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The SNARE protein SNAP23 and the SNARE-interacting protein Munc18c in human skeletal muscle are implicated in insulin resistance/type 2 diabetes.

Journal article
Authors Pontus Boström
Linda Andersson
Birgitte Vind
Liliana Håversen
Mikael Rutberg
Ylva Wickström
Erik Larsson
Per-Anders Jansson
M.K Svensson
Rickard Brånemark
Charlotte Ling
Henning Beck-Nielsen
Jan Borén
Kurt Højlund
Sven-Olof Olofsson
Published in Diabetes
Volume 59
Issue 8
Pages 1870-8
ISSN 1939-327X
Publication year 2010
Published at Institute of Biomedicine, Department of Medical Biochemistry and Cell Biology
Institute of Medicine, Department of Molecular and Clinical Medicine
Institute of Clinical Sciences
Pages 1870-8
Language en
Links dx.doi.org/10.2337/db09-1503
https://gup.ub.gu.se/file/69482
Keywords Biopsy, Blood Glucose, metabolism, Cytosol, metabolism, Diabetes Mellitus, Type 2, genetics, metabolism, Environment, Gene Expression Regulation, Glucose Clamp Technique, Humans, Insulin Resistance, genetics, Microsomes, Liver, metabolism, Munc18 Proteins, genetics, metabolism, Muscle, Skeletal, cytology, metabolism, pathology, Obesity, complications, genetics, metabolism, Proto-Oncogene Proteins c-akt, metabolism, Qb-SNARE Proteins, genetics, metabolism, Qc-SNARE Proteins, genetics, metabolism, Reference Values, Twins, Monozygotic
Subject categories Biomaterials, Surgical research

Abstract

OBJECTIVE: Our previous studies suggest that the SNARE protein synaptosomal-associated protein of 23 kDa (SNAP23) is involved in the link between increased lipid levels and insulin resistance in cardiomyocytes. The objective was to determine whether SNAP23 may also be involved in the known association between lipid accumulation in skeletal muscle and insulin resistance/type 2 diabetes in humans, as well as to identify a potential regulator of SNAP23. RESEARCH DESIGN AND METHODS: We analyzed skeletal muscle biopsies from patients with type 2 diabetes and healthy, insulin-sensitive control subjects for expression (mRNA and protein) and intracellular localization (subcellular fractionation and immunohistochemistry) of SNAP23, and for expression of proteins known to interact with SNARE proteins. Insulin resistance was determined by a euglycemic hyperinsulinemic clamp. Potential mechanisms for regulation of SNAP23 were also investigated in the skeletal muscle cell line L6. RESULTS: We showed increased SNAP23 levels in skeletal muscle from patients with type 2 diabetes compared with that from lean control subjects. Moreover, SNAP23 was redistributed from the plasma membrane to the microsomal/cytosolic compartment in the patients with the type 2 diabetes. Expression of the SNARE-interacting protein Munc18c was higher in skeletal muscle from patients with type 2 diabetes. Studies in L6 cells showed that Munc18c promoted the expression of SNAP23. CONCLUSIONS: We have translated our previous in vitro results into humans by showing that there is a change in the distribution of SNAP23 to the interior of the cell in skeletal muscle from patients with type 2 diabetes. We also showed that Munc18c is a potential regulator of SNAP23.

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