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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.

Artikel i vetenskaplig tidskrift
Författare 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
Publicerad i Diabetes
Volym 59
Nummer/häfte 8
Sidor 1870-8
ISSN 1939-327X
Publiceringsår 2010
Publicerad vid Institutionen för biomedicin, avdelningen för medicinsk kemi och cellbiologi
Institutionen för medicin, avdelningen för molekylär och klinisk medicin
Institutionen för kliniska vetenskaper
Sidor 1870-8
Språk en
Länkar dx.doi.org/10.2337/db09-1503
https://gup.ub.gu.se/file/69482
Ämnesord 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
Ämneskategorier Biomaterial, Kirurgisk forskning

Sammanfattning

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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