Munc18c: a controversial regulator of peripheral insulin action

Latha Ramalingam, Stephanie M Yoder, Eunjin Oh, Debbie C Thurmond

Research output: Contribution to journalReview articlepeer-review

9 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)601-8
Number of pages8
JournalTrends in Endocrinology and Metabolism
Issue number11
StatePublished - Nov 2014
Externally publishedYes


  • Adipose Tissue/metabolism
  • Animals
  • Glucose/metabolism
  • Humans
  • Insulin/metabolism
  • Insulin Resistance/genetics
  • Multiprotein Complexes/metabolism
  • Munc18 Proteins/physiology
  • Muscle, Skeletal/metabolism
  • SNARE Proteins/metabolism


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