Abstract

Epidemiological data has associated coffee consumption with a lower prevalence of type 2 diabetes, metabolic syndrome and chronic liver disease. However, the mechanisms and coffee substances responsible for these effects remain unclear. In the present study, mice received caffeinated or decaffeinated instant coffee ad libitum during a two week period after inducing obesity by introducing a high-fat diet over a 10week period. Body weight, glucose homeostasis, and liver and visceral adipose tissue inflammation were assessed. In addition, AKT signaling, the fatty acid profile and liver histopathological analyses were performed. Ingestion of caffeinated or decaffeinated coffee for 2weeks resulted in reductions in glucose and insulin blood levels, and insulin tolerance was improved without reductions in final body weight or adiposity. Only caffeinated coffee modified the adipokine profile in visceral adipose tissue, resulting in a restoration of adiponectin levels. However, deleterious liver alterations, which manifested as reductions in steatosis, inhibition of iNOS expression and restoration of insulin inducing-AKT phosphorylation, were reversed by the ingestion of both caffeinated and decaffeinated coffee. Serum AST and ALT levels were also improved in mice after coffee ingestion, while the fatty acid profile in the liver and the cytokine profiles in adipose and liver tissues were not altered by coffee ingestion. Thus, instant coffee consumption reverses obesity-induced alterations in mice, and our results corroborate those of epidemiological studies that associated coffee consumption with a lower prevalence of obesity-related pathologies.

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call