Exposure to cold ameliorates glucose intolerance caused by high fat fed rats although enhancing obesity

Background: Browning, the process by which white adipocytes acquire characteristics of brown adipocytes, is emerging as a potential therapeutic strategy to combat obesity-related metabolic dysfunction. Intermittent cold exposure (ICE) has been shown to induce browning of WAT and enhance thermogenesis, which may improve glucose and lipid metabolism.Objective: To evaluate the effects of intermittent cold exposure (ICE) on glucose homeostasis and adipose tissue browning in obese rats, focusing on changes in glucose tolerance, insulin sensitivity, and adipose tissue morphology.Methods: A 32 male Sprague-Dawley rats were divided into four groups (8 rats/group): 1) Control (normal diet), 2) Control exposed to ICE, 3) high-fat high-fructose diet (HFFD), 4) HFFD exposed to ICE. Measured parameters including; body weight, food intake, fasting glucose, insulin sensitivity (HOMA-IR), and lipid profile, were assessed. Histopathological and molecular analyses of adipose tissue were conducted to evaluate browning markers (UCP1, CD137).Results: Although ICE led to increased body weight in both control and obese groups, ICE significantly improved glucose homeostasis in obese rats with reduction fasting insulin and HOMA-IR. ICE significantly ameliorated dyslipidaemia in obese rats. ICE activated BAT and induced browning of WAT, as evidenced by increased UCP1 expression in interscapular fat and enhanced CD137 expression in inguinal fat. Conclusion:Intermittent cold exposure enhances the browning of white adipose tissue and improves glucose and lipid metabolism in obese rats.