The role of mTOR and oral intervention of combined Zingiber officinale ‐ Terminalia chebula extract in type 2 diabetes rat models

Abstract

The present study examined the potential of Zingiber officinale‐Terminalia chebula extract alone (ZO and TC) and in combination (ZOTC) against type 2 diabetes via downregulation of mechanistic target of rapamycin (mTOR). The 1:4 (ZOTC) ratio showed high cell survival percentage against the rat insulinoma cell line (RIN‐5F) when compared to other possible ratios of ZOTC. Oral administration of ZO alone, TC alone, combined ZOTC (1:4), and the positive control metformin (Met) in fructose‐streptozotocin (STZ) ‐induced diabetic rats showed reduced blood glucose levels, reduced insulin resistance (HOMA‐IR), increased insulin levels, and increased pancreatic beta cell function (HOMA‐β). ZOTC treatment in diabetic rats ameliorated the antioxidant status without affecting liver and serum parameters. Histological evaluation of the pancreas was performed to find pathological changes; the transcriptional and immunohistochemistry results showed reduced mTOR expression in the pancreas during ZOTC treatment. Conclusively, the results obtained suggest that ZOTC treatment against fructose‐STZ‐induced type 2 diabetes rat models can help regulate blood glucose, insulin levels, and normalize pancreatic β cell damage. Practical applications Type 2 diabetes is a chronic metabolic disorder that affects a large number of populations worldwide. Zingiber officinale (ZO) and Terminalia chebula (TC) has been used in traditional medicine since ancient times against various ailments, including diabetes. In this study, we reported the effect of the combined ZOTC that showed significant blood glucose reduction and increased insulin levels via mTOR when compared to individual treatments. This finding is valuable for food technologists and alternative medicine practitioners to know the antidiabetic effect of the ZOTC combination.

Negative Effects of Chronic High Intake of Fructose on Lung Diseases

“…Moreover, fructose intake upregulates S6 phosphorylation, a marker of the mTORC1 signaling pathway, in muscle and liver tissues [ 147 ]. Another study showed that mTORC1 protein levels were increased in the pancreatic tissue of rats with diabetes induced by fructose-streptozotocin [ 148 ]. A recent report showed that fructose enhanced the production of pro-inflammatory cytokines in response to LPS by increasing mTORC1 activity in monocytes [ 149 ].…”