Regulation of synthesis and oxidation of fatty acids by adiponectin receptors (AdipoR1/R2) and insulin receptor substrate isoforms (IRS-1/-2) of the liver in a nonalcoholic steatohepatitis animal model

Matsunami, Tokio; Sato, Yukita; Ariga, Satomi; Sato, Takuya; Shimomura, Toshiko; Kashimura, Haruka; Hasegawa, Yuki; Yukawa, Masayoshi

doi:10.1016/j.metabol.2010.07.032

Cited by 37 publications

(21 citation statements)

References 49 publications

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“…Liver fibrosis in individuals infected with hepatitis C virus was associated with hyperadiponectinemia and, interestingly, reduced AdipoR1 expression (Corbetta et al, 2011). A study in humans showed no change in AdipoR expression in patients with NASH (Uribe et al, 2008), but an important role for changes in AdipoR expression was also shown in a study using a high-fat and high-cholesterol diet in obese fa/fa Zucker rats to induce NASH was associated with decreased AdipoR1 and AdipoR2 expression (Matsunami et al, 2011). In addition, liver expression and localization of adiponectin were increased in wild-type mice in response to carbon tetrachloride induced hepatofibrosis (Yoda-Murakami et al, 2001).…”

Section: Adiponectin Physiology and Evidence For Contribution Of Endomentioning

confidence: 97%

Adiponectin Action: A Combination of Endocrine and Autocrine/Paracrine Effects

Dadson

Liu²,

Sweeney

2011

Front. Endocrin.

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The widespread physiological actions of adiponectin have now been well characterized as clinical studies and works in animal models have established strong correlations between circulating adiponectin level and various disease-related outcomes. Thus, conventional thinking attributes many of adiponectin’s beneficial effects to endocrine actions of adipose-derived adiponectin. However, it is now clear that several tissues can themselves produce adiponectin and there is growing evidence that locally produced adiponectin can mediate functionally important autocrine or paracrine effects. In this review article we discuss regulation of adiponectin production, its mechanism of action via receptor isoforms and signaling pathways, and its principal physiological effects (i.e., metabolic and cardiovascular). The role of endocrine actions of adiponectin and changes in local production of adiponectin or its receptors in whole body physiology is discussed.

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Section: Adiponectin Physiology and Evidence For Contribution Of Endomentioning

confidence: 97%

Adiponectin Action: A Combination of Endocrine and Autocrine/Paracrine Effects

Dadson

Liu²,

Sweeney

2011

Front. Endocrin.

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“…Though not consistently seen in either human or animal studies (41), some reports indicate downregulation of adiponectin receptor transcription may be seen in livers of NAFLD and NASH patients (42, 43). Decreased expression of AdipoR2 has also been observed in murine models of hepatic steatosis (44). Conversely direct manipulation of adiponectin receptor expression demonstrates a potential causal relationship between adiponectin signaling and steatosis (45).…”

Section: Adiponectin Improves Hepatic Lipid Metabolismmentioning

confidence: 99%

Regulation of glucose and lipid homeostasis by adiponectin: Effects on hepatocytes, pancreatic β cells and adipocytes

Tao

Sifuentes

Holland

2014

Best Practice & Research Clinical Endocrinology & Metab

119

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Adiponectin has received considerable attention for its potential anti-diabetic actions. The adipokine exerts control of glucose and lipid homeostasis via critical effects within the liver, adipose, and pancreas. By stimulating adipogenesis, opposing inflammation, and influencing rates of lipid oxidation and lipolysis, adiponectin critically governs lipid spillover into non-adipose tissues. Ceramide, a cytotoxic and insulin desensitizing lipid metabolite formed when peripheral tissues are exposed to excessive lipid deposition, is potently opposed by adiponectin. Via adiponectin receptors, AdipoR1 and AdipoR2, adiponectin stimulates the deacylation of ceramide- yielding sphingosine for conversion to sphingosine 1-phosphate (S1P) by sphingosine kinase. The resulting conversion from ceramide to S1P promotes survival of functional beta cell mass, allowing for insulin production to meet insulin demands. Alleviation of ceramide burden on the liver allows for improvements in hepatic insulin action. Here, we summarize how adiponectin-induced changes in these tissues lead to improvements in glucose metabolism, highlighting the sphingolipid signaling mechanisms linking adiponectin to each action.

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“…For instance, TNF-α is involved in SREBP activation [24] . On the contrary adiponectin activates fatty acid oxidation [83,84] , but decreases the activity of fatty acid synthase and acetylcoenzyme A carboxylase [85] . Moreover, it inhibits liver production of TNF [86] .…”

Section: Fat As An Endocrine Organ: Cytokinesmentioning

confidence: 99%

Liver steatosis in hepatitis C patients

González‐Reimers¹

2015

WJH

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would affect HCV patients who are also obese or diabetics. In fact, several genotypes exert metabolic effects which overlap with some of those observed in the metabolic syndrome. In this review we will analyse the pathogenic pathways involved in the development of steatosis in HCV patients. Several cytokines and adipokines also become activated and are involved in "pure" steatosic effects, in addition to inflammation. They are probably responsible for the evolution of simple steatosis to steatohepatitis, making it difficult to explain why such alterations only affect a proportion of steatosic patients. Core tip: Chronic hepatitis C virus (HCV) infection can lead to steatosis and steatohepatitis. Increased liver triglyceride synthesis is mediated by several transcription factors such as sterol regulatory elementbinding protein (SREBP) whose expression is enhanced, in turn, by HCV core protein. Chronic HCV infection is also associated with insulin resistance that seems to be selective because although it activates systemic lipolysis, it increases triglyceride synthesis within the liver. This is due to the stimulatory effect of insulin on SREBP. It remains to be answered why not all patients with HCV infection and steatosis develop steatohepatitis despite early cytokine activation and metabolic derangements. AbstractThere is controversy regarding some aspects of hepatitis C virus (HCV) infection-associated liver steatosis, and their relationship with body fat stores. It has classically been found that HCV, especially genotype 3, exerts direct metabolic effects which lead to liver steatosis. This supports the existence of a so called viral steatosis and a metabolic steatosis, which REVIEWSubmit a

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Regulation of synthesis and oxidation of fatty acids by adiponectin receptors (AdipoR1/R2) and insulin receptor substrate isoforms (IRS-1/-2) of the liver in a nonalcoholic steatohepatitis animal model

Cited by 37 publications

References 49 publications

Adiponectin Action: A Combination of Endocrine and Autocrine/Paracrine Effects

Adiponectin Action: A Combination of Endocrine and Autocrine/Paracrine Effects

Regulation of glucose and lipid homeostasis by adiponectin: Effects on hepatocytes, pancreatic β cells and adipocytes

Liver steatosis in hepatitis C patients

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