Chemerin gene expression is regulated by food restriction and food restriction–refeeding in rat adipose tissue but not in liver

Stelmańska, Ewa; Śledziński, Tomasz; Turyn, Jacek; Presler, Malgorzata; Korczyńska, Justyna; Świerczyński, Julian

doi:10.1016/j.regpep.2012.12.001

Cited by 22 publications

(19 citation statements)

References 38 publications

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“…Evidence has proved that circulating chemerin is down-regulated by food restriction or exercise, and rose again by refeeding [23][24][25][26][27]. We presume that the reduction of serum chemerin in obese-GDM group may ascribe to reasonable diet and/or movement intervention.…”

Section: Discussionmentioning

confidence: 82%

Chemerin expression in Chinese pregnant women with and without gestational diabetes mellitus

et al. 2015

Annales d'Endocrinologie

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Section: Discussionmentioning

confidence: 82%

Chemerin expression in Chinese pregnant women with and without gestational diabetes mellitus

et al. 2015

Annales d'Endocrinologie

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“…Hepatic chemerin expression is not affected by food restriction and food restrictionrefeeding [23]. Adipocyte chemerin synthesis is upregulated by insulin but whether this contributes to higher serum chemerin levels is still a matter of debate [23][24][25].…”

Section: Regulating Of Hepatocyte Chemerin and Cmklr1mentioning

confidence: 99%

Chemerin in Liver Diseases

2014

Endocrinol Metab Synd

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Chemerin is a chemoattractant protein and moreover has a role in adipogenesis, angiogenesis and glucose homeostasis. Chemerin is primarily synthesized and secreted by adipocytes and hepatocytes. Chemerin receptors chemokine-like receptor 1 (CMKLR1), G-protein coupled receptor 1 (GPR1) and CC-motif chemokine receptorlike 2 (CCRL2) are all expressed in the liver suggesting that chemerin may be relevant in liver physiology and pathophysiology. Non-alcoholic fatty liver disease (NAFLD) is associated with obesity and is the most common cause of chronic liver injury. NAFLD and chronic hepatitis C virus infection are risk factors for hepatocellular carcinoma. Hepatic and serum chemerin have been analyzed in human and rodent NAFLD, in patients with chronic hepatitis C and patients with hepatocellular carcinoma. Chemerin, GPR1 and CMKLR1 deficient mice have been used to elucidate the role of these proteins in body weight gain and glucose homeostasis. The regulation of chemerin and CMKLR1 by adipokines, hormones and cytokines relevant in liver diseases has been studied in hepatocytes. The data published so far are briefly summarized herein. Current experimental findings do not provide evidence for a crucial role of chemerin in chronic liver diseases and further research is needed to evaluate a possible protective function of this protein in hepatocellular carcinoma.

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Section: Discussionmentioning

confidence: 99%

“…Other studies have demonstrated that short-term or long-term changes in nutritional status (fasting and re-feeding) affected chemerin mRNA expression and chemerin protein secretion from adipocytes and/or serum chemerin concentrations (22, 45). These latter effects may have been related to insulin stimulation of prochemerin secretion by adipocytes (26, 45). Despite these observations, the majority of clinical experimental studies have assessed plasma or serum chemerin concentrations in a single sample after an overnight fast and have thus not accounted for potential effects of time of day or nutritional effects on chemerin.…”

Section: Discussionmentioning

confidence: 99%

CMKLR1 activation ex vivo does not increase proportionally to serum total chemerin in obese humans

Toulany¹,

Parlee²,

Sinal³

et al. 2016

Endocrine Connections

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Prochemerin is the inactive precursor of the adipokine chemerin. Proteolytic processing is obligatory for the conversion of prochemerin into active chemerin and subsequent regulation of cellular processes via the chemokine-like receptor 1 (CMKLR1). Elevated plasma or serum chemerin concentrations and differential processing of prochemerin have been reported in obese humans. The impact of these changes on CMKLR1 signalling in humans is unknown. The objective of this pilot study was to develop a cellular bioassay to measure CMKLR1 activation by chemerin present in human serum and to characterise how obesity modifies serum activation of CMKLR1 under fasted and fed conditions. Blood samples were collected from control (N = 4, BMI 20–25) and obese (N = 4, BMI >30) female subjects after an overnight fast (n = 2) and at regular intervals (n = 7) following consumption of breakfast over a period of 6 h. A cellular CMKLR1-luminescent reporter assay and a pan-chemerin ELISA were used to determine CMKLR1 activation and total chemerin concentrations, respectively. Serum total chemerin concentration (averaged across all samples) was higher in obese vs control subjects (17.9 ± 1.8 vs 10.9 ± 0.5 nM, P < 0.05), but serum activation of CMKLR1 was similar in both groups. The CMKLR1 activation/total chemerin ratio was lower in obese vs control subjects (0.33 ± 0.04 vs 0.58 ± 0.05, P < 0.05). After breakfast, serum total chemerin or CMKLR1 activation did not differ from baseline values. In conclusion, the unexpected observation that obese serum activation of CMKLR1 did not match increased total chemerin concentrations suggests impaired processing to and/or enhanced degradation of active chemerin in serum of obese humans.

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Chemerin gene expression is regulated by food restriction and food restriction–refeeding in rat adipose tissue but not in liver

Cited by 22 publications

References 38 publications

Chemerin expression in Chinese pregnant women with and without gestational diabetes mellitus

Chemerin expression in Chinese pregnant women with and without gestational diabetes mellitus

Chemerin in Liver Diseases

CMKLR1 activation ex vivo does not increase proportionally to serum total chemerin in obese humans

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