Mitochondrial Dysfunction in Type 2 Diabetes Mellitus: Imeglimin as a Novel Therapeutic Approach

Dr SURENDER KUMAR; Dr RISHI SHUKLA; Dr SHAMBO SAMAJDAR; Dr SOUMIK GOSWAMI; Dr OM LAKHANI; Dr PREM KUMAR; Dr SAMEER MUCHHALA; Dr NIDDHI BAXI

doi:10.59793/0vmn8208

Authors

Dr SURENDER KUMAR Senior Endocrinologist, Dept. of Endocrinology and Metabolism, Sir Ganga Ram Hospital, New Delhi, India
Dr RISHI SHUKLA †Director and Head, Dept. of Endocrinology, Regency Health, Kanpur; Founder, Center for Diabetes and Endocrine Diseases, Kanpur, Uttar Pradesh, India
Dr SHAMBO SAMAJDAR Independent Clinical Pharmacologist and Assistant Professor, JMN Medical College and Hospital, Chakdaha, Nadia, West Bengal, India
Dr SOUMIK GOSWAMI Assistant Professor, Endocrinology, NRS Medical College, Kolkata, West Bengal, India
Dr OM LAKHANI Consultant Endocrinologist, Zydus Hospitals, Ahmedabad, Gujarat, India
Dr PREM KUMAR Consultant Endocrinologist, Diaplus Multi Speciality Hospital, Salem, Tamil Nadu, India
Dr SAMEER MUCHHALA General Manager, Zydus Healthcare Ltd., Mumbai, Maharashtra, India
Dr NIDDHI BAXI Medical Advisor, Zydus Healthcare Ltd., Mumbai, Maharashtra, India

DOI:

https://doi.org/10.59793/0vmn8208

Keywords:

Beta-cells,, imeglimin,, insulin secretion,, mitochondrial dysfunction

Abstract

Insulin resistance (IR) in peripheral tissues, such as skeletal muscle and adipose tissue, is
recognized as a precursor to type 2 diabetes mellitus (T2DM). Mitochondria play a vital role in
the pathogenesis of T2DM, primarily attributed to the oxidative stress and systemic inflammation
caused by the compromised mitochondrial function, which further results in IR. Imeglimin, a
mitochondrial modulator, has been shown to enhance insulin secretion, achieve optimal glucose
control, and improve insulin sensitivity. The available evidence suggests that imeglimin can boost
mitochondrial bioenergetics, regulate respiratory chain functions, and reduce reactive oxygen
species (ROS) production, while protecting endothelial cells without affecting mitochondrial
respiration. In T2DM patients, imeglimin improves beta-cell glucose responsiveness and
stimulates insulin secretion via multiple pathways. Imeglimin has been shown to be well-tolerated
and effective in the management of T2DM, both as a standalone treatment and in combination
with other oral therapies, with evidence indicating improvements in insulin sensitivity and
reductions in blood glucose levels. All these insights point towards imeglimin being a unique
drug in the management of T2DM, making it an important addition to the armamentarium of
diabetes treatment.