Effects of a low-fat diet on the hepatic expression of adiponectin and its receptors in rats with NAFLD

Ma, Hong; You, Guo-Ping; Cui, Fan; Chen, Lu-Fang; Yang, Xiao; Chen, Ligang; Lu, Hua-Dong; Zhang, Wenqiang

doi:10.1016/s1665-2681(19)30807-5

Cited by 16 publications

(7 citation statements)

References 29 publications

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“…Our results showed that Ad supplementation, even under CIH conditions, partially ameliorated hepatic injury; Ma, H et al showed that Ad might play an important role in the development of NALFD, and up regulating the level of Ad alleviated the hepatic injury 53 . All of these findings suggested that the Ad played a protective role in hepatic injury.…”

Section: Discussionsupporting

confidence: 50%

Adiponectin protects the rats liver against chronic intermittent hypoxia induced injury through AMP-activated protein kinase pathway

Ding

Zhang

Dong

et al. 2016

Sci Rep

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This study was performed to assess the effect of chronic intermittent hypoxia (CIH) on the liver, the associated mechanisms and the potential therapeutic roles of adiponectin (Ad). Sixty rats were randomly assigned to four groups: the normal control (NC), NC and Ad supplement (NC + Ad), CIH, and CIH and Ad supplement (CIH + Ad) groups. The rats in the CIH and CIH + Ad groups were exposed to a hypoxic environment for 4 months. Rats in the NC + Ad and CIH + Ad groups were also treated with an intravenous injection of Ad (10 ug), twice a week. The plasma levels of hepatic enzymes, serum triglyceride, liver triglyceride, fasting blood glucose and hepatic cell apoptosis in hepatic tissue, were higher in the CIH group than in the NC and NC + Ad groups. However, the Ad supplementation in the CIH + Ad group rescued the hepatic tissue insult by activating the AMP-activated protein kinase (AMPK) pathway. In conclusion, Ad could protect against CIH-induced hepatic injury partly through the AMPK pathway.

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Section: Discussionsupporting

confidence: 50%

Adiponectin protects the rats liver against chronic intermittent hypoxia induced injury through AMP-activated protein kinase pathway

Ding

Zhang

Dong

et al. 2016

Sci Rep

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“…The expansion of adipose tissue, independently of other concomitant factors, deprives patients with NAFLD of the anti-inflammatory and antifibrotic effects of adiponectin, effects which are inversely related to total adiposity 39. Adiponectin is a potent cytokine exerting insulin sensitizing, anti-inflammatory and anti-steatotic activity in hepatocytes through increasing oxidation of free fatty acids and decreasing gluconeogenesis, FFA flow and de novo lipogenesis 40,41. In addition, adiponectin protects hepatocytes from apoptosis in the NAFLD-associated hepatic inflammatory microenvironment 42.…”

Section: Nafld and Cancer: The Adipocytokine Networkmentioning

confidence: 99%

Obesity, Nonalcoholic Fatty Liver Disease and Adipocytokines Network in Promotion of Cancer

Divella¹,

Mazzocca²,

Daniele³

et al. 2019

Int. J. Biol. Sci.

131

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Western populations are becoming increasingly sedentary and the incidence of nonalcoholic fatty liver disease (NAFLD) is increasing and becoming one of the most common causes of liver disease worldwide. Also, NAFLD is considered one the new emerging risk factors for development of tumors of the gastro-intestinal tract, particularly hepatocellular carcinoma (HCC). Visceral obesity is an important risk factor for the onset of NAFLD. An accumulation of ectopic fat, including visceral obesity and fatty liver leads to a dysfunction of the adipose tissue with impaired production of adipocytokines which, in turn, favor an increase in pro-inflammatory cytokines. In this review, we discuss how the obesity-related chronic state of low-grade inflammation and the presence of NAFLD lead to the emergence of a microenvironment favorable to the development of cancer.

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“…Hepatic histopathology was considerably improved after dietary intervention but did not reach statistical significance. Reports from rats have shown that switching to a normal low‐fat diet for 8 weeks after 8 weeks of high‐fat diet ameliorated dyslipidaemia as well as hepatic steatosis and inflammation . Thus, prolonged treatment duration may be necessary to reverse NASH via dietary intervention, especially considering the advanced disease stage in the current model, exhibiting hepatic fibrosis, which was not apparent in the rat model .…”

Section: Discussionmentioning

confidence: 91%

Liraglutide Decreases Hepatic Inflammation and Injury in Advanced Lean Non‐Alcoholic Steatohepatitis

Ipsen

Rolin

Rakipovski

et al. 2018

Basic Clin Pharma Tox

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Although commonly associated with obesity, non-alcoholic fatty liver disease (NAFLD) is also present in the lean population representing a unique disease phenotype. Affecting 25% of the world's population, NAFLD is associated with increased mortality especially when progressed to non-alcoholic steatohepatitis (NASH). However, no approved pharmacological treatments exist. Current research focuses mainly on NASH associated with obesity, leaving the effectiveness of promising treatments in lean NASH virtually unknown. This study therefore aimed to evaluate the effect of liraglutide (glucagon-like peptide 1 analogue) and dietary intervention, alone and in combination, in guinea pigs with non-obese NASH. After 20 weeks of high-fat feeding (20% fat, 15% sucrose, 0.35% cholesterol), 40 female guinea pigs were block-randomized based on weight into four groups receiving one of four treatments for 4 weeks: continued high-fat diet (HF, control), high-fat diet and liraglutide treatment (HFL), chow diet (4% fat, 0% sucrose, 0% cholesterol; HFC) or chow diet and liraglutide treatment (HFCL). High-fat feeding induced NASH with severe fibrosis. Liraglutide decreased inflammation (p < 0.05) and hepatocyte ballooning (p < 0.05), while increasing hepatic α-tocopherol (p = 0.0154). Dietary intervention did not improve liver histopathology significantly, but decreased liver weight (p = 0.004), plasma total cholesterol (p = 0.0175), LDL-cholesterol (p = 0.0063), VLDL-cholesterol (p = 0.0034), hepatic cholesterol (p < 0.0001) and increased hepatic vitamin C (p = 0.0099). Combined liraglutide and dietary intervention induced a rapid weight loss, necessitating periodical liraglutide dose adjustment/discontinuation, limiting the strength of the findings from this group. Collectively, this pre-clinical study supports the beneficial effect of liraglutide on NASH and extends this notion to lean NASH.

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Effects of a low-fat diet on the hepatic expression of adiponectin and its receptors in rats with NAFLD

Cited by 16 publications

References 29 publications

Adiponectin protects the rats liver against chronic intermittent hypoxia induced injury through AMP-activated protein kinase pathway

Adiponectin protects the rats liver against chronic intermittent hypoxia induced injury through AMP-activated protein kinase pathway

Obesity, Nonalcoholic Fatty Liver Disease and Adipocytokines Network in Promotion of Cancer

Liraglutide Decreases Hepatic Inflammation and Injury in Advanced Lean Non‐Alcoholic Steatohepatitis

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