Nov 6, 2009

Combined effects of ghrelin and higher food intake enhance skeletal muscle mitochondrial oxidative capacity and AKT phosphorylation in rats with chronic kidney disease

Kidney International
Rocco BarazzoniDaniel L Marks


Skeletal muscle mitochondrial dysfunction and insulin resistance occur in chronic kidney disease. Ghrelin is a gastric hormone previously shown to enhance muscle mitochondrial enzyme activities and AKT-mediated insulin signaling independent of food intake in healthy rats. Here we determined the impact of ghrelin treatment on anorexia, skeletal muscle mitochondrial oxidative capacity, AKT phosphorylation as a measure of insulin signaling, and lean body mass in a rat model of chronic kidney disease. Ghrelin infusion promoted higher food intake and lean body mass. Further, although muscle mitochondrial enzyme activities were low in the rats with CKD (chronic kidney disease), they normalized with ghrelin treatment, a change that was consistent with the increase in the transcript levels of regulators of mitochondrial biogenesis and lipid metabolism. This was associated with a lower muscle triglyceride content and higher AKT phosphorylation. Pair-feeding showed that mitochondrial effects of ghrelin are independent of changes in food intake, whereas combined ghrelin treatment and higher food intake were needed to enhance AKT phosphorylation. Thus, ghrelin-induced muscle mitochondrial changes and lower tissue triglycerides could favor ...Continue Reading

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Mentioned in this Paper

Metabolic Process, Cellular
Morbidity Aspects
Chronic Kidney Insufficiency
Protein Phosphorylation
Protein kinase B gamma
Soleus Muscle Structure
Insulin Resistance
Desire for Food

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