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Hyperinsulinemic-euglycemic Clamps in Conscious, Unrestrained Mice
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Published on: November 16, 2011

Increased insulin action in SKIP heterozygous knockout mice.

Takeshi Ijuin1, Y Eugene Yu, Kiyohito Mizutani

  • 1Division of Lipid Biochemistry, Kobe University Graduate School of Medicine, Kobe 650-0017, Hyogo, Japan.

Molecular and Cellular Biology
|June 25, 2008
PubMed
Summary

Mice lacking the SKIP gene show improved insulin sensitivity and reduced obesity. This suggests SKIP is a potential therapeutic target for treating insulin resistance and diabetes.

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Published on: January 4, 2018

Area of Science:

  • Metabolic research
  • Molecular biology
  • Endocrinology

Background:

  • Insulin is crucial for glucose and lipid metabolism; its impairment contributes to diabetes.
  • Human skeletal muscle and kidney-enriched inositol polyphosphate phosphatase (SKIP) negatively regulates insulin signaling.
  • SKIP is a member of the phosphatidylinositol 3,4,5-trisphosphate phosphatase family.

Purpose of the Study:

  • To investigate the role of SKIP in insulin signaling and glucose homeostasis.
  • To generate and analyze mice with a targeted mutation in the mouse SKIP gene (Pps).

Main Methods:

  • Generation of Pps mutant mice.
  • Assessment of insulin sensitivity using hyperinsulinemic-euglycemic clamp studies.
  • Measurement of 2-deoxyglucose uptake in isolated soleus muscle.
  • In vitro knockdown studies in L6 myoblast cells to assess Akt/protein kinase B (PKB) phosphorylation and glucose uptake.

Main Results:

  • Heterozygous Pps mutant mice exhibited increased insulin sensitivity and reduced diet-induced obesity.
  • Enhanced Akt/PKB phosphorylation was observed in skeletal muscle but not adipose tissue of mutant mice.
  • Insulin-induced 2-deoxyglucose uptake was significantly increased in isolated soleus muscle from Pps mutant mice.
  • Systemic glucose disposal rate increased in Pps mutant mice without affecting hepatic glucose production.
  • In vitro SKIP knockdown enhanced insulin-stimulated Akt/PKB phosphorylation and glucose uptake in L6 myoblasts.

Conclusions:

  • SKIP negatively regulates insulin signaling in skeletal muscle.
  • Targeting SKIP could be a promising therapeutic strategy for insulin resistance and diabetes mellitus.