Adiponectin as a protective factor in hepatic steatosis

Méndez-Sánchez, Nahúm; Chávez-Tapia, Norberto C.; Villa, Antonio; Sánchez-Lara, Karla; Zamora-Valdés, Daniel; Ramos, Martha H.; Uribe, Misael

doi:10.3748/wjg.v11.i12.1737

Cited by 41 publications

(25 citation statements)

References 34 publications

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“…52) Another GLP-1 analogue, exendin-4, has been demonstrated to decrease the fatty acid load in hepatocytes and reverse hepatic steatosis in obese mice. 53,54) In the present study, our results confirmed that liraglutide decreased body weight, increased insulin sensitivity, reduced hepatic lipid accumulation and consequently decreased serum ALT levels, which indicated that liraglutide might have a liver protective effect in the rats with HFHC diet-induced NAFLD. Previous studies have reported that MDA levels in the liver were reduced by administration of exendin-4 in ob/ob mice.…”

Section: Discussionsupporting

confidence: 76%

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The Glucagon-Like Peptide-1 Analogue Liraglutide Inhibits Oxidative Stress and Inflammatory Response in the Liver of Rats with Diet-Induced Non-alcoholic Fatty Liver Disease

Gao

Zeng

Zhang

et al. 2015

Biological & Pharmaceutical Bulletin

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Liraglutide, a glucagon-like peptide-1 (GLP-1) analogue, has been demonstrated to reduce hepatic steatosis. However, the mechanism of the lipid-lowering effect of liraglutide in the liver remains unclear. The aim of the present study was to investigate the beneficial effect of liraglutide on diet-induced non-alcoholic fatty liver disease (NAFLD) and the underlying mechanism in rats. NAFLD was induced in Sprague-Dawley rats by feeding a high fat and high cholesterol (HFHC) diet. Liraglutide (0.6 mg/kg body weight/d) was injected intraperitoneally to the rats subjected to HFHC diet four weeks before sacrificing the animals. Body and liver weight, fasting blood glucose (FBG), fasting insulin, serum aminotransferase (ALT) and lipid accumulation in the liver were determined. Markers of oxidative stress, such as malondialdehyde (MDA), free fatty acid (FFAs), superoxide dismutase (SOD), and pro-inflammatory cytokine tumor necrosis factor-α (TNF-α) were detected by colorimetric detection or enzyme-linked immunosorbent assay (ELISA). Serum and hepatic adiponectin were measured by ELISA. The expression of c-Jun N-terminal kinase-1 (JNK-1) and phosphorylated JNK-1 were examined by Western blotting. Liraglutide improved insulin resistance, decreased hepatic steatosis and reversed liver dysfunction. The hepatic levels of MDA, FFAs, and TNF-α were significantly decreased versus controls. Meanwhile, administration of liraglutide significantly increased SOD and adiponectin levels in the liver and inhibited the expression of JNK-1 and phosphorylated JNK-1 versus control rats. Liraglutide exerted anti-oxidative and anti-inflammatory effects in the liver and consequently reversed hepatic steatosis and insulin resistance. Such effects might be mediated by the elevation of adiponectin levels and the inactivation of JNK-1.

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Section: Discussionsupporting

confidence: 76%

“…54) A large number of studies in experimental animals and patients have found that the level of adiponectin is closely related to obesity, insulin resistance, coronary heart disease and NAFLD. 55,56) In addition, adiponectin has been reported to be tightly associated with oxidative stress and inflammatory respons.…”

Section: Discussionmentioning

confidence: 99%

The Glucagon-Like Peptide-1 Analogue Liraglutide Inhibits Oxidative Stress and Inflammatory Response in the Liver of Rats with Diet-Induced Non-alcoholic Fatty Liver Disease

Gao

Zeng

Zhang

et al. 2015

Biological & Pharmaceutical Bulletin

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“…Diagn. 7(2), (2007) are significantly lower in NAFLD patients than in their matched controls [26,27]. This is also true for the patients with coronary artery disease [28].…”

supporting

confidence: 58%

Adipokines and melanocortins in the hepatic manifestation of metabolic syndrome: nonalcoholic fatty liver disease

Jarrar¹

2018

Preprint

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Metabolic syndrome is associated with nonalcoholic fatty liver disease and its more aggressive form, nonalcoholic steatohepatitis. Adipokines produced by white adipose tissue possess broad physiological activity and play an important autocrine role in obesity-associated complications, including metabolic syndrome, nonalcoholic fatty liver disease and cardiovascular disease. Various adipokines may have beneficial or harmful effects. Other tissues, particularly stomach and intestine, produce active molecules that can influence the function of adipocytes and, possibly, the levels of adipokine secretion. In some cases, the production sites of these molecules remain unknown. The review focuses on our current understanding of the disease-related effects of the adipokines and the melanocortins on various peripheral tissues, and discusses some of their potential interactions with each other. Potential therapeutic applications are also considered.Expert Rev. Mol. Diagn. 7(2), 195-205 (2007) Multiple facets of metabolic syndromeMetabolic syndrome (MS) was first introduced as a clinical entity by Reaven in 1988 [1]. MS represents a cluster of risk factors commonly associated with central obesity, insulin-resistance, hypertension and elevated triglycerides, as well as decreased high-density lipoprotein cholesterol. In turn, MS is associated with an increased risk of cardiovascular disease and is a common early abnormality in the development of Type 2 diabetes. Additionally, MS plays a well-recognized role in the development of the obstructive sleep apnea, erectile dysfunction, polycystic ovary syndrome and malignant tumors. It is noteworthy that, despite tremendous clinical impact of MS, there is no clear consensus regarding the diagnostic criteria for this important nosological entity. To date, different criteria have been proposed by the WHO, by the third report of the National Cholesterol Education Program Adult Treatment Panel III (ATPIII) on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults, International Diabetes Federation, European Group for the Study of Insulin Resistance, and American College of Endocrinology. The problem of multiple MS definitions was recently addressed in a joint statement of The American Diabetes Association and the European Association for the Study of Diabetes [2]. The statement and other publications stress the necessity of introduction of additional criteria for MS including concentrations of the proand anti-inflammatory proteins in the serum. It is most likely that the list of the etiological factors driving the development of MS includes abnormalities in visceral adipose tissue or an altered inflammatory background that, in turn, stimulate the development of the secondary complications of MS.Recently, nonalcoholic fatty liver disease (NAFLD) and its more aggressive form, nonalcoholic steatohepatitis (NASH), have come to be regarded as the hepatic manifestation of MS. In this context, insulin resistance (IR) is 196Expert Rev. Mol. Diagn. 7(2), (2007) the key eve...

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“…2A, 10) were detected in CM. As hepatocyte growth factor, leptin, and adiponectin have been shown to act as protective factors against steatosis, [15][16][17] we investigated the effect of blocking antibodies against IL-6, GRO, IL-8, and MCP-1. Only anti-MCP-1 blocked CM-induced lipid accumulation in Huh-7 cells, albeit not completely (Fig.…”

Section: Of Human Scwat Explants Induces Significantmentioning

confidence: 99%

Monocyte chemoattractant protein-1 secreted by adipose tissue induces direct lipid accumulation in hepatocytes

et al. 2008

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For many years, adipose tissue has been mainly considered as an inert reservoir for storing triglycerides. Since the discovery that adipocytes may secrete a variety of bioactive molecules (hormones, chemokines, and cytokines), an endocrine and paracrine role for white adipose tissue (WAT) in the regulation of energy balance and other physiological processes has been established, particularly with regard to brain and muscle. In contrast, little is known about the interactions of WAT with liver. Hence, we examined the effect of the secretory products of WAT on hepatocytes. Conditioned medium of human WAT explants induced significant steatosis in hepatocyte cell lines. Factor(s) responsible for the conditioned medium-induced steatosis were screened by a battery of blocking antibodies against different cytokines/chemokines shown to be secreted by WAT. In contrast to interleukin-8 and interleukin-6, the monocyte chemoattractant protein-1 was capable of inducing steatosis in hepatocytes in a time-dependent manner at concentrations similar to those found in conditioned medium. Incubation of conditioned medium with antimonocyte chemoattractant protein-1 antibodies prevented triglyceride accumulation. Investigation of the mechanism leading to the triglyceride accumulation showed that both a diminution of apolipoprotein B secretion and an increase in phosphoenolpyruvate carboxykinase messenger RNA may be involved. Conclusion: The monocyte chemoattractant protein-1 secreted by adipose tissue may induce steatosis not only recruiting macrophages but also acting directly on hepatocytes. (HEPATOLOGY 2008;48:799-807.)

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Adiponectin as a protective factor in hepatic steatosis

Cited by 41 publications

References 34 publications

The Glucagon-Like Peptide-1 Analogue Liraglutide Inhibits Oxidative Stress and Inflammatory Response in the Liver of Rats with Diet-Induced Non-alcoholic Fatty Liver Disease

The Glucagon-Like Peptide-1 Analogue Liraglutide Inhibits Oxidative Stress and Inflammatory Response in the Liver of Rats with Diet-Induced Non-alcoholic Fatty Liver Disease

Adipokines and melanocortins in the hepatic manifestation of metabolic syndrome: nonalcoholic fatty liver disease

Monocyte chemoattractant protein-1 secreted by adipose tissue induces direct lipid accumulation in hepatocytes

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