit from enteral administration of arginine, omega 3 and RNA, as well as parenteral glutamine supplementation. When proximal sutures are used, tubes allowing early jejunal feeding should be used.

Published
2014

27. Surgical infection and malnutrition

Author

Daniel A. de Luis, Jesus M. Culebras, Rocio Aller, and Jose Maria Eiros-Bouza

Subjects
Complicación infecciosa, Nutrición, Cirugía, Nutritional diseases. Deficiency diseases, RC620-627
Abstract

Background: Malnutrition in surgical patients is associated with delayed recovery, higher rates of morbidity and mortality, prolonged hospital stay, increased healthcare costs and a higher early re-admission rate. Methods: Data synthesis after review of pertinent literature. Results: The aetiology of malnutrition is multifactorial. In cancer patients, there is an abnormal peripheral glucose disposal, gluconeogenesis, and whole-body glucose turnover. Malnourished cancer patients undergoing major operations are at significant risk from perioperative complications such as infectious complications. Surgical aggression generates an inflammatory response which worsens intermediary metabolism. Conclusions: Nutritional evaluation and nutritional support must be performed in all surgical patients, in order to minimize infectious complications. Enteral nutrition early in the postoperative period is effective and well tolerated reducing infectious complications, improving wound healing and reducing length of hospital stay. Pharmaconutrition is indicated in those patients, who benefit from enteral administration of arginine, omega 3 and RNA, as well as parenteral glutamine supplementation. When proximal sutures are used, tubes allowing early jejunal feeding should be used.

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28. Relationship of -55C/T polymorphism of uncoupling protein 3 (UCP3) gene with metabolic syndrome by ATP III classification

Author

Daniel Antonio, de Luis, Rocio, Aller, Olatz, Izaola, Manuel Gonzalez, Sagrado, Rosa, Conde, David, Primo, Beatriz, de la Fuente, Hilda F, Ovalle, and Marta Ruiz, Mambrilla

Subjects
Adult, Male, Metabolic Syndrome, Middle Aged, Polymorphism, Single Nucleotide, Ion Channels, Statistics, Nonparametric, Mitochondrial Proteins, Cross-Sectional Studies, Adipokines, Risk Factors, Odds Ratio, Humans, Uncoupling Protein 3, Body Weights and Measures, Female, Obesity, Research Articles
Abstract

BACKGROUND AND AIMS: The relation of ‐55C/T polymorphism of uncoupling protein 3 (UCP3) with metabolic syndrome (MS) has been evaluated only in one previous study with contradictory results. The aim of our study was to investigate the association of ‐55C/T polymorphism of UCP3 gene with MS. DESIGN: A population of 817 obese Caucasian patients was analyzed in a cross‐sectional survey. Genotype of UCP3 gene ‐55C/T was studied. To estimate the prevalence of MS , the definitions of the ATPIII were considered. RESULTS: Five hundred and ninety‐four patients (72.7%) had the genotype ‐55CC (wild group), whereas 223 patients (27.3%) had the genotype ‐55C/T. Genotype ‐5TT was not detected. Prevalence of mutant UCP genotypes was similar in patients with MS (75.7% wild genotype and 24.3% mutant genotype) and without MS (69.7% wild genotype and 30.3% mutant genotype). Odds ratio of MS wild vs. mutant genotype was 1.17 CI 95%: 0.99–1.38). Total cholesterol and low density lipoprotein (LDL) cholesterol concentrations were lower in mutant‐type group than wild‐type group in patients with MS. No differences in other parameters were detected between genotypes in the same group of MS. CONCLUSION: ‐55C/T UCP polymorphism is not major risk factor for the MS. However, in mutant group of ‐55CC UCP3 gene in patients with MS, total cholesterol and LDL cholesterol were lower than wild‐type patients. J. Clin. Lab. Anal. 26:272‐278, 2012. © 2012 Wiley Periodicals, Inc.

Published
2012

29. Increased Th1, Th17 and pro-fibrotic responses in hepatitis C-infected patients are down-regulated after 12 weeks of treatment with pegylated interferon plus ribavirin

Author

Maria Angeles, Jimenez-Sousa, Raquel, Almansa, Concha, de la Fuente, Agustín, Caro-Paton, Lourdes, Ruiz, Gloria, Sanchez-Antolín, Jose Manuel, Gonzalez, Rocio, Aller, Noelia, Alcaide, Pilar, Largo, Salvador, Resino, Raul Ortiz, de Lejarazu, and Jesus F, Bermejo-Martin

Subjects
Down-Regulation, Interferon-alpha, T-Lymphocytes, Helper-Inducer, Interferon alpha-2, Viral Load, Antiviral Agents, Fibrosis, Hepatitis C, Recombinant Proteins, Polyethylene Glycols, Case-Control Studies, Ribavirin, Cytokines, Humans, Drug Therapy, Combination, Chemokines
Abstract

Hepatitis C virus causes significant morbidity and mortality worldwide. The infection induces up-regulation of cytokine and chemokines commonly linked to the development of cellular and pro-inflammatory antiviral responses. The current standard in hepatitis C treatment consists of combination regimens of pegylated interferon-alpha plus ribavirin. The impact of combined treatment in the host immune response is still poorly understood. In the present study, we profiled 27 cytokines, chemokines and growth factors involved in the innate and adaptive responses to the virus in the serum of 27 hepatitis C virus-infected patients, before and after 12 weeks of combined treatment, and compared them to 10 healthy controls. Hepatitis C virus infection induced not only the secretion of chemokines and cytokines participating in Th1 responses (MIP-1 alpha, IP-10, TNF-alpha, IL-12p70, IL-2), but also cytokines involved in the development of Th17 responses (IL-6, IL-8, IL-9 and IL-17) and two pro-fibrotic factors (FGF-b, VEGF). The most important increases included MIP-1 alpha (4.7-fold increase compared to the control group), TNF-alpha (3.0-fold), FGF-b (3.4-fold), VEGF (3.5-fold), IP-10 (3.6-fold), IL-17 (107.0-fold), IL-9 (7.5-fold), IL-12p70 (7.0-fold), IL-2 (5.6-fold) and IL-7 (5.6-fold). Combined treatment with pegylated interferon-alpha plus ribavirin down-modulated the secretion of key Th1 and Th17 pro-inflammatory mediators, and pro-fibrotic growth factors as early as 12 weeks after treatment initiation. MIP-1 alpha, FGF-b, IL-17 decreased in a more dramatic manner in the group of responder patients than in the group of non-responders (fold-change in cEVR; fold-change in NcEVR): MIP-1 alpha (4.72;1.71), FGF-b (4.54;1.21), IL-17 (107.1;1.8). Correlation studies demonstrated that the decreases in the levels of these mediators were significantly associated with each other, pointing to a coordinated effect of the treatment on their secretion (r coefficient; p value): [ FGF-b versus IL-17 (0.90; 0.00), IL-17 versus VEGF (0.88; 0.00), MIP-1 alpha versus IL-17 (0.84;0.00), FGF-b versus MIP-1 alpha (0.96;0.00), FGF-b versus IL-12p70 (0.90; 0.00), VEGF versus IL-12p70 (0.89; 0.00)]. Th17 immunity has been previously associated with autoimmune diseases and asthma, but this is the first work reporting a role for this profile in viral hepatitis. These results provide an opportunity to evaluate the impact of the treatment with Peg-INF-alpha and RBV on the prevention of immune-driven tissue damage in infected patients.

Published
2010

30. [The effects of a low-fat versus a low carbohydrate diet in obese adults]

Author

Daniel A, De Luis, Rocio, Aller, Olatz, Izaola, Manuel, González Sagrado, and Rosa, Conde

Subjects
Adult, Male, Diet, Carbohydrate-Restricted, Humans, Female, Obesity, Prospective Studies, Diet, Fat-Restricted
Abstract

The aim of our study was to compare the effect of a high fat and a high protein diet vs a fat restricted diet on weight loss in obese patients.A population of 74 obesity non diabetic outpatients was analyzed in a prospective way. Patients were randomly allocated to two groups: a) diet I (low fat diet: 1500kcal/day, 52% carbohydrates, 20% proteins, 27% fats) with a distribution of fats and b) diet II (high fat and high protein diet: 1507kcal/day, 38% carbohydrates, 26% proteins, 36% fats). After three months with diet, weight, blood pressure, glucose, C reactive protein, insulin, insulin resistance, total cholesterol, LDL-cholesterol, HDL-cholesterol and triglycerides were evaluated.There were randomized 35 patients (4 males and 31 females) in the group I and 39 patients (6 males and 33 females) in diet group II. In group I, systolic pressure, BMI, weight, fat free mass, fat mass total body water, intracellular body water and waist circumference decreased significantly. In group II, glucose, total cholesterol, LDL cholesterol, systolic blood, BMI, weight, fat mass, total body water and waist circumference decreased significantly. Differences among averages of parameters before treatment with both diets were not detected.No differences were detected on weight loss between a fat-restricted diet and a high fat and high protein enhanced diet.

Published
2007

32. Influence of Insulin Resistance and Adipokines in the Grade of Steatosis of Nonalcoholic Fatty Liver Disease.

Author

Rocio Aller, Daniel de Luis, Luis Fernandez, Fernando Calle, Benito Velayos, Jose Olcoz, Olatz Izaola, Manuel Sagrado, Rosa Conde, and Jose Gonzalez

Subjects
*FATTY degeneration, *ISOPENTENOIDS, *CLINICAL pathology, *DRUG resistance
Abstract

Abstract  The objective of this work was to study the influence of insulin resistance and adipokines on the grade of steatosis in patients with NAFLD (nonalcoholic fatty liver disease) diagnosed by liver biopsy. A sample of 24 NAFLD patients was analyzed in a cross-sectional study. All patients with a two-week weight-stabilization period before recruitment were enrolled. A liver biopsy was realized. Weight, basal glucose, insulin, insulin resistance (HOMA), total cholesterol, LDL-cholesterol, HDL-cholesterol, triglycerides, and adipokines blood levels were measured. A nutritional evaluation (dietary intake, indirect calorimetry, and bioimpedance) was performed. The mean age was 41.6 ± 8.7 years and the mean body mass index (BMI) 29.4 ± 4.7. Twelve patients had a low grade of steatosis (grade 1 of the Brunt classification) and 12 patients had a high grade of steatosis (grade 2 or 3). Only HOMA was higher in patients with a high grade of steatosis (1.4 ± 0.5 vs. 2.8 ± 1.7 units; P −1; P −1; P  [ABSTRACT FROM AUTHOR]

Published
2008
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33. Pathogenesis of occult chronic hepatitis B virus infection.

Author

de la Fuente RA, Gutiérrez ML, Garcia-Samaniego J, Fernández-Rodriguez C, Lledó JL, and Castellano G

Subjects
Animals, Biomarkers blood, DNA, Viral blood, Hepatitis B Surface Antigens blood, Hepatitis B virus genetics, Hepatitis B virus growth & development, Hepatitis B virus immunology, Hepatitis B, Chronic diagnosis, Hepatitis B, Chronic therapy, Hepatitis B, Chronic transmission, Hepatitis C Antibodies blood, Humans, Infectious Disease Transmission, Vertical, Risk Factors, Virus Activation, Virus Replication, Hepatitis B virus pathogenicity, Hepatitis B, Chronic virology, Liver virology
Abstract

Occult hepatitis B infection (OBI) is characterized by hepatitis B virus (HBV) DNA in serum in the absence of hepatitis B surface antigen (HBsAg) presenting HBsAg-negative and anti-HBc positive serological patterns. Occult HBV status is associated in some cases with mutant viruses undetectable by HBsAg assays; but more frequently it is due to a strong suppression of viral replication and gene expression. OBI is an entity with world-wide diffusion. The failure to detect HBsAg, despite the persistence of the viral DNA, is due in most cases to the strong suppression of viral replication and gene expression that characterizes this "occult" HBV infection; although the mechanisms responsible for suppression of HBV are not well understood. The majority of OBI cases are secondary to overt HBV infection and represent a residual low viremia level suppressed by a strong immune response together with histological derangements which occurred during acute or chronic HBV infection. Much evidence suggests that it can favour the progression of liver fibrosis and the development of hepatocellular carcinoma.

Published
2011
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