Mar 6, 2012

Absence of RIP140 reveals a pathway regulating glut4-dependent glucose uptake in oxidative skeletal muscle through UCP1-mediated activation of AMPK

PloS One
Asmaa FritahMalcolm G Parker

Abstract

Skeletal muscle constitutes the major site of glucose uptake leading to increased removal of glucose from the circulation in response to insulin. Type 2 diabetes and obesity are often associated with insulin resistance that can be counteracted by exercise or the use of drugs increasing the relative proportion of oxidative fibers. RIP140 is a transcriptional coregulator with a central role in metabolic tissues and we tested the effect of modulating its level of expression on muscle glucose and lipid metabolism in two mice models. Here, we show that although RIP140 protein is expressed at the same level in both oxidative and glycolytic muscles, it inhibits both fatty acid and glucose utilization in a fiber-type dependent manner. In RIP140-null mice, fatty acid utilization increases in the extensor digitorum longus and this is associated with elevated expression of genes implicated in fatty acid binding and transport. In the RIP140-null soleus, depletion of RIP140 leads to increased GLUT4 trafficking and glucose uptake with no change in Akt activity. AMPK phosphorylation/activity is inhibited in the soleus of RIP140 transgenic mice and increased in RIP140-null soleus. This is associated with increased UCP1 expression and mitochond...Continue Reading

Mentioned in this Paper

CD36 Antigens
Metabolic Process, Cellular
Diabetes Mellitus, Non-Insulin-Dependent
NRIP1 wt Allele
Brown Fat
Colforsin
Biochemical Pathway
Carbonyl Cyanide p-Trifluoromethoxyphenylhydrazone
Cyclic AMP-Responsive DNA-Binding Protein
Hydrogen sulfite

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