2018
DOI: 10.1016/j.cellsig.2017.10.005
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Impairment of energy sensors, SIRT1 and AMPK, in lipid induced inflamed adipocyte is regulated by Fetuin A

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Cited by 29 publications
(20 citation statements)
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“…Fetuin-A is abundant, but its roles in disease progression are poorly understood. Previous studies reported that fetuin-A is crucial in lipid metabolism [22]. In this study, fetuin-A was not correlated with HDL-C or LDL-C, although HDL-C was nonsignificantly lower in persons with moderate/severe periodontitis.…”
Section: Discussioncontrasting
confidence: 53%
“…Fetuin-A is abundant, but its roles in disease progression are poorly understood. Previous studies reported that fetuin-A is crucial in lipid metabolism [22]. In this study, fetuin-A was not correlated with HDL-C or LDL-C, although HDL-C was nonsignificantly lower in persons with moderate/severe periodontitis.…”
Section: Discussioncontrasting
confidence: 53%
“…In particular, fetuin-A is the contributor which plays a critical role in the impairment of two metabolic sensors, Sirtuin 1 and AMP-activated protein kinase, in inflamed adipocytes of high fat diet mice [20]. Several studies was proposed that increased circulating fetuin-A in humans after a chronic exercise program may promote increased weight loss and improved metabolic control through elevation of adiponectin expression [20] and decrease of inflammatory cytokines in the liver and muscle [21] via fetuin-A inhibition through the AMP-activated protein kinase-nuclear factor kappa-light-chain-enhancer of activated B cells pathway [4]. Furthermore, fetuin-A directly correlated with two cardiometabolic risk markers, Apo B and C-reactive protein that, together with insulin resistance, are important components of the metabolic syndrome.…”
Section: Introductionmentioning
confidence: 99%
“…On the other hand, the role of FetA in the pathogenesis of inflammation, both in the systemic and tissue-specific inflammation, has received substantial attention in recent years. As described previously, FetA could induce the synthesis and secretion of pro-inflammatory adipokines and synergistically inhibit the lipid efflux especially within macrophages [117, 118]. In addition, the adipocyte-derived FetA shows the effect on the transformation of the anti-inflammatory M2-phenotype macrophages into the pro-inflammatory M1-phenotype macrophages, thus promoting the inflammatory process in humans [116].…”
Section: Adipokines Are Pathogenic Factors Which Link Psoriasis and Omentioning
confidence: 87%