Associations of a Panel of Adipokines with Fat Deposits and Metabolic Phenotypes in a General Population

Abstract

Objective: This study provides a comprehensive overview of the associations of five adipokines (adiponectin, chemerin, galectin-3, leptin, and resistin) with fat deposits, behavioral risk factors, and metabolic phenotypes. Methods: Using multivariable linear and logistic regression models, cross-sectional data from 4,116 participants of the population-based Study of Health in Pomerania were analyzed. Results: Participants with obesity showed higher chemerin, galectin-3, and leptin but showed lower adiponectin concentrations. Independently of other fat compounds, liver fat content, visceral adipose tissue, and subcutaneous adipose tissue (SAT) were inversely associated with adiponectin. Independent positive associations of liver fat content and SAT with chemerin as well as of SAT with galectin-3 and leptin were observed. Physically inactive participants had higher chemerin and leptin concentrations. Smokers had higher chemerin and galectin-3 as well as lower leptin. Alcohol consumption was associated with adiponectin (positive) and resistin (inverse). All adipokines were associated with at least one lipid marker. Associations with glucose metabolism were seen for adiponectin, chemerin, galectin-3, and leptin. Conclusions: High adiponectin concentrations were related to favorable metabolic conditions, whereas high chemerin, galectin-3, and leptin were associated with an unfavorable metabolic profile. High leptin seems to be primarily indicative of obesity, whereas high adiponectin and chemerin are associated with a broader range of metabolic phenotypes.

Proprotein convertase subtilisin/kexin type 9 (PCSK9) levels are not associated with severity of liver disease and are inversely related to cholesterol in a cohort of thirty eight patients with liver cirrhosis

“…Recombinant chemerin added to culture media did not regulate PCSK9 in hepatocellular carcinoma cell lines [64] and there is no evidence that PCSK9 affects hepatocyte chemerin expression. Serum chemerin is positively and adiponectin is negatively associated with an unfavourable metabolic phenotype in a population-based cohort study [65]. Such associations may change in severely ill patients including patients with liver cirrhosis [20].…”

SHIP-MR and Radiology: 12 Years of Whole-Body Magnetic Resonance Imaging in a Single Center

“…A role of adipokines in the development of fatty liver disease could be confirmed independently of inflammatory or metabolic diseases. Fischer et al [ 114 ] published a further analysis in which MR-quantified liver fat content and visceral and subcutaneous fat were investigated in relation to various adipokines including chemerin, leptin, adiponectin, resistin, and galectin-3.…”

Thromboinflammatory Processes at the Nexus of Metabolic Dysfunction and Prostate Cancer: The Emerging Role of Periprostatic Adipose Tissue

“…Chemerin (retinoic acid receptor 2, RARRES2) is an endogenous leukocyte chemoattractant that, through its cognate G protein-coupled receptor CMKLR1, participates in the early stages of acute inflammation [ 402 ]. Although states of metabolic dysfunction including insulin resistance, obesity, and T2D are associated with increased levels of circulating chemerin and CMKLR1 expression in SAT and VAT [ 402 , 403 , 404 , 405 , 406 , 407 , 408 , 409 ], there remain controversies concerning whether chemerin upregulation participates in disease pathogenesis or represents a compensatory mechanism. Particularly, and prior to the proteolytic cleavage of its C-terminal by various proteases including plasmin, FXIa, and FXIIa, circulating prochemerin is biologically inert [ 410 ].…”