Muscle Response to IL-6 Defective in Type 2 Diabetes

Fewer Mitochondria in Offspring of Parents With Diabetes
Fewer Mitochondria in Offspring of Parents With Diabetes
Skeletal muscle cells from people with type 2 diabetes have defects in glucose metabolism but have normal lipid metabolism after treatment with interleukin-6 (IL-6).

(HealthDay News) – Skeletal muscle cells from people with type 2 diabetes have defects in glucose metabolism but have normal lipid metabolism after treatment with interleukin-6 (IL-6), according to a study published online Oct 18 in Diabetes.

Noting that IL-6 both enhances and inhibits the action of insulin, Lake Q Jiang, from the Karolinska Institutet in Stockholm, and colleagues investigated how IL-6 affected glucose and lipid metabolism in cultured myotubes from people with normal glucose tolerance and from people with type 2 diabetes.

The researchers found that, in myotubes from people with normal glucose tolerance, IL-6 treatment increased glycogen synthesis, glucose uptake, and phosphorylation of signal transducer and activator of transcription 3 (STAT3). In contrast, IL-6 had no effect on glucose metabolism or STAT3 signaling but did increase expression of suppressor of cytokine signaling 3 in people with type 2 diabetes. IL-6 increased fatty acid oxidation in myotubes from both groups. Cultured myotubes from both groups had similar levels of IL-6, IL-6 receptor, and glycoprotein 130, as well as similar IL-6 secretion.

“In summary, skeletal muscle cells from type 2 diabetic patients display selective IL-6 resistance for glucose rather than lipid metabolism,” Jiang and colleagues conclude. “IL-6 appears to play a differential role in regulating metabolism in type 2 diabetic patients compared with normal glucose-tolerant subjects.”

The study was funded in part by the Novo Nordisk Research Foundation.

Abstract
Full Text (subscription or payment may be required)