LKB1 and AMPK and the regulation of skeletal muscle metabolism.
- Posted by Trawkin on April 23rd, 2008 filed in Uncategorized
LKB1 and AMPK and the regulation of skeletal muscle metabolism.
Anabolic and catabolic signals Current Opinion in Clinical Nutrition & Metabolic Care. 11(3):227-232, May 2008.
Koh, Ho-Jin; Brandauer, Josef; Goodyear, Laurie J
Abstract:
Purpose of review: To address the role of LKB1 and AMP-activated protein kinase (AMPK) in glucose transport, fatty acid oxidation, and metabolic adaptations in skeletal muscle.
Recent findings: Contraction-mediated skeletal muscle glucose transport is decreased in muscle-specific LKB1 knockout mice, but not in whole body AMPK[alpha]2 knockout mice or AMPK[alpha]2 inactive transgenic mice.
Chronic activation of AMPK by 5-aminoimidazole-4-carboxamide-1-[beta]-D-ribofuranoside (AICAR) and [beta]-guanadinopropionic acid enhances mitochondrial function in skeletal muscle, but AICAR or exercise-induced increases in mitochondrial markers are preserved in skeletal muscles from whole body AMPK[alpha]2 or muscle-specific LKB1 knockout mice.
Pharmacological activation of AMPK increases glucose transport and fatty acid oxidation in skeletal muscle. Therefore, chronic activation of AMPK may be beneficial in the treatment of obesity and type 2 diabetes.
Summary: LKB1 and AMPK play important roles in regulating metabolism in resting and contracting skeletal muscle.
(C) 2008 Lippincott Williams & Wilkins, Inc.
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