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1 Nutraceuticals and Functional Foods Institute, 2 Department of Food Science and Nutrition, 3 Department of Anatomy and Physiology, and 4 Center for Research on Energy Metabolism, Laval University, Ste-Foy, Quebec, Canada G1K 7P4; and 5 Lipid Research Unit, Laval University Hospital Research Center, Ste-Foy, Quebec, Canada G1V 4G2
In the present study, we tested the
hypothesis that fish protein may represent a key constituent of fish
with glucoregulatory activity. Three groups of rats were fed a high-fat
diet in which the protein source was casein, fish (cod) protein, or soy
protein; these groups were compared with a group of chow-fed controls. High-fat feeding led to severe whole body and skeletal muscle insulin
resistance in casein- or soy protein-fed rats, as assessed by the
euglycemic clamp technique coupled with measurements of 2-deoxy-D-[3H]glucose uptake rates by
individual tissues. However, feeding cod protein fully prevented the
development of insulin resistance in high fat-fed rats. These animals
exhibited higher rates of insulin-mediated muscle glucose disposal that
were comparable to those of chow-fed rats. The beneficial effects of
cod protein occurred without any reductions in body weight gain,
adipose tissue accretion, or expression of tumor necrosis factor-
in
fat and muscle. Moreover, L6 myocytes exposed to cod protein-derived
amino acids showed greater rates of insulin-stimulated glucose uptake compared with cells incubated with casein- or soy protein-derived amino
acids. These data demonstrate that feeding cod protein prevents obesity-induced muscle insulin resistance in high fat-fed obese rats at
least in part through a direct action of amino acids on insulin-stimulated glucose uptake in skeletal muscle cells.
amino acids; high-fat diet; adipose tissue
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