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.