Inverse Relationship of theCMKLR1Relative Expression and Chemerin Serum Levels in Obesity with Dysmetabolic Phenotype and Insulin Resistance

Abstract

Background. In obesity there is a subclinical chronic low-grade inflammatory response where insulin resistance (IR) may develop. Chemerin is secreted in white adipose tissue and promotes low-grade inflammatory process, where it expressed CMKLR1 receptor. The role of chemerin and CMKLR1 in inflammatory process secondary to obesity is not defined yet. Methods. Cross-sectional study with 134 individuals classified as with and without obesity by body mass index (BMI) and IR. Body fat storage measurements and metabolic and inflammatory markers were measured by routine methods. Soluble chemerin and basal levels of insulin by ELISA and relative expression of CMKLR1 were evaluated with qPCR and 2−ΔΔCT method. Results. Differences (P < 0.05) were observed between obesity and lean individuals in body fat storage measurements and metabolic-inflammatory markers. Both CMKLR1 expression and chemerin levels were increased in obesity without IR. Soluble chemerin levels correlate with adiposity and metabolic markers (r = 8.8% to 38.5%), P < 0.05. Conclusion. The increment of CMKLR1 expression was associated with insulin production. Increased serum levels of chemerin in obesity were observed, favoring a dysmetabolic response. The results observed in this study suggest that both chemerin and CMKLR1 have opposite expression in the context of low-grade inflammatory response manifested in the development of IR.

Diabetes and Obesity—Cumulative or Complementary Effects On Adipokines, Inflammation, and Insulin Resistance

“…Initially, it was believed that the secretion of chemerin increases significantly in parallel to adipogenesis. It was assumed that the alteration of this process, or the change in the expression of the chemerin receptor CMKLR1 or chemerin-CMKLR1 signaling, affected adipocyte differentiation [7,56,68,69], impaired glucose homeostasis [70] and glucose-stimulated pancreatic insulin release [7], affected insulin sensitivity [71], and even modified the genes involved in lipid and glucose metabolism [7]. Recently, given chemerin's multiple roles, a new hypothesis was formed-chemerin itself can be a link between inflammation, obesity and atherosclerosis [72].…”

Low CD36 and LOX-1 Levels andCD36Gene Subexpression Are Associated with Metabolic Dysregulation in Older Individuals with Abdominal Obesity

“…To determine obesity and adiposity indexes, the following math calculations were used, BMI, kg/m 2 = weight (kg)/height 2 (m); WHR = WC cm/HC cm; WHtR = WC cm/height (cm); conicity index (CI) = WC (cm)/0.109√weight (kg)/height (cm); total adipose area (TAA, cm 2 ) = WC 2 /4 π ; visceral area (VA, cm 2 ) = π (WC/2 π − abdominal skinfold) 2 ; subcutaneous abdominal area (cm 2 ) = TAA − VA [ 26 ]; visceral adipose index (VAI): for males, VAI = (WC/36.58 + (1.896 ∗ BMI))6(TG/0.81)6(1.52/HDLc), and for females, VAI = (WC/39.68 + (1.886 ∗ BMI))6(TG/1.03)6(1.31/HDLc); abdominal volume index (AVI, L) = [2 × WC 2 + (0.7 cm)(WC − HC) 2 /1000] [ 32 ]; and homeostasis model assessment-insulin resistance (HOMA-IR) = [basal glucose mg/dL × (basal insulin μ UI/mL)/405] [ 33 , 34 ], in addition to the sum of the 5 skin fold thicknesses (ST5) [ 35 ].…”

Chemerin serum level and insulin resistance in hypertensive patients with obesity

“…The revealed relations between serum chemerin levels and carbohydrate metabolism indices in patients with hypertension on the background of the highest chemerin levels in patients with concomitant obesity of the I gr. with subsequent decrease in higher grades of obesity, as well as significant increase in the rate of patients with IR ( Fig.1) in groups with morbid obesity can be explained by the data presented in [11]. It is known that macrophages play a decisive role in the formation of IR [12].…”