Searching across hundreds of databases

Our searching services are busy right now. Your search will reload in five seconds.

Forgot Password

If you have forgotten your password you can enter your email here and get a temporary password sent to your email.

A muscle-specific insulin receptor knockout exhibits features of the metabolic syndrome of NIDDM without altering glucose tolerance.

Molecular cell | Nov 24, 1998

Skeletal muscle insulin resistance is among the earliest detectable defects in humans with type 2 diabetes mellitus. To determine the contribution of muscle insulin resistance to the metabolic phenotype of diabetes, we used the Cre-loxP system to disrupt the insulin receptor gene in mouse skeletal muscle. The muscle-specific insulin receptor knockout mice exhibit a muscle-specific > 95% reduction in receptor content and early signaling events. These mice display elevated fat mass, serum triglycerides, and free fatty acids, but blood glucose, serum insulin, and glucose tolerance are normal. Thus, insulin resistance in muscle contributes to the altered fat metabolism associated with type 2 diabetes, but tissues other than muscle appear to be more involved in insulin-regulated glucose disposal than previously recognized.

Pubmed ID: 9844629 RIS Download

Mesh terms: Animals | Blood Glucose | Body Weight | Cells, Cultured | Cholesterol | Creatine Kinase | Diabetes Mellitus, Type 2 | Female | Glucose | Glucose Tolerance Test | Insulin | Insulin Resistance | Integrases | Isoenzymes | Lipids | Liver | Male | Mice | Mice, Knockout | Mice, Transgenic | Muscle, Skeletal | Phosphotyrosine | Receptor, Insulin | Signal Transduction | Viral Proteins

Research resources used in this publication

None found

Research tools detected in this publication

None found

Data used in this publication

None found

Associated grants

  • Agency: NIDDK NIH HHS, Id: 2P30DK36836
  • Agency: NIDDK NIH HHS, Id: DK 31036

Publication data is provided by the National Library of Medicine ® and PubMed ®. Data is retrieved from PubMed ® on a weekly schedule. For terms and conditions see the National Library of Medicine Terms and Conditions.

We have not found any resources mentioned in this publication.