Munc18c: a controversial regulator of peripheral insulin action
ORCID
Latha Ramalingam: 0000-0002-4856-7327
Document Type
Article
Date
11-2014
Keywords
GLUT4 vesicle exocytosis, SNARE proteins, adipose, glucose uptake, skeletal muscle
Disciplines
Nutrition
Description/Abstract
Insulin resistance, a hallmark of impaired glucose tolerance and type 2 diabetes (T2D), arises from dysfunction of insulin action and subsequent glucose uptake by peripheral tissues, predominantly skeletal muscle and fat. Exocytosis of glucose transporter (GLUT4)-containing vesicles facilitated by soluble NSF (N-ethylmaleimide-sensitive factor) attachment receptor (SNARE) protein isoforms, and Munc18c (mammalian homolog of Unc-18c) mediates this glucose uptake. Emerging evidences, including recent human clinical studies, point to pivotal roles for Munc18c in peripheral insulin action in adipose and skeletal muscle. Intriguing new advances are also initiating debates regarding the molecular mechanism(s) controlling Munc18c action. The objective of this review is therefore to present a balanced perspective of new continuities and controversies surrounding the regulation and requirement for Munc18c in the regulation of peripheral insulin action.
Recommended Citation
Ramalingam L, Yoder SM, Oh E, Thurmond DC. Munc18c: a controversial regulator of peripheral insulin action. Trends Endocrinol Metab. 2014 Nov;25(11):601-8. doi: 10.1016/j.tem.2014.06.010. Epub 2014 Jul 12. PMID: 25028245; PMCID: PMC4253632.
Creative Commons License
This work is licensed under a Creative Commons Attribution 4.0 International License.
