Green Tea and Decaffeinated Light Roasted Green Coffee Extract Combination Improved Cardiac Insulin Resistance through Free Fatty Acids and Adiponectin/FAS Pathways Amelioration in Metabolic Syndrome Rat Model.

BACKGROUND

Insulin resistance has been independently associated with cardiac diseases. Free fatty acids (FFAs) are known to induce cardiac insulin resistance via low-grade inflammation. Therefore, lowering FFA levels may improve cardiac insulin resistance. This study investigated the effects of a combination of green tea and decaffeinated light-roasted green coffee extract on free fatty acid-induced cardiac insulin resistance by modulating the adiponectin/FAS pathways.

METHODS

This study used 25 male Sprague-Dawley rats. Metabolic syndrome (MS) was induced using a high-fat, high-sucrose (HFHS) diet and a low-dose streptozotocin (STZ) injection, while a normal chow (NC) diet served as the healthy control. The MS rats were treated for 9 weeks with green tea (300 mg/kg b.w.), decaffeinated light-roasted green coffee (200 mg/kg b.w.), or a combination of both extracts. The experimental subjects were divided into five groups: 1) MS (HFHS diet + STZ), 2) NC (normal chow), 3) GT (green tea extract), 4) GC (decaffeinated light-roasted green coffee extract), and 5) CM (combination of both extracts). Adiponectin and HOMA-IR levels were analysed using ELISA, while the gene expression of Adipo-R1, FAS, PI3K, PDK1, Akt, and GLUT4 was measured using RT-PCR.

RESULTS

The combination of green tea and decaffeinated light-roasted green coffee demonstrated synergistic effects in reducing FFA levels. The adiponectin/FAS pathways were attenuated in the CM group. Furthermore, the combination therapy improved cardiac insulin resistance marker expressions, including IRS-1/2, PI3K, PDK1, Akt, and GLUT4.

CONCLUSIONS

The combination of green tea and decaffeinated light-roasted green coffee extract improved cardiac insulin resistance more effectively than the administration of either extract alone, by reducing FFA levels through the modulation of the adiponectin/FAS pathways.