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12. Intestinal alkaline phosphatase prevents metabolic syndrome in mice

Author

Kaliannan, Kanakaraju, Hamarneh, Sulaiman R., Economopoulos, Konstantinos P., Alam, Sayeda Nasrin, Moaven, Omeed, Patel, Palak, Malo, Nondita S., Ray, Madhury, Abtahi, Seyed M., Muhammad, Nur, Raychowdhury, Atri, Teshager, Abeba, Mohamed, Mussa M. Rafat, Moss, Angela K., Ahmed, Rizwan, Hakimian, Shahrad, Narisawa, Sonoko, Millán, José Luis, Hohmann, Elizabeth, Warren, H. Shaw, Bhan, Atul K., Malo, Madhu S., and Hodin, Richard A.

Published
2013

13. Intestinal alkaline phosphatase deficiency increases the risk of diabetes

Author

Malo, Jagannath, Alam, Md Jahangir, Islam, Salequl, Mottalib, Md Abdul, Rocki, Md Mehedi Hasan, Barmon, Ginok, Tinni, Shamema Akter, Barman, Swapan K, Sarker, Tapas, Khan, Md Nayeemul Islam, Kaliannan, Kanakaraju, Hasanat, Muhammad Abul, Rahman, Salimur, Pathan, Md Faruque, Khan, A K Azad, and Malo, Madhu S

Subjects
Adult, Incidence, Endocrinology, Diabetes and Metabolism, Fasting, Middle Aged, Alkaline Phosphatase, RC648-665, Diseases of the endocrine glands. Clinical endocrinology, type 2, Diabetes Mellitus, Type 2, diabetes mellitus, Humans, Epidemiology/Health services research, Obesity
Abstract

IntroductionOur previous case–control study demonstrated that a high level of intestinal alkaline phosphatase (IAP), an endotoxin-detoxifying anti-inflammatory enzyme secreted by villus-associated enterocytes and excreted with stool, plays a protective role against type 2 diabetes mellitus (T2DM) irrespective of obesity. In the current study, we investigated the long-term effect of IAP deficiency (IAPD) on the pathogenesis of T2DM.Research design and methodsA healthy cohort of participants without diabetes (30–60 years old), comprising 188 without IAPD (IAP level: ≥65 U/g stool) and 386 with IAPD (IAP level: ResultsT2DM incidence rates were 8.0%, 11.7%, 25.6%, and 33.3% in participants with ‘persistent no IAPD’ (IAP level: always ≥65 U/g stool), ‘remittent IAPD’ (IAP level: increased from 2 p=0.0541). Sensitivity analyses of persistent IAP levels revealed that, compared with participants of the highest persistent IAP pentile (always >115 U/g stool), the rate of increase of fasting glycemia was double and the risk of developing T2DM was 1280% higher (RR: 13.80 (95% CI 1.87 to 101.3), p=0.0099) in participants of the lowest persistent IAP pentile (always ConclusionsIAPD increases the risk of developing T2DM, and regular STAP tests would predict individual vulnerability to T2DM. Oral IAP supplementation might prevent T2DM.

Published
2022

17. Associations of homocysteine status and homocysteine metabolism enzyme polymorphisms with hypertension and dyslipidemia in a Chinese hypertensive population

Author

Yuan, Xiaojie, primary, Wang, Tingcai, additional, Gao, Jie, additional, Wang, Yunchao, additional, Chen, Yajun, additional, Kaliannan, Kanakaraju, additional, Li, Xiaochun, additional, Xiao, Jing, additional, Ma, Tianyou, additional, Zhang, Lei, additional, and Shao, Zhongjun, additional

Published
2019
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19. Associations of homocysteine status and homocysteine metabolism enzyme polymorphisms with hypertension and dyslipidemia in a Chinese hypertensive population.

Author

Yuan, Xiaojie, Wang, Tingcai, Gao, Jie, Wang, Yunchao, Chen, Yajun, Kaliannan, Kanakaraju, Li, Xiaochun, Xiao, Jing, Ma, Tianyou, Zhang, Lei, and Shao, Zhongjun

Subjects
ENZYME metabolism, DYSLIPIDEMIA, DISEASE risk factors, HYPERTENSION, GENETIC polymorphisms, ANGIOTENSIN I
Abstract

Background: Hypertension (HTN), dyslipidemia and hyperhomocysteinemia (HHcy) are risk factors for cardiovascular disease (CVD). Methods: Hypertensive Chinese subjects (n = 228) were enrolled. MTHFR C667T, MTHFR A1298C, MTR A2756G, and MTRR A66G genotypes were determined. Unconditional logistic regression was performed to determine the associations of serum Hcy status and genotypes with HTN and dyslipidemia. Results: The mean age of hypertensive adults was 65.53 ± 9.94 years, including 88 (38.6%) men and 140 (61.4%) women. Patients with MTHFR 667TT and MTRR GG carriers showed higher serum Hcy levels (P = 0.019 and 0.018, respectively), which is associated with higher serum triacylglycerols (TAG) and total cholesterol (TC) levels (P = 0.014 and 0.044, respectively) and a higher risk for hypertriglyceridemia (OR = 1.889, 95% CI: 1.105–3.229, P = 0.020). Compared with low Hcy and MTRR 66AA, those with high Hcy and 66AA or 66AG+GG showed higher odd\s of hypertriglyceridemia (MTRR 66AA+ high Hcy: OR: 2.692, 95% CI: 1.189–6.096, Pcombined = 0.018; MTRR 66AG/GG+ high Hcy: OR: 3.433, 95% CI: 1.517–7.772, Pcombined = 0.003, respectively). Patients with high Hcy and MTHFR 667CC, as well as those with low Hcy and 667CT+TT, showed lower odds of uncontrolled SBP (MTHFR 667CC+ high Hcy: OR: 0.338, 95% CI: 0.115–0.996, Pcombined = 0.049; MTHFR 667CT/TT+ low Hcy: OR: 0.421, 95% CI: 0.193–0.921, Pcombined = 0.030) compared to patients with low Hcy and MTHFR 667CC. Conclusions: Serum Hcy status and Hcy metabolism gene polymorphisms (MTHFR C667T and MTRR A66G) may have synergistic effects on the prevalence of HTN and dyslipidemia. [ABSTRACT FROM AUTHOR]

Published
2020
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20. Green Tea Liquid Consumption Alters the Human Intestinal and Oral Microbiome

Author

Yuan, Xiaojie, primary, Long, Yong, additional, Ji, Zhaohua, additional, Gao, Jie, additional, Fu, Ting, additional, Yan, Min, additional, Zhang, Lei, additional, Su, Haixia, additional, Zhang, Weilu, additional, Wen, Xiaohui, additional, Pu, Zhongshu, additional, Chen, Hui, additional, Wang, Yufei, additional, Gu, Xu, additional, Yan, Binyuan, additional, Kaliannan, Kanakaraju, additional, and Shao, Zhongjun, additional

Published
2018
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21. Erratum for Kang et al., “Gut Microbiota Mediates the Protective Effects of Dietary Capsaicin against Chronic Low-Grade Inflammation and Associated Obesity Induced by High-Fat Diet”

Author

Kang, Chao, primary, Wang, Bin, additional, Kaliannan, Kanakaraju, additional, Wang, Xiaolan, additional, Lang, Hedong, additional, Hui, Suocheng, additional, Huang, Li, additional, Zhang, Yong, additional, Zhou, Ming, additional, Chen, Mengting, additional, and Mi, Mantian, additional

Published
2017
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24. Effects of vitamin C supplementation on blood pressure and hypertension control in response to ambient temperature changes in patients with essential hypertension.

Author

Yuan, Xiaojie, Li, Xiaochun, Ji, Zhaohua, Xiao, Jing, Zhang, Lei, Zhang, Weilu, Su, Haixiao, Kaliannan, Kanakaraju, Long, Yong, and Shao, Zhongjun

Subjects
BLOOD pressure, VITAMIN C, ESSENTIAL hypertension, EARTH temperature, BLOOD pressure measurement
Abstract

Evidence for blood pressure-lowering effects of vitamin C (VC) supplementation in clinical trials is inconsistent and limited studies have examined the effect of VC supplementation on hypertension (HTN) control. In this study, eligible patients were cluster assigned to receive 300 mg VC per day or nothing for 6 months. During the 6-month follow-up period, a questionnaire survey was obtained and standardized blood pressure measurements were performed on all subjects. Oral administration of VC significantly decreased the diastolic blood pressure and pulse pressure with a significant increase in HTN control. After adjusting for confounding variables, treatment with VC was associated with ~ 0.5 risk reduction of uncontrolled HTN in subjects received anti-hypertensive medications, whereas lower indoor and outdoor and ground temperature were significantly associated with an increased risk of uncontrolled HTN in all patients. Our results warrant further studies investigating the mechanisms underlying the association between VC and HTN control. [ABSTRACT FROM AUTHOR]

Published
2019
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27. A Novel Approach to Maintain Gut Mucosal Integrity Using an Oral Enzyme Supplement

Author

Hamarneh, Sulaiman R., primary, Mohamed, Mussa M. Rafat, additional, Economopoulos, Konstantinos P., additional, Morrison, Sara A., additional, Phupitakphol, Tanit, additional, Tantillo, Tyler J., additional, Gul, Sarah S., additional, Gharedaghi, Mohammad Hadi, additional, Tao, Qingsong, additional, Kaliannan, Kanakaraju, additional, Narisawa, Sonoko, additional, Millán, José L., additional, van der Wilden, Gwendolyn M., additional, Fagenholz, Peter J., additional, Malo, Madhu S., additional, and Hodin, Richard A., additional

Published
2014
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28. Intestinal Alkaline Phosphatase Prevents Antibiotic-Induced Susceptibility to Enteric Pathogens

Author

Alam, Sayeda Nasrin, primary, Yammine, Halim, additional, Moaven, Omeed, additional, Ahmed, Rizwan, additional, Moss, Angela K., additional, Biswas, Brishti, additional, Muhammad, Nur, additional, Biswas, Rakesh, additional, Raychowdhury, Atri, additional, Kaliannan, Kanakaraju, additional, Ghosh, Sathi, additional, Ray, Madhury, additional, Hamarneh, Sulaiman R., additional, Barua, Soumik, additional, Malo, Nondita S., additional, Bhan, Atul K., additional, Malo, Madhu S., additional, and Hodin, Richard A., additional

Published
2014
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30. Tu1620 Intestinal Alkaline Phosphatase Is an Endogenous Anti-Inflammatory Factor

Author

Mohamed, Mussa, primary, Economopoulos, Konstantinos P., additional, Patel, Palak, additional, Muhammad, Nur, additional, Moaven, Omeed, additional, Moss, Angela K., additional, Hamarneh, Sulaiman R., additional, Teshager, Abeba, additional, Kaliannan, Kanakaraju, additional, Abtahi, Seyed M., additional, Alam, Sayeda Nasrin, additional, Malo, Nondita S., additional, Tao, Qingsong, additional, Malo, Madhu S., additional, and Hodin, Richard A., additional

Published
2013
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32. Intestinal alkaline phosphatase inhibits the proinflammatory nucleotide uridine diphosphate

Author

Moss, Angela K., primary, Hamarneh, Sulaiman R., additional, Mohamed, Mussa M. Rafat, additional, Ramasamy, Sundaram, additional, Yammine, Halim, additional, Patel, Palak, additional, Kaliannan, Kanakaraju, additional, Alam, Sayeda N., additional, Muhammad, Nur, additional, Moaven, Omeed, additional, Teshager, Abeba, additional, Malo, Nondita S., additional, Narisawa, Sonoko, additional, Millán, José Luis, additional, Warren, H. Shaw, additional, Hohmann, Elizabeth, additional, Malo, Madhu S., additional, and Hodin, Richard A., additional

Published
2013
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34. 632 Prevention of Antibiotic-Associated DSS Colitis by Intestinal Alkaline Phosphatase

Author

Ahmed, Rizwan, primary, Alam, Sayeda Nasrin, additional, Economopoulos, Konstantinos P., additional, Moaven, Omeed, additional, Ray, Madhury, additional, Kaliannan, Kanakaraju, additional, Hamarneh, Sulaiman R., additional, Muhammad, Nur, additional, Barua, Soumik, additional, Raychowdhury, Atri, additional, Mohamed, Mussa, additional, Bhan, Atul K., additional, Malo, Madhu S., additional, and Hodin, Richard A., additional

Published
2012
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35. Sa2066 A Novel Function of Intestinal Alkaline Phosphatase as an Endogenous Prebiotic

Author

Moaven, Omeed, primary, Alam, Sayeda Nasrin, additional, Ray, Madhury, additional, Kaliannan, Kanakaraju, additional, Ahmed, Rizwan, additional, Hamarneh, Sulaiman R., additional, Economopoulos, Konstantinos P., additional, Moss, Angela K., additional, Muhammad, Nur, additional, Mohamed, Mussa, additional, Malo, Madhu S., additional, and Hodin, Richard A., additional

Published
2012
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37. Mo1177 The Effects of Orally Administered Intestinal Alkaline Phosphatase on High-Fat Diet-Induced Metabolic Disorders

Author

Kaliannan, Kanakaraju, primary, Alam, Sayeda Nasrin, additional, Moaven, Omeed, additional, Moss, Angela K., additional, Ray, Madhury, additional, Ahmed, Rizwan, additional, Hamarneh, Sulaiman R., additional, Muhammad, Nur, additional, Economopoulos, Konstantinos P., additional, Mohamed, Mussa, additional, Bhan, Atul K., additional, Malo, Madhu S., additional, and Hodin, Richard A., additional

Published
2012
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38. Mo1820 Oral Supplementation With Intestinal Alkaline Phosphatase: A Novel Therapy to Treat Salmonella Colitis

Author

Alam, Sayeda Nasrin, primary, Yammine, Halim, additional, Ahmed, Rizwan, additional, Hamarneh, Sulaiman R., additional, Economopoulos, Konstantinos P., additional, Moaven, Omeed, additional, Kaliannan, Kanakaraju, additional, Moss, Angela K., additional, Ray, Madhury, additional, Muhammad, Nur, additional, Mohamed, Mussa, additional, Raychowdhury, Atri, additional, Barua, Soumik, additional, Bhan, Atul K., additional, Malo, Madhu S., additional, and Hodin, Richard A., additional

Published
2012
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39. ATP-Induced Activation of NLRP3 Inflammasome and IL-1β Secretion Prevented by Intestinal Alkaline Phosphatase

Author

Ramasamy, Sundaram, primary, Malo, Madhu S., additional, Nasrin Alam, Sayeda, additional, Yammine, Halim, additional, Kaliannan, Kanakaraju, additional, Moss, Angela K., additional, Muhammad, Nur, additional, Biswas, Rakesh, additional, Batal, Obaida H., additional, Raychowdhury, Atri, additional, Warren, H. Shaw, additional, Hohmann, Elizabeth, additional, Bhan, Atul K., additional, and Hodin, Richard A., additional

Published
2011
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40. Intestinal Alkaline Phosphatase Detoxifies Bacterial Components

Author

Moss, Angela K., primary, Malo, Madhu S., additional, Yammine, Halim, additional, Nasrin Alam, Sayeda, additional, Ramasamy, Sundaram, additional, Biswas, Rakesh, additional, Muhammad, Nur, additional, Kaliannan, Kanakaraju, additional, Batal, Obaida H., additional, Warren, H. Shaw, additional, Hohmann, Elizabeth, additional, and Hodin, Richard A., additional

Published
2011
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41. Intestinal alkaline phosphatase has beneficial effects in mouse models of chronic colitis

Author

Ramasamy, Sundaram, primary, Nguyen, Deanna D., additional, Eston, Michelle A., additional, Nasrin Alam, Sayeda, additional, Moss, Angela K., additional, Ebrahimi, Farzad, additional, Biswas, Brishti, additional, Mostafa, Golam, additional, Chen, Kathryn T., additional, Kaliannan, Kanakaraju, additional, Yammine, Halim, additional, Narisawa, Sonoko, additional, Millán, José Luis, additional, Warren, Shaw H., additional, Hohmann, Elizabeth L., additional, Mizoguchi, Emiko, additional, Reinecker, Hans-Christian, additional, Bhan, Atul K., additional, Snapper, Scott B., additional, Malo, Madhu S., additional, and Hodin, Richard A., additional

Published
2011
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42. Gut Microbiota Mediates the Protective Effects of Dietary Capsaicin against Chronic Low-Grade Inflammation and Associated Obesity Induced by High-Fat Diet

Author

Kang, Chao, Wang, Bin, Kaliannan, Kanakaraju, Wang, Xiaolan, Lang, Hedong, Hui, Suocheng, Huang, Li, Zhang, Yong, Zhou, Ming, Chen, Mengting, and Mi, Mantian

Subjects
capsaicin, chronic low-grade inflammation, gut barrier, gut microbiota, metabolic endotoxemia
Abstract

Metabolic endotoxemia originating from dysbiotic gut microbiota has been identified as a primary mediator for triggering the chronic low-grade inflammation (CLGI) responsible for the development of obesity. Capsaicin (CAP) is the major pungent bioactivator in chili peppers and has potent anti-obesity functions, yet the mechanisms linking this effect to gut microbiota remain obscure. Here we show that mice fed a high-fat diet (HFD) supplemented with CAP exhibit lower levels of metabolic endotoxemia and CLGI associated with lower body weight gain. High-resolution responses of the microbiota were examined by 16S rRNA sequencing, short-chain fatty acid (SCFA) measurements, and phylogenetic reconstruction of unobserved states (PICRUSt) analysis. The results showed, among others, that dietary CAP induced increased levels of butyrate-producing Ruminococcaceae and Lachnospiraceae, while it caused lower levels of members of the lipopolysaccharide (LPS)-producing family S24_7. Predicted function analysis (PICRUSt) showed depletion of genes involved in bacterial LPS synthesis in response to CAP. We further identified that inhibition of cannabinoid receptor type 1 (CB1) by CAP also contributes to prevention of HFD-induced gut barrier dysfunction. Importantly, fecal microbiota transplantation experiments conducted in germfree mice demonstrated that dietary CAP-induced protection against HFD-induced obesity is transferrable. Moreover, microbiota depletion by a cocktail of antibiotics was sufficient to block the CAP-induced protective phenotype against obesity, further suggesting the role of microbiota in this context. Together, our findings uncover an interaction between dietary CAP and gut microbiota as a novel mechanism for the anti-obesity effect of CAP acting through prevention of microbial dysbiosis, gut barrier dysfunction, and chronic low-grade inflammation.

Published
2017
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43. Non-invasive diagnosis of non-alcoholic fatty liver disease (NAFLD) using ultrasound image echogenicity.

Author

Benjamin A, Zubajlo R, Thomenius K, Dhyani M, Kaliannan K, Samir AE, and Anthony BW

Subjects
Animals, Liver, Mice, Phantoms, Imaging, Sheep, Sound, Ultrasonography, Non-alcoholic Fatty Liver Disease
Abstract

This paper introduces a non-invasive, quantitative technique to diagnose the progression of non-alcoholic fatty liver disease (NAFLD). The method is predicated on two fundamental principles: 1) the speed of sound in a fatty liver is lower than that in a healthy liver and 2) the quality of an ultrasound image is maximized when the beamformer's speed of sound matches the true speed of sound in the tissue being examined. The proposed method uses the echogenicity of an ultrasound image as a quantitative measure to estimate the true speed of sound within the liver parenchyma and capture its correlation with the underlying fat content. The proposed technique was evaluated in simulations and then tested ex vivo on sheep liver, mice liver (healthy and fatty) and tissue-mimicking phantoms. In the case of the phantom and sheep liver, the method was able to estimate the true speed of sound with errors of less than 0.5%; in the case of the mice livers, the method was able to accurately estimate the speed of sound within the livers (less than 1% error) and capture the correlation between fat content and speed of sound. Thereby, demonstrating the capability of ultrasound technology to non-invasively, quantitatively, and accurately diagnose NAFLD at point of care.

Published
2017
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44. Intestinal alkaline phosphatase inhibits the proinflammatory nucleotide uridine diphosphate.

Author

Moss AK, Hamarneh SR, Mohamed MM, Ramasamy S, Yammine H, Patel P, Kaliannan K, Alam SN, Muhammad N, Moaven O, Teshager A, Malo NS, Narisawa S, Millán JL, Warren HS, Hohmann E, Malo MS, and Hodin RA

Subjects
Animals, Bacterial Proteins antagonists & inhibitors, Bacterial Proteins metabolism, Cells, Cultured, Humans, Interleukin-8 analysis, Interleukin-8 metabolism, Intestinal Mucosa immunology, Lipopolysaccharides metabolism, Mice, Mice, Knockout, Receptors, Purinergic P2 metabolism, Alkaline Phosphatase metabolism, Disease Models, Animal, Inflammation Mediators antagonists & inhibitors, Inflammation Mediators metabolism, Inflammatory Bowel Diseases, Intestine, Small metabolism, Uridine Diphosphate metabolism
Abstract

Uridine diphosphate (UDP) is a proinflammatory nucleotide implicated in inflammatory bowel disease. Intestinal alkaline phosphatase (IAP) is a gut mucosal defense factor capable of inhibiting intestinal inflammation. We used the malachite green assay to show that IAP dephosphorylates UDP. To study the anti-inflammatory effect of IAP, UDP or other proinflammatory ligands (LPS, flagellin, Pam3Cys, or TNF-α) in the presence or absence of IAP were applied to cell cultures, and IL-8 was measured. UDP caused dose-dependent increase in IL-8 release by immune cells and two gut epithelial cell lines, and IAP treatment abrogated IL-8 release. Costimulation with UDP and other inflammatory ligands resulted in a synergistic increase in IL-8 release, which was prevented by IAP treatment. In vivo, UDP in the presence or absence of IAP was instilled into a small intestinal loop model in wild-type and IAP-knockout mice. Luminal contents were applied to cell culture, and cytokine levels were measured in culture supernatant and intestinal tissue. UDP-treated luminal contents induced more inflammation on target cells, with a greater inflammatory response to contents from IAP-KO mice treated with UDP than from WT mice. Additionally, UDP treatment increased TNF-α levels in intestinal tissue of IAP-KO mice, and cotreatment with IAP reduced inflammation to control levels. Taken together, these studies show that IAP prevents inflammation caused by UDP alone and in combination with other ligands, and the anti-inflammatory effect of IAP against UDP persists in mouse small intestine. The benefits of IAP in intestinal disease may be partly due to inhibition of the proinflammatory activity of UDP.

Published
2013
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