11 results on '"Egan, Josephine M"'
Search Results
2. Cannabinoids Regulate Bcl-2 and Cyclin D2 Expression in Pancreatic β Cells
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Kim, Jihye, primary, Lee, Kyung Jin, additional, Kim, Jung Seok, additional, Rho, Jun Gi, additional, Shin, Jung Jae, additional, Song, Woo Keun, additional, Lee, Eun Kyung, additional, Egan, Josephine M., additional, and Kim, Wook, additional
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- 2016
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3. Sustained exendin-4 secretion through gene therapy targeting salivary glands in two different rodent models of obesity/type 2 diabetes
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Miguel, López, Giovanni Di Pasquale, Ilaria, Dicembrini, Laura, Raimondi, Pagano, Claudio, Egan, Josephine M., Andrea, Cozzi, Lorenzo, Cinci, Andrea, Loreto, Manni, Maria E., Silvia, Berretti, Annamaria, Morelli, Changyu, Zheng, Michael, Drew G., Mario, Maggi, Vettor, Roberto, Chiorini, John A., Edoardo, Mannucci, and Rotella, Carlo M.
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Blood Glucose ,Male ,Anatomy and Physiology ,medicine.medical_treatment ,Gene Expression ,Adipose tissue ,Type 2 diabetes ,Weight Gain ,Biochemistry ,Salivary Glands ,Impaired glucose tolerance ,Mice ,Endocrinology ,Viral classification ,Receptors, Glucagon ,Glucose tolerance test ,Multidisciplinary ,Salivary gland ,medicine.diagnostic_test ,Neurochemistry ,Gene Therapy ,Dependovirus ,medicine.anatomical_structure ,Medicine ,Neurochemicals ,Research Article ,medicine.medical_specialty ,Science ,Genetic Vectors ,Adipokine ,Endocrine System ,Diet, High-Fat ,Microbiology ,Glucagon-Like Peptide-1 Receptor ,Virology ,Internal medicine ,Diabetes mellitus ,medicine ,Animals ,Humans ,Obesity ,Biology ,Nutrition ,Diabetic Endocrinology ,Clinical Genetics ,Endocrine Physiology ,Venoms ,business.industry ,Insulin ,Neuropeptides ,Genetic Therapy ,Glucose Tolerance Test ,Diabetes Mellitus Type 2 ,medicine.disease ,Hormones ,Rats ,Rats, Zucker ,Disease Models, Animal ,Diabetes Mellitus, Type 2 ,Exenatide ,Peptides ,DNA viruses ,business - Abstract
Exendin-4 (Ex-4) is a Glucagon-like peptide 1 (GLP-1) receptor agonist approved for the treatment of Type 2 Diabetes (T2DM), which requires daily subcutaneous administration. In T2DM patients, GLP-1 administration is reported to reduce glycaemia and HbA1c in association with a modest, but significant weight loss. The aim of present study was to characterize the site-specific profile and metabolic effects of Ex-4 levels expressed from salivary glands (SG) in vivo, following adeno-associated virus-mediated (AAV) gene therapy in two different animal models of obesity prone to impaired glucose tolerance and T2DM, specifically, Zucker fa/fa rats and high fed diet (HFD) mice. Following percutaneous injection of AAV5 into the salivary glands, biologically active Ex-4 was detected in the blood of both animal models and expression persisted in salivary gland ductal cell until the end of the study. In treated mice, Ex-4 levels averaged 138.9±42.3 pmol/L on week 6 and in treated rats, mean circulating Ex-4 levels were 238.2±72 pmol/L on week 4 and continued to increase through week 8. Expression of Ex-4 resulted in a significant decreased weight gain in both mice and rats, significant improvement in glycemic control and/or insulin sensitivity as well as visceral adipose tissue adipokine profile. In conclusion, these results suggest that sustained site-specific expression of Ex-4 following AAV5-mediated gene therapy is feasible and may be useful in the treatment of obesity as well as trigger improved metabolic profile.
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- 2012
4. Sustained Exendin-4 Secretion through Gene Therapy Targeting Salivary Glands in Two Different Rodent Models of Obesity/Type 2 Diabetes
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Di Pasquale, Giovanni, primary, Dicembrini, Ilaria, additional, Raimondi, Laura, additional, Pagano, Claudio, additional, Egan, Josephine M., additional, Cozzi, Andrea, additional, Cinci, Lorenzo, additional, Loreto, Andrea, additional, Manni, Maria E., additional, Berretti, Silvia, additional, Morelli, Annamaria, additional, Zheng, Changyu, additional, Michael, Drew G., additional, Maggi, Mario, additional, Vettor, Roberto, additional, Chiorini, John A., additional, Mannucci, Edoardo, additional, and Rotella, Carlo M., additional
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- 2012
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5. Insulin and Glucagon Regulate Pancreatic α-Cell Proliferation
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Liu, Zhuo, primary, Kim, Wook, additional, Chen, Zhike, additional, Shin, Yu-Kyong, additional, Carlson, Olga D., additional, Fiori, Jennifer L., additional, Xin, Li, additional, Napora, Joshua K., additional, Short, Ryan, additional, Odetunde, Juliana O., additional, Lao, Qizong, additional, and Egan, Josephine M., additional
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- 2011
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6. Ghrelin Is Produced in Taste Cells and Ghrelin Receptor Null Mice Show Reduced Taste Responsivity to Salty (NaCl) and Sour (Citric Acid) Tastants
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Shin, Yu-Kyong, primary, Martin, Bronwen, additional, Kim, Wook, additional, White, Caitlin M., additional, Ji, Sunggoan, additional, Sun, Yuxiang, additional, Smith, Roy G., additional, Sévigny, Jean, additional, Tschöp, Matthias H., additional, Maudsley, Stuart, additional, and Egan, Josephine M., additional
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- 2010
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7. Circulating Brain-Derived Neurotrophic Factor and Indices of Metabolic and Cardiovascular Health: Data from the Baltimore Longitudinal Study of Aging
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Golden, Erin, primary, Emiliano, Ana, additional, Maudsley, Stuart, additional, Windham, B. Gwen, additional, Carlson, Olga D., additional, Egan, Josephine M., additional, Driscoll, Ira, additional, Ferrucci, Luigi, additional, Martin, Bronwen, additional, and Mattson, Mark P., additional
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- 2010
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8. Bitter Taste Receptors Influence Glucose Homeostasis
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Dotson, Cedrick D., primary, Zhang, Lan, additional, Xu, Hong, additional, Shin, Yu-Kyong, additional, Vigues, Stephan, additional, Ott, Sandra H., additional, Elson, Amanda E. T., additional, Choi, Hyun Jin, additional, Shaw, Hillary, additional, Egan, Josephine M., additional, Mitchell, Braxton D., additional, Li, Xiaodong, additional, Steinle, Nanette I., additional, and Munger, Steven D., additional
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- 2008
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9. Conserved and Differential Effects of Dietary Energy Intake on the Hippocampal Transcriptomes of Females and Males
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Martin, Bronwen, primary, Pearson, Michele, additional, Brenneman, Randall, additional, Golden, Erin, additional, Keselman, Alex, additional, Iyun, Titilola, additional, Carlson, Olga D., additional, Egan, Josephine M., additional, Becker, Kevin G., additional, Wood, William, additional, Prabhu, Vinayakumar, additional, de Cabo, Rafael, additional, Maudsley, Stuart, additional, and Mattson, Mark P., additional
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- 2008
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10. Ghrelin Is Produced in Taste Cells and Ghrelin Receptor Null Mice Show Reduced Taste Responsivity to Salty (NaCl) and Sour (Citric Acid) Tastants.
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Yu-Kyong Shin, Martin, Bronwen, Wook Kim, White, Caitlin M., Sunggoan Ji, Yuxiang Sun, Smith, Roy G., évigny, Jean, Tschöp, Matthias H., Maudsley, Stuart, and Egan, Josephine M.
- Subjects
TASTE buds ,GHRELIN ,CELLS ,CITRIC acid ,SALT ,LABORATORY mice ,FOOD habits ,BARBEL (Anatomy) ,CHEMICAL senses - Abstract
Background: The gustatory system plays a critical role in determining food preferences, food intake and energy balance. The exact mechanisms that fine tune taste sensitivity are currently poorly defined, but it is clear that numerous factors such as efferent input and specific signal transduction cascades are involved. Methodology/Principal Findings: Using immunohistochemical analyses, we show that ghrelin, a hormone classically considered to be an appetite-regulating hormone, is present within the taste buds of the tongue. Prepro-ghrelin, prohormone convertase 1/3 (PC 1/3), ghrelin, its cognate receptor (GHSR), and ghrelin-O-acyltransferase (GOAT , the enzyme that activates ghrelin) are expressed in Type I, II, III and IV taste cells of mouse taste buds. In addition, ghrelin and GHSR co-localize in the same taste cells, suggesting that ghrelin works in an autocrine manner in taste cells. To determine a role for ghrelin in modifying taste perception, we performed taste behavioral tests using GHSR null mice. GHSR null mice exhibited significantly reduced taste responsivity to sour (citric acid) and salty (sodium chloride) tastants. Conclusions/Significance: These findings suggest that ghrelin plays a local modulatory role in determining taste bud signaling and function and could be a novel mechanism for the modulation of salty and sour taste responsivity. [ABSTRACT FROM AUTHOR]
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- 2010
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11. A genome-wide association search for type 2 diabetes genes in African Americans.
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Palmer ND, McDonough CW, Hicks PJ, Roh BH, Wing MR, An SS, Hester JM, Cooke JN, Bostrom MA, Rudock ME, Talbert ME, Lewis JP, Ferrara A, Lu L, Ziegler JT, Sale MM, Divers J, Shriner D, Adeyemo A, Rotimi CN, Ng MC, Langefeld CD, Freedman BI, Bowden DW, Voight BF, Scott LJ, Steinthorsdottir V, Morris AP, Dina C, Welch RP, Zeggini E, Huth C, Aulchenko YS, Thorleifsson G, McCulloch LJ, Ferreira T, Grallert H, Amin N, Wu G, Willer CJ, Raychaudhuri S, McCarroll SA, Langenberg C, Hofmann OM, Dupuis J, Qi L, Segrè AV, van Hoek M, Navarro P, Ardlie K, Balkau B, Benediktsson R, Bennett AJ, Blagieva R, Boerwinkle E, Bonnycastle LL, Boström KB, Bravenboer B, Bumpstead S, Burtt NP, Charpentier G, Chines PS, Cornelis M, Couper DJ, Crawford G, Doney AS, Elliott KS, Elliott AL, Erdos MR, Fox CS, Franklin CS, Ganser M, Gieger C, Grarup N, Green T, Griffin S, Groves CJ, Guiducci C, Hadjadj S, Hassanali N, Herder C, Isomaa B, Jackson AU, Johnson PR, Jørgensen T, Kao WH, Klopp N, Kong A, Kraft P, Kuusisto J, Lauritzen T, Li M, Lieverse A, Lindgren CM, Lyssenko V, Marre M, Meitinger T, Midthjell K, Morken MA, Narisu N, Nilsson P, Owen KR, Payne F, Perry JR, Petersen AK, Platou C, Proença C, Prokopenko I, Rathmann W, Rayner NW, Robertson NR, Rocheleau G, Roden M, Sampson MJ, Saxena R, Shields BM, Shrader P, Sigurdsson G, Sparsø T, Strassburger K, Stringham HM, Sun Q, Swift AJ, Thorand B, Tichet J, Tuomi T, van Dam RM, van Haeften TW, van Herpt T, van Vliet-Ostaptchouk JV, Walters GB, Weedon MN, Wijmenga C, Witteman J, Bergman RN, Cauchi S, Collins FS, Gloyn AL, Gyllensten U, Hansen T, Hide WA, Hitman GA, Hofman A, Hunter DJ, Hveem K, Laakso M, Mohlke KL, Morris AD, Palmer CN, Pramstaller PP, Rudan I, Sijbrands E, Stein LD, Tuomilehto J, Uitterlinden A, Walker M, Wareham NJ, Watanabe RM, Abecasis GR, Boehm BO, Campbell H, Daly MJ, Hattersley AT, Hu FB, Meigs JB, Pankow JS, Pedersen O, Wichmann HE, Barroso I, Florez JC, Frayling TM, Groop L, Sladek R, Thorsteinsdottir U, Wilson JF, Illig T, Froguel P, van Duijn CM, Stefansson K, Altshuler D, Boehnke M, McCarthy MI, Soranzo N, Wheeler E, Glazer NL, Bouatia-Naji N, Mägi R, Randall J, Johnson T, Elliott P, Rybin D, Henneman P, Dehghan A, Hottenga JJ, Song K, Goel A, Egan JM, Lajunen T, Doney A, Kanoni S, Cavalcanti-Proença C, Kumari M, Timpson NJ, Zabena C, Ingelsson E, An P, O'Connell J, Luan J, Elliott A, McCarroll SA, Roccasecca RM, Pattou F, Sethupathy P, Ariyurek Y, Barter P, Beilby JP, Ben-Shlomo Y, Bergmann S, Bochud M, Bonnefond A, Borch-Johnsen K, Böttcher Y, Brunner E, Bumpstead SJ, Chen YD, Chines P, Clarke R, Coin LJ, Cooper MN, Crisponi L, Day IN, de Geus EJ, Delplanque J, Fedson AC, Fischer-Rosinsky A, Forouhi NG, Frants R, Franzosi MG, Galan P, Goodarzi MO, Graessler J, Grundy S, Gwilliam R, Hallmans G, Hammond N, Han X, Hartikainen AL, Hayward C, Heath SC, Hercberg S, Hicks AA, Hillman DR, Hingorani AD, Hui J, Hung J, Jula A, Kaakinen M, Kaprio J, Kesaniemi YA, Kivimaki M, Knight B, Koskinen S, Kovacs P, Kyvik KO, Lathrop GM, Lawlor DA, Le Bacquer O, Lecoeur C, Li Y, Mahley R, Mangino M, Manning AK, Martínez-Larrad MT, McAteer JB, McPherson R, Meisinger C, Melzer D, Meyre D, Mitchell BD, Mukherjee S, Naitza S, Neville MJ, Oostra BA, Orrù M, Pakyz R, Paolisso G, Pattaro C, Pearson D, Peden JF, Pedersen NL, Perola M, Pfeiffer AF, Pichler I, Polasek O, Posthuma D, Potter SC, Pouta A, Province MA, Psaty BM, Rayner NW, Rice K, Ripatti S, Rivadeneira F, Rolandsson O, Sandbaek A, Sandhu M, Sanna S, Sayer AA, Scheet P, Seedorf U, Sharp SJ, Shields B, Sijbrands EJ, Silveira A, Simpson L, Singleton A, Smith NL, Sovio U, Swift A, Syddall H, Syvänen AC, Tanaka T, Tönjes A, Uitterlinden AG, van Dijk KW, Varma D, Visvikis-Siest S, Vitart V, Vogelzangs N, Waeber G, Wagner PJ, Walley A, Ward KL, Watkins H, Wild SH, Willemsen G, Witteman JC, Yarnell JW, Zelenika D, Zethelius B, Zhai G, Zhao JH, Zillikens MC, Borecki IB, Loos RJ, Meneton P, Magnusson PK, Nathan DM, Williams GH, Silander K, Salomaa V, Smith GD, Bornstein SR, Schwarz P, Spranger J, Karpe F, Shuldiner AR, Cooper C, Dedoussis GV, Serrano-Ríos M, Lind L, Palmer LJ, Franks PW, Ebrahim S, Marmot M, Kao WH, Pramstaller PP, Wright AF, Stumvoll M, Hamsten A, Buchanan TA, Valle TT, Rotter JI, Siscovick DS, Penninx BW, Boomsma DI, Deloukas P, Spector TD, Ferrucci L, Cao A, Scuteri A, Schlessinger D, Uda M, Ruokonen A, Jarvelin MR, Waterworth DM, Vollenweider P, Peltonen L, Mooser V, and Sladek R
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- Adult, Aged, Case-Control Studies, Cohort Studies, Female, Genetic Predisposition to Disease, Genotype, Humans, Male, Meta-Analysis as Topic, Middle Aged, Polymorphism, Single Nucleotide, Validation Studies as Topic, Black or African American genetics, Diabetes Mellitus, Type 2 ethnology, Diabetes Mellitus, Type 2 genetics, Genome-Wide Association Study
- Abstract
African Americans are disproportionately affected by type 2 diabetes (T2DM) yet few studies have examined T2DM using genome-wide association approaches in this ethnicity. The aim of this study was to identify genes associated with T2DM in the African American population. We performed a Genome Wide Association Study (GWAS) using the Affymetrix 6.0 array in 965 African-American cases with T2DM and end-stage renal disease (T2DM-ESRD) and 1029 population-based controls. The most significant SNPs (n = 550 independent loci) were genotyped in a replication cohort and 122 SNPs (n = 98 independent loci) were further tested through genotyping three additional validation cohorts followed by meta-analysis in all five cohorts totaling 3,132 cases and 3,317 controls. Twelve SNPs had evidence of association in the GWAS (P<0.0071), were directionally consistent in the Replication cohort and were associated with T2DM in subjects without nephropathy (P<0.05). Meta-analysis in all cases and controls revealed a single SNP reaching genome-wide significance (P<2.5×10(-8)). SNP rs7560163 (P = 7.0×10(-9), OR (95% CI) = 0.75 (0.67-0.84)) is located intergenically between RND3 and RBM43. Four additional loci (rs7542900, rs4659485, rs2722769 and rs7107217) were associated with T2DM (P<0.05) and reached more nominal levels of significance (P<2.5×10(-5)) in the overall analysis and may represent novel loci that contribute to T2DM. We have identified novel T2DM-susceptibility variants in the African-American population. Notably, T2DM risk was associated with the major allele and implies an interesting genetic architecture in this population. These results suggest that multiple loci underlie T2DM susceptibility in the African-American population and that these loci are distinct from those identified in other ethnic populations.
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- 2012
- Full Text
- View/download PDF
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