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

Abstract

Background: Insulin resistance has been independently associated with cardiac diseases. Free fatty acids are recently known to induce cardiac insulin resistance due to low-grade inflammation. Therefore, the improvement of free fatty acid levels can also improve cardiac insulin resistance. This study investigated the combination of green tea and decaffeinated-light roasted green coffee extract in the improvement of free fatty acid-induced cardiac insulin resistance by improving the adiponectin/FAS pathways. Methods: This study used 25 males Sprague-Dawley rats induced by a high-fat high sucrose diet and injection of low dose streptozotocin to make a metabolic syndrome (MS) rat model and standard chow as healthy control rats. The MS rats were treated with green tea (200 mg/ b. w.), decaffeinated-light roasted green coffee (300 mg/ b. w.), and the combination of both extracts in 9 weeks. Experimental groups in this study were divided into 5 groups: 1) MS (HFHS diet + STZ) group, 2) NC (normal chow) group, 3) GT (green tea extract) group, 4) GC (decaffeinated-light roasted green coffee extract), 5) CM (combination of both extracts) group. Adiponectin and HOMA-IR level was analysed using ELISA, and the gene expression of Adipo-R1, FAS, PI3K, PDK1, Akt, GLUT4 was measured by RT-PCR. Results: The combination of green tea and decaffeinated-light roasted green coffee showed synergistic effects in improving FFA levels. The adiponectin/FAS pathways was attenuated in the CM group. Moreover, the combination also showed improvement in cardiac insulin resistance markers such as IRS1/2, PI3K, PDK1, Akt, and GLUT4. Conclusions:  The combination of green tea and decaffeinated-light roasted green coffee extract improved cardiac insulin resistance better than green tea and green coffee extract administration alone by reducing free fatty acids levels through adiponectin/FAS pathways modulation.