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1 Division of Diabetes and Endocrine Research, Department of Medicine, Mount Zion Medical Center, University of California, San Francisco 94143-1616; and 2 Department of Physiological Science, University of California, Los Angeles, California 90095-1606
High-fat feeding results in
impaired insulin signaling in skeletal muscle, but the role of the
insulin receptor (IR) remains controversial. In the present
study, female Fischer 344 rats were fed diets either low in fat [low
fat, complex carbohydrate (LFCC)] or high in fat and sucrose (HFS).
Insulin-stimulated skeletal muscle glucose transport, measured in
purified sarcolemmal vesicles, was lower in rats consuming the HFS diet
for 2 and 8 wk compared with LFCC controls (72.9 ± 3.5, 67.6 ± 3.5, and 86.1 ± 3.5 pmol · mg
1 · 15 s1,
respectively; P < 0.05). Muscle IR content was
unchanged in 2-wk HFS animals but was 50% lower in the 8-wk HFS group
(P < 0.001). However, compared with LFCC,
insulin-stimulated IR autophosphorylation was 26% lower in 2-wk HFS
and 40% lower in 8-wk HFS animals (P < 0.005). Total
muscle content of the proposed IR inhibitors cytokine tumor necrosis
factor-
and membrane glycoprotein PC-1 was not significantly changed
in HFS animals at either 2 or 8 wk. These results demonstrate
that high-fat feeding induces insulin resistance in muscle concomitant
with a diminished IR signaling capacity, although the mechanism remains unknown.
dietary fat; insulin receptor substrate-1; insulin receptor; membrane glycoprotein PC-1; tyrosine kinase; tumor necrosis factor-
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