Some individuals with type 2 diabetes (which is characterized by abnormally high blood glucose levels) have lower than normal amounts of the protein PGC-1-alpha in their skeletal muscles, but it is not known whether this has a role in the onset of diabetes or if it is caused by the diabetes.
Using mice that lack PGC-1-alpha in their skeletal muscle (MKO mice), Bruce Spiegelman and colleagues from the Dana-Farber Cancer Institute, Boston, have now shown that decreased expression of PGC-1-alpha can cause dysregulation of blood glucose levels.
When fed either a normal or high-fat diet MKO mice had much higher blood glucose levels than wild-type mice. This was because the beta-cells of the pancreas secreted less insulin, the hormone that prevents blood glucose levels from soaring. Higher levels of the soluble factor IL-6 were also detected in the blood. As IL-6 treatment decreased insulin secretion by wild-type and MKO pancreatic islets, the authors suggested that PGC-1-alpha mediates crosstalk between skeletal muscle and pancreatic islets through IL-6.
TITLE: Abnormal glucose homeostasis in skeletal muscle–specific PGC-1-alpha knockout mice reveals skeletal muscle–pancreatic beta-cell crosstalk
Bruce M. Spiegelman
Dana-Farber Cancer Institute, Boston, Massachusetts, USA.
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