Endocrine Abstracts

Background: Chemerin is a multifunctional adipokine involved in pathogenesis of metabolic disease by regulating inflammation, adipocyte plasticity and glucose metabolism. It is known to be influenced by age, adiposity and triglycerides, and supports important roles in systemic lipid and glucose metabolism.However, the direct acute effects of circulating chemerin on varying metabolic disease states given a high–saturated fat meal has not been addressed.

Methods: Subjects (n = 54) were given a high-fat meal (75g fat, 5g carbohydrate, 6g protein) after an overnight fast (non-obese control (NOC): age 39.0±4.04, BMI 25.7±1.31, n = 7; impaired glucose tolerance (IGT): age 39.4±4.43, BMI 32.4±1.73, n = 8; obese: age 40.0±4.87, BMI 33.7±0.73, n = 5; type 2 diabetes mellitus (T2DM): age 45.4±2.34, BMI 29.0±1.07, n = 18). Serum was collected before and 4hr post meal for biochemical analysis.

Results: Circulating chemerin was significantly increased across the metabolic states from baseline assessment (NOC: (107.3±8.17ng/mL) Vs IGT: (132.1±4.43ng/mL) 1.2-fold↑, P < 0.05; NOC Vs Obese (179.4±4.87ng/mL) 1.7-fold↑, P < 0.0001). Obese participants had significantly raised chemerin levels compared with IGT (1.36-fold↑, P < 0.05) and T2DM participants (1.48-fold↑, P < 0.001). Across the entire cohort there was association between chemerin and increased body fat percentage pre- (R²=0.37↑, P < 0.01) and post-high-fat meal (R²=0.46↑, P < 0.001). These findings also showed that, 4hr after a meal, obese subjects had higher circulating chemerin levels (91%↑) than NOC subjects (P < 0.001).

Conclusions: This study highlights that irrespective of a single high-fat meal, circulating chemerin in an IGT and obese metabolic state remain elevated. Noting this elevation was substantial in obese subjects prior to an IGT or T2DM metabolic state. In Conclusions, these data suggest that prior to a compromised metabolic state such as T2DM, in obesity, chemerin levels remain high irrespective of fasting or high-fat meal, and may promote glucose dysfunction more rapidly due to the greater exposure to chemerin.