Bioenergetics and Type 2 DiabetesDoliba NM*
Department of Biochemistry and Biophysics, Institute for Diabetes, Obesity and Metabolism, University of Pennsylvania School of Medicine, PA, USA
- *Corresponding Author:
- Doliba NM
Department of Biochemistry
Biophysics and Institute for Diabetes
Obesity and Metabolism
University of Pennsylvania School of Medicine
PA 19104, USA
E-mail: [email protected]
Received Date: January 05, 2017; Accepted Date: January 16, 2017; Published Date: January 23, 2017
Citation: Doliba NM (2017) Bioenergetics and Type 2 Diabetes. Biochem Pharmacol (Los Angel) 5:222. doi: 10.4172/2167-0501.1000222
Copyright: © 2017 Doliba NM. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Hyperglycemia of type 2 diabetes mellitus (T2DM) develops when pancreatic β-cells damaged by chronic exposure to elevated blood glucose and lipids (glucolipotoxicity) fail to synthesize and secrete sufficient quantities of insulin for maintaining plasma glucose level. Despite intensive studies in this field, the molecular mechanism by which fatty acids (FA) cause β-cell impairment is not well understood. It still remains unknown what are the lipid- or glucose-derived molecules directly responsible for the impairment of β-cell function? Our studies showed that in addition to impaired insulin secretion and loss of biphasicity, T2D islets exhibited altered cell bioenergetics as evidenced by decreased oxygen consumption rate as compared to those of the control islets. We also discovered that fuel overload (high level of FA and glucose leads to incomplete FA oxidation and results in accumulation of "toxic" long-chain 3-OH-fatty acids that could induce oxidative stress and disrupt mitochondrial function. Timedependent impairments of bioenergetics due to chronic exposure to elevated blood glucose and lipids would be the consequence leading to pancreatic β-cell failure.