Adiponectin upregulates hepatocyte CMKLR1 which is reduced in human fatty liver

Wanninger, Josef; Walter, Roland; Bauer, Sabrina; Weiß, TS; Eisinger, Kristina; Hellerbrand, Claus; Schäffler, Andréas; Higuchi, Akiko; Walsh, Kenneth; Buechler, Christa

doi:10.1055/s-0031-1295836

Cited by 10 publications

(19 citation statements)

References 36 publications

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“…Chemerin acts by binding the G protein-coupled receptor, chemokine receptor-like 1 (CMKLR1) (also known as chemerin receptor 23 (ChemR23)) [7,26], expressed by a variety of cells [26,27,28,29]. CMKLR1 was highly abundant in the liver and is expressed by primary human hepatocytes, hepatic stellate cells, Kupffer cells, and bile duct cells [30]. The data with respect to chemerin and CMKLR1 mRNA is very limited and equivocal.…”

Section: Introductionmentioning

confidence: 99%

Hepatic chemerin mRNA in morbidly obese patients with nonalcoholic fatty liver disease

Kajor¹,

Kukla²,

Waluga³

et al. 2017

pjp

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The aim of this study was to investigate hepatic chemerin mRNA, serum chemerin concentration, and immunohistochemical staining for chemerin and and chemokine receptor-like 1 (CMKLR1) in hepatic tissue in 56 morbidly obese women with nonalcoholic fatty liver disease (NAFLD) and to search for a relationship with metabolic and histopathological features. Chemerin mRNA was assessed by quantitative real-time PCR, chemerin, and CMKLR1 immunohistochemical expression with specific antibodies, while serum chemerin concentration was assessed with commercially available enzyme-linked immunosorbent assays. Serum chemerin concentration reached 874.1 ±234.6 ng/ml. There was no difference in serum chemerin levels between patients with BMI < 40 kg/m 2 and ≥ 40 kg/m 2 . Serum chemerin concentration tended to be higher in patients with hepatocyte ballooning, greater extent of steatosis, and definite nonalcoholic steatohepatitis (NASH). Liver chemerin mRNA was observed in all included patients and was markedly, but insignificantly, higher in those with BMI ≥ 40 kg/ m 2 , hepatocyte ballooning, greater extent of steatosis, and definite NASH. Hepatic chemerin mRNA might be a predictor of hepatic steatosis, hepatocyte ballooning, and NAFLD activity score (NAS) but seemed not to be a primary driver regulating liver necroinflammatory activity and fibrosis. The lack of association between serum chemerin and hepatic chemerin mRNA may suggest that adipose tissue but not the liver is the main source of chemerin in morbidly obese women.

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Section: Introductionmentioning

confidence: 99%

Hepatic chemerin mRNA in morbidly obese patients with nonalcoholic fatty liver disease

Kajor¹,

Kukla²,

Waluga³

et al. 2017

pjp

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show abstract

“…CMKLR1 was detected in primary human hepatocytes, Kupffer cells, bile-duct cells and hepatic stellate cells, but was decreased in human and rodent fatty liver and in fibrotic liver of mice. Adiponectin strongly upregulated CMKLR1 in primary human hepatocytes and in liver tissue while hepatic CMKLR1 was suppressed in the liver of adiponectin deficient mice (86). A recent study showed that pretreatment with resolvin D1 attenuated endoplasmic reticulum stress-induced apoptosis and decreased caspase 3 activity in HepG2 cells (87).…”

Section: Omega-3 Fatty Acids and Resolution Of Inflammation In Nafld:mentioning

confidence: 98%

Data Uncertainty in Virtual Network Embedding: Robust Optimization and Protection Levels

2016

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“…Mechanistically, autophagy activation by adiponectin causes digestion of Bax, thereby preventing caspase activation. 6) In addition, adiponectin enhances the expression of chemokine-like receptor 1 and CXCL8 by adipoR1 signaling in human hepatocytes, 17,18) which behave as survival factors in the liver. Adiponectin also attenuates ceramide accumulation in liver.…”

Section: Anti-apoptotic and Pro-survival Effects Of Adiponectin In LImentioning

confidence: 99%

Modulation of Cell Death and Survival by Adipokines in the Liver

Nepal

Park

2015

Biological & Pharmaceutical Bulletin

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Adipokines, hormones predominantly produced from adipose tissue, have been shown to impart dynamic functions in the liver. Emerging evidence has shown that adipokines are also involved in modulating liver cell survival and/or death. Among the various adipokines, adiponectin and leptin directly regulate proliferation of hepatocytes, Kupffer cells, and hepatic stellate cells. Moreover, these adipokines control apoptosis and cell cycle of hepatic cancer cells in a complex manner. Adiponectin possesses both pro-and anti-proliferative properties, whereas leptin appears to play roles as a pro-survival hormone. Recent studies have revealed that regulation of cell death and proliferation is one of the critical factors regulating liver physiology by adipokines. In this review, we summarize the effects of adipokines on apoptosis and survival of liver cells and also demonstrate their implications in regulating various liver functions and decipher the underlying molecular mechanisms.

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Adiponectin upregulates hepatocyte CMKLR1 which is reduced in human fatty liver

Cited by 10 publications

References 36 publications

Hepatic chemerin mRNA in morbidly obese patients with nonalcoholic fatty liver disease

Hepatic chemerin mRNA in morbidly obese patients with nonalcoholic fatty liver disease

Data Uncertainty in Virtual Network Embedding: Robust Optimization and Protection Levels

Modulation of Cell Death and Survival by Adipokines in the Liver

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