Visceral Adipose Tissue-A Common Link to the Development of Nonalcoholic Fatty Liver Disease and Metabolic Syndrome

Objectives: Nonalcoholic fatty liver disease (NAFLD) is a major cause of liver-related morbidity and is frequently associated with obesity and metabolic syndrome. The recently discovered hormone adiponectin is produced by adipose tissue, and low plasma adiponectin is considered a key factor in the development of the insulin resistance underlying metabolic syndrome. Animal studies suggest that adiponectin may protect against non-alcoholic steatohepatitis, but direct evidence in humans is lacking. We therefore conducted this study to assess the relationship between plasma adiponectin and nonalcoholic fatty liver disease to explore its role in the pathogenesis of this disease. Design and methods: We measured plasma adiponectin and anthropometric, biochemical, hormonal and metabolic correlates in a group of 17 NAFLD patients with diagnosis confirmed by biopsy, and 20 controls with comparable age, body-mass index and sex. Furthermore we compared plasma adiponectin in patients with simple steatosis and steatohepatitis. Results: Plasma adiponectin was significantly lower in NAFLD patients than controls (5.93±0.45 vs 15.67±1.60 ng/ml). Moreover, NAFLD patients were significantly more insulin resistant while having similar serum leptin. Adiponectin was similar in simple steatosis and in steatohepatitis (6.16±0.78 vs 5.69±0.49 ng/ml). An inverse correlation was observed between adiponectin and homeostatic model assessment (HOMA) of insulin resistance (P = 0.008), while adiponectin did not correlate with serum transaminases and lipid values. Conclusions: These data support a role for low circulating adiponectin in the pathogenesis of NAFLD and confirm the strict association between reduced adiponectin production by adipose tissue, NAFLD and insulin resistance.

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Ectopic fat depots as a factor of cardiovascular risk in patients with nonalcoholic fatty liver disease

Clinical Medicine (Russian Journal) ◽

10.30629/0023-2149-2020-98-11-12-759-765 ◽

2021 ◽

Vol 98 (11-12) ◽

pp. 759-765

Author(s):

M. E. Statsenko ◽

S. V. Turkina ◽

I. A. Tyshchenko ◽

E. E. Gorbacheva

Keyword(s):

Adipose Tissue ◽

Liver Disease ◽

Fatty Liver ◽

Nonalcoholic Fatty Liver Disease ◽

Fatty Liver Disease ◽

Nonalcoholic Fatty Liver ◽

Fat Depots ◽

Increased Risk ◽

Visceral Adipose

The review represents evaluation of the ectopic fatty depots effect on the development of cardiovascular diseases (CVD) in patients with nonalcoholic fatty liver disease (NAFLD). Nowadays, NAFLD is the most common cause of chronic liver disease in most countries of the world. A number of studies have confirmed the important role of NAFLD in the formation and progression of CVD, which is manifested by an increased risk of cardiovascular events in patients with NAFLD according to Framingham Risk Score. The statement that NAFLD should be recognized as an independent risk factor for CVD, in addition to other metabolic disorders, is often confirmed. One of the possible mechanisms of interrelation between NAFLD and CVD is the paracrine activity of visceral adipose tissue; the possibility of local effects of various ectopic depots of visceral fat is being discussed. There is no doubt that epicardial adipose tissue plays an important role in the formation of the hepato-cardiac continuum. Тhere are more and more studies evaluating the effect of other ectopic depots on the development of CVD in patients with NAFLD. The article provides an analysis of publications devoted to the interrelation between fatty ectopic depots and CVD risks in patients with NAFLD. MedLine and PubMed databases in English and Russian languages were used for the search. The review includes articles published from 2000 to 2020.

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

10.31221/osf.io/brkq4 ◽

2018 ◽

Author(s):

Mohammed H Jarrar

Keyword(s):

Cardiovascular Disease ◽

Metabolic Syndrome ◽

Adipose Tissue ◽

Liver Disease ◽

Fatty Liver ◽

Nonalcoholic Fatty Liver Disease ◽

Fatty Liver Disease ◽

Physiological Activity ◽

Peripheral Tissues ◽

Nonalcoholic Fatty Liver

Metabolic syndrome is associated with nonalcoholic fatty liver disease and its moreaggressive 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 liverdisease and cardiovascular disease. Various adipokines may have beneficial or harmfuleffects. Other tissues, particularly stomach and intestine, produce active molecules thatcan influence the function of adipocytes and, possibly, the levels of adipokine secretion. Insome 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 potentialinteractions with each other. Potential therapeutic applications are also considered.

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Multidisciplinary Pharmacotherapeutic Options for Nonalcoholic Fatty Liver Disease

International Journal of Hepatology ◽

10.1155/2012/950693 ◽

2012 ◽

Vol 2012 ◽

pp. 1-13 ◽

Cited By ~ 11

Author(s):

Kei Nakajima

Keyword(s):

Type 2 Diabetes ◽

Metabolic Syndrome ◽

Liver Disease ◽

Fatty Liver ◽

Nonalcoholic Fatty Liver Disease ◽

Fatty Liver Disease ◽

Lipid Lowering ◽

Nonalcoholic Fatty Liver ◽

Ras Blockers

Nonalcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH) are multidisciplinary liver diseases that often accompany type 2 diabetes or metabolic syndrome, which are characterized by insulin resistance. Therefore, effective treatment of type 2 diabetes and metabolic syndrome should target not only the cardiometabolic abnormalities, but also the associated liver disorders. In the last decade, it has been shown that metformin, thiazolidinediones, vitamin E, ezetimibe, n-3 polyunsaturated fatty acids, renin-angiotensin system (RAS) blockers, and antiobesity drugs may improve hepatic pathophysiological disorders as well as clinical parameters. Accordingly, insulin sensitizers, antioxidative agents, Niemann-Pick C1-like 1 (NPC1L1) inhibitors, RAS blockers, and drugs that target the central nervous system may represent candidate pharmacotherapies for NAFLD and possibly NASH. However, the efficacy, safety, and tolerability of long-term treatment (potentially for many years) with these drugs have not been fully established. Furthermore, clinical trials have not comprehensively examined the efficacy of lipid-lowering drugs (i.e., statins, fibrates, and NPC1L1 inhibitors) for the treatment of NAFLD. Although clinical evidence for RAS blockers and incretin-based agents (GLP-1 analogs and dipeptidyl peptidase-4 inhibitors) is also lacking, these agents are promising in terms of their insulin-sensitizing and anti-inflammatory effects without causing weight gain.

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