Insulin :: In insulin resistance, all fingers point to diminished levels of PKC-lambda

Obesity, the metabolic syndrome, and type 2 diabetes are frequently characterized by insulin resistance ? a condition in which normal amounts of insulin are not adequate to produce a normal insulin response from fat, muscle, and liver cells.

The result is an elevation in blood glucose levels.

While the causes of insulin resistance are not completely defined, previous studies have suggested that an atypical protein kinase C (aPKC), PKC-lambda, regulates insulin-stimulated glucose transport.

In a study appearing online on July 19 in advance of publication in the August print issue of the Journal of Clinical Investigation, a team led by Robert Farese at the University of South Florida generated mice lacking PKC-lambda specifically in muscle tissue and found that glucose transport and the activity of the glucose transporter GLUT4 were reduced in these animals and accompanied by body-wide insulin resistance, diabetes, abnormal insulin-producing beta cells, high cholesterol, and excess fat deposition in the abdomen and liver. The results show that insulin resistance and resultant effects, owing to a specific defect in muscle PKC-lambda, is sufficient to cause abdominal obesity and other abnormalities characteristic of the metabolic syndrome and type 2 diabetes.

TITLE: Muscle-specific knockout of PCK-lambda impairs glucose transport and induces metabolic and diabetic sydnromes

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