<i>Macaca radiata</i> (bonnet monkey): a spontaneous model of nonalcoholic fatty liver disease

Nagarajan, Priyadharsini; Venkatesan, R.; Kumar, Mahesh; Usmani, Abul; Majumdar, Subeer S.

doi:10.1111/j.1478-3231.2008.01706.x

Cited by 14 publications

(20 citation statements)

References 21 publications

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“…Another recent study has identified a nonhuman primate model of NAFLD resembling features of human NAFLD [51]. This will be useful in understanding the mechanism of the onset of this disease and for developing novel therapeutic modalities.…”

Section: Iron/hfe Gene Mutationsmentioning

confidence: 99%

Nonalcoholic fatty liver disease in India – a lot done, yet more required!

Duseja

2010

Indian J Gastroenterol

110

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Nonalcoholic fatty liver disease (NAFLD) is emerging as an important cause of liver disease in India. Epidemiological studies suggest prevalence of NAFLD in around 9% to 32% of general population in India with higher prevalence in those with overweight or obesity and those with diabetes or prediabetes. Clinicopathological studies show that NAFLD is an important cause of unexplained rise in hepatic transaminases, cryptogenic cirrhosis and cryptogenic hepatocellular carcinoma in Indian patients. There is high prevalence of insulin resistance and nearly half of Indian patients with NAFLD have evidence of full-blown metabolic syndrome. Though oxidative stress is involved in the pathogenesis of NAFLD/nonalcoholic steatohepatitis, serum or liver iron and HFE gene mutations appear not to play a role in the pathogenesis of NAFLD in Indian patients. Imaging modalities are not useful in differentiating simple steatosis from NASH and liver biopsy may be useful in those with risk factors for significant liver disease. Pilot studies on treatment strategies have shown that weight reduction and exercise, ursodeoxycholic acid, metformin, vitamin E and pentoxyfylline are effective in normalizing transaminases and or in improving hepatic steatosis and inflammation in Indian patients with NAFLD. Randomized controlled treatment trials involving large number of patients with histological end point are required to assess the efficacy of different modalities. In conclusion, a lot has been done, yet more is required to understand various aspects of NAFLD in India.

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Section: Iron/hfe Gene Mutationsmentioning

confidence: 99%

Nonalcoholic fatty liver disease in India – a lot done, yet more required!

Duseja

2010

Indian J Gastroenterol

110

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“…However, the features of human ESC differ significantly from those of mouse ESC, and it is hard to evaluate the safety of ESC‐derived cell transplantation in human. Rhesus macaque is over 90% DNA homologous with human and has long been used as a model for studying various human diseases . Before ESC‐derived hepatocyte‐like cells can be transplanted in human, their safety should be evaluated in a non‐human primate.…”

Section: Discussionmentioning

confidence: 99%

“…Rhesus macaque is over 90% DNA homologous with human and has long been used as a model for studying various human diseases. [6][7][8] Before ESC-derived hepatocyte-like cells can be transplanted in human, their safety should be evaluated in a nonhuman primate. In this study ORMES6, a rhesus monkey ESC line, was induced into hepatocyte-like cells.…”

Section: Discussionmentioning

confidence: 99%

“…Due to their close evolutionary relationship to human beings, rhesus monkey has been frequently used as a model in preclinical trials to study various human diseases including fatty liver, liver fibrosis and hepatocellular carcinoma. [6][7][8][9][10] ESC of human and rhesus monkey share similar features, such as their morphology, surface marker expression and developmental potential. 11 Therefore, ESC of rhesus monkey may be an ideal intermediate translational model to assess the application of human ESC in clinical trials.…”

Section: Introductionmentioning

confidence: 99%

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Differentiation of nonhuman primate embryonic stem cells into hepatocyte‐like cells

Kuai

Shao

et al. 2013

J of Digest Diseases

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“…Importantly, moderate steatosis and inflammation developed in MetS‐predisposed monkeys fed a normal chow diet, and they also exhibit clear increases in the hepatic expression of profibrotic genes . When fed an HFD or even a simple high‐carbohydrate diet, MetS‐predisposed monkeys rapidly become obese and insulin resistant and develop hepatic inflammation with fibrosis . The similarities between the pathophysiology, anatomy, and histopathological disease spectrum in nonhuman primate and humans suggest that the MetS‐predisposed monkey is more representatively faithful to the clinical situation than murine models, and thus enable much more relevant studies of molecular mechanisms of NASH.…”

mentioning

confidence: 99%