A new way to control blood sugar levels in diabetics

This study, therefore, may lead to the development of newer drugs

Researchers at SGPGIMS , Lucknow discover a new way to control blood sugar levels in diabetics .

India remains the diabetes capital of the world and around 9% of adult Indian population has diabetes. Patients with type 2 diabetes secrete not only too little insulin but also too much glucagon, which contributes to poor blood glucose control. Glucagon like insulin is a hormone secreted by our pancreas. However, it acts opposite to insulin and increase blood sugar levels in humans. After a meal, the secretion of glucagon is blocked to prevent excessive production of glucose by the liver.
When this fails in diabetic patients, too much glucagon contributes to increased hepatic glucose production that exacerbates the already high blood sugar levels of diabetics. Despite this vital function of glucagon, relatively little is known about how its secretion is regulated.

In a recent study, performed by the group led by Dr. Rohit A. Sinha, Dept of Endocrinology, SGPGIMS, and supported by the WellcomeTrust/DBT, his lab discovered a new way to reduce glucagon release. Using cell culture and animal models, Dr. Sinha’s Lab showed how glucagon release can be reduced by inhibiting the activity of a protein called as MTORC1 in the pancreas.

Inhibition of MTORC1 leads to degradation of stored glucagon by cellular structures known as lysosomes and stops glucagon from increasing blood sugar levels.

This study, therefore, may lead to the development of newer drugs that would control glucagon levels in humans and manage blood sugar levels in diabetics. This work has been recently published in an international journal “Molecular Metabolism”.

Reference:

Sangam Rajak, Sherwin Xie, Archana Tewari, Sana Raza, Wu Yajun, Boon-Huat Bay, Paul M. Yen, Rohit A. Sinha. MTORC1 inhibition drives crinophagic degradation of glucagon. Molecular Metabolism 2021, 101286, ISSN 2212-8778. https://doi.org/10.1016/j.molmet.2021.101286.

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