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Lipid Storage Protein Linked to Insulin Sensitivity

Last Updated: July 24, 2012.

 

PLIN2 regulates lipid storage in skeletal muscle and correlates with improved insulin sensitivity

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Perilipin 2 plays a role in regulating lipid storage in skeletal muscle and can improve insulin sensitivity, according to a study published online July 17 in Diabetes.

TUESDAY, July 24 (HealthDay News) -- Perilipin 2 (PLIN2) plays a role in regulating lipid storage in skeletal muscle and can improve insulin sensitivity, according to a study published online July 17 in Diabetes.

Noting that excessive lipid storage in skeletal muscle is characteristic of type 2 diabetes, Madeleen Bosma, from the Maastricht University Medical Centre in the Netherlands, and colleagues varied the expression of PLIN2, a lipid droplet-coating protein abundantly expressed in skeletal muscle, to examine its role in lipid handling and insulin sensitivity.

The researchers found that knocking down PLIN2 in vitro was associated with reduced formation of lipid droplets, reduced triacylglycerol storage, slightly increased fatty acid oxidation, and increased palmitate incorporation into diacylglycerols and phospholipids. Overexpressing PLIN2 in vitro was associated with increased intramyocellular triacylglycerol storage and improved insulin sensitivity. When PLIN2 was overexpressed in muscle in vivo there was an increase in lipid droplet accumulation and, in spite of increased intramyocellular lipid storage, there was improved skeletal muscle insulin sensitivity.

"We conclude that PLIN2 is essential for lipid storage in skeletal muscle by enhancing the partitioning of excess fatty acids toward triacylglycerol storage in lipid droplets, thereby blunting lipotoxicity-associated insulin resistance," Bosma and colleagues write.

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Copyright © 2012 HealthDay. All rights reserved.


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