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[A1CR]

[posted on behalf of CRON4healthyfuture; 2003-01-15]

Can somebody help me out here? Whenever I hear people talk about the
differences between protein sources, it is sometimes hard for me to
appreciate how there could be that significant of a difference, considering
how proteins are degraded into a soup of the constituent amino acids, but
differences are still being demarcated by study after study, so who am I to
argue?

In any case, these folks are contending that cod protein, but *not* casein
or soy, "fixed" these fat rats, in regards to their insulinemic axis.

Now what is so special about cod protein? Is it at some sort of sweet spot
of essential amino acid content? I mean, animal protein is animal protein,
up to a point. I wonder what the mechanism of this observed effect is?

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Diabetes 2003 Jan;52(1):29-37 Related Articles, Links

Dietary cod protein restores insulin-induced activation of
phosphatidylinositol 3-kinase/Akt and GLUT4 translocation to the T-tubules
in skeletal muscle of high-fat-fed obese rats.

Tremblay F, Lavigne C, Jacques H, Marette A.

Department of Anatomy and Physiology, Laval University Hospital Research
Center, Ste-Foy, Quebec, Canada.

Diet-induced obesity is known to cause peripheral insulin resistance in
rodents. We have recently found that feeding cod protein to high-fat-fed
rats prevents the development of insulin resistance in skeletal muscle. In
the present study, we have further explored the cellular mechanisms behind
this beneficial effect of cod protein on skeletal muscle insulin
sensitivity. Rats were fed a standard chow diet or a high-fat diet in which
the protein source was either casein, soy, or cod proteins for 4 weeks.
Whole-body and muscle glucose disposal were reduced by approximately 50% in
rats fed high-fat diets with casein or soy proteins, but these impairments
were not observed in animals fed cod protein. Insulin-induced tyrosine
phosphorylation of the insulin receptor and insulin receptor substrate
(IRS) proteins were similar in muscle of chow- and high-fat-fed rats
regardless of the dietary protein source. However, IRS-1-associated
phosphatidylinositol (PI) 3-kinase activity was severely impaired (-60%) in
muscle of high-fat-fed rats consuming casein or soy protein. In marked
contrast, feeding rats with cod protein completely prevented the
deleterious effect of fat feeding on insulin-stimulated PI 3-kinase
activity. The activation of the downstream kinase Akt/PKB by insulin,
assessed by in vitro kinase assay and phosphorylation of GSK-3beta, were
also impaired in muscle of high-fat-fed rats consuming casein or soy
protein, but these defects were also fully prevented by dietary cod
protein. However, no effect of cod protein was observed on atypical protein
kinase C activity. Normalization of PI 3-kinase/Akt activation by insulin
in rats fed high-fat diets with cod protein was associated with improved
translocation of GLUT4 to the T-tubules but not to the plasma membrane.
Taken together, these results show that dietary cod protein is a natural
insulin-sensitizing agent that appears to prevent obesity-linked muscle
insulin resistance by normalizing insulin activation of the PI 3-kinase/Akt
pathway and by selectively improving GLUT4 translocation to the T-tubules.

PMID: 12502490 [PubMed - in process]