title: Relationships between serum adiponectin and soluble TNF-α receptors and glucose and lipid oxidation in lean and obese subjects.
abstract: Insulin resistance might be associated with an impaired ability of insulin to stimulate glucose oxidation and inhibit lipid oxidation. Insulin action is also inversely associated with TNF-α system and positively related to adiponectin. The aim of the present study was to analyze the associations between serum adiponectin, soluble TNF-α receptors concentrations and the whole-body insulin sensitivity, lipid and glucose oxidation, non-oxidative glucose metabolism (NOGM) and metabolic flexibility in lean and obese subjects. We examined 53 subjects: 25 lean (BMI < 25 kg × m(-2)) and 28 with overweight or obesity (BMI > 25 kg × m(-2)) with normal glucose tolerance. Hyperinsulinemic euglycemic clamp and indirect calorimetry were performed. An increase in respiratory exchange ratio in response to insulin was used as a measure of metabolic flexibility. Obese subjects had lower insulin sensitivity, adiponectin and higher sTNFR1 (all P < 0.001) and sTNFR2 (P = 0.001). Insulin sensitivity was positively related to adiponectin (r = 0.49, P < 0.001) and negatively related to sTNFR1 (r = -0.40, P = 0.004) and sTNFR2 (r = -0.52, P < 0.001). Adiponectin was related to the rate of glucose (r = 0.47, P < 0.001) and lipid (r = -0.40, P = 0.003) oxidation during the clamp, NOGM (r = 0.41, P = 0.002) and metabolic flexibility (r = 0.36, P = 0.007). Serum sTNFR1 and sTNFR2 were associated with the rate of glucose (r = -0.45, P = 0.001; r = -0.51, P < 0.001, respectively) and lipid (r = 0.52, P < 0.001; r = 0.46, P = 0.001, respectively) oxidation during hyperinsulinemia, NOGM (r = -0.31, P = 0.02; r = -0.43, P = 0.002, respectively) and metabolic flexibility (r = -0.47 and r = -0.51, respectively, both P < 0.001) in an opposite manner than adiponectin. Our data suggest that soluble TNF-α receptors and adiponectin have multiple effects on glucose and lipid metabolism in obesity.
authors.affiliation: Department of Endocrinology, Diabetology and Internal Medicine, Medical University of Białystok, Poland.
authors.forename: A
authors.initials: A
authors.lastname: Adamska
authors.forename: A
authors.initials: A
authors.lastname: Nikołajuk
authors.forename: M
authors.initials: M
authors.lastname: Karczewska-Kupczewska
authors.forename: I
authors.initials: I
authors.lastname: Kowalska
authors.forename: E
authors.initials: E
authors.lastname: Otziomek
authors.forename: M
authors.initials: M
authors.lastname: Górska
authors.forename: M
authors.initials: M
authors.lastname: Strączkowski
mesh_terms: D052242:Adiponectin / Q000097:blood*; D000328:Adult; D001786:Blood Glucose / Q000378:metabolism*; D015992:Body Mass Index; D005260:Female; D006801:Humans; D050356:Lipid Metabolism / Q000502:physiology*; D008055:Lipids / Q000097:blood; D008297:Male; D009765:Obesity / Q000097:blood* / Q000378:metabolism; D010084:Oxidation-Reduction; D018124:Receptors, Tumor Necrosis Factor / Q000097:blood* / Q000378:metabolism; D012995:Solubility; D013851:Thinness / Q000097:blood* / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D055815:Young Adult
chemical_list: C499918:ADIPOQ protein, human; D052242:Adiponectin; D001786:Blood Glucose; D008055:Lipids; D018124:Receptors, Tumor Necrosis Factor; D014409:Tumor Necrosis Factor-alpha