X-Message-Number: 31310
Date: Wed, 31 Dec 2008 19:22:30 -0800 (PST)
From: 
Subject: dietary cod may increase human lifespan

[Dietary cod may slow human aging by increasing insulin sensitivity. This
effect on insulin is not due to fatty acids.]

Diabetes Care. 2007 Nov;30(11):2816-21. Epub 2007 Aug 6.
Dietary cod protein improves insulin sensitivity in insulin-resistant men
and women: a randomized controlled trial.
  Ouellet V, Marois J, Weisnagel SJ, Jacques H. Institute of Nutraceuticals
and Functional Foods, Laval University, Quebec City, Quebec, Canada.
  OBJECTIVE: The purpose of this article was to compare the effects of cod
protein to those of other animal proteins on insulin sensitivity in
insulin-resistant human subjects. RESEARCH DESIGN AND METHODS: Insulin
sensitivity (M/I) was assessed using a hyperinsulinemic-euglycemic clamp in
19 insulin-resistant subjects fed a cod protein diet and a similar diet
containing lean beef, pork, veal, eggs, milk, and milk products (BPVEM) for
4 weeks in a crossover design study. Both diets were formulated to differ
only in protein source, thus providing equivalent amounts of dietary fibers
and monounsaturated, polyunsaturated (including n-3), and saturated fatty
acids (1.1:1.8:1.0). Beta-cell function, estimated by oral glucose tolerance
test-derived parameters, was also assessed. RESULTS: There was a significant
improvement in insulin sensitivity (P = 0.027) and a strong tendency for a
better disposition index (beta-cell function x M/I) (P = 0.055) in subjects
consuming the cod protein diet compared with those consuming the BPVEM diet.
When median baseline M/I (4.8 x 10(-3) mg x kg(-1) x min(-1) x pmol(-1)) was
taken into account, an interaction on the 30-min C-peptide-to-30-min glucose
ratio, used as an index of beta-cell function, was observed between diet and
M/I status (P = 0.022). Indeed, this ratio strongly tended to increase in
subjects with low M/I consuming the cod protein diet compared with those
consuming the BPVEM diet (P = 0.065). CONCLUSIONS: Dietary cod protein
improves insulin sensitivity in insulin-resistant individuals and thus could
contribute to prevention of type 2 diabetes by reducing the metabolic
complications related to insulin resistance.
PMID: 17682120

Nutr Metab Cardiovasc Dis. 2007 Oct;17(8):572-80. Epub 2006 Nov 28.
Fish oil, insulin sensitivity, insulin secretion and glucose tolerance in
healthy people: is there any effect of fish oil supplementation in relation
to the type of background diet and habitual dietary intake of n-6 and n-3
fatty acids?
  Giacco R, Cuomo V, Vessby B, Uusitupa M, Hermansen K, Meyer BJ, Riccardi
G, Rivellese AA; KANWU Study Group. Institute of Food Science, Italian
National Research Council, Avellino, Italy.
  AIM: To evaluate whether a moderate supplementation of long-chain n-3
fatty acids is able to modulate insulin sensitivity, insulin secretion,
beta-cell function and glucose tolerance in healthy individuals consuming a
diet rich in either saturated or monounsaturated fat, also in relation to
their habitual dietary intake of n-6 and n-3 fatty acid. METHODS AND
RESULTS: One hundred and sixty-two healthy individuals were randomly
assigned to follow either one of two isoenergetic diets for 3 months, one
rich in monounsaturated fats and the other rich in saturated fats. Within
each group there was a second randomisation to fish oil (n-3 fatty acids 3.6
g/day) or placebo. At the beginning and at the end of the treatment periods
insulin sensitivity (SI), first phase insulin response (FPIR) and glucose
tolerance (K(G)-value) were evaluated by the intravenous glucose tolerance
test (IVGTT). Fish oil did not have any effect on SI, FPIR, K(G)-value and
disposition index in either diet. Even after dividing subjects according to
the median value of n-6/n-3 ratio of serum phospholipids at baseline, there
was no change in SI (Delta SI 0.42+/-0.34 on fish oil vs 0.14+/-0.23 on
placebo for those with n-6/n-3 <4.85; -1.03+/-0.47 on fish oil
vs -0.27+/-0.32 on placebo for those with n-6/n-3 >4.85) (M+/-SE), FPIR
(Delta FPIR 135.9+/-78.9 vs 157.2+/-157.5 pmol/L; 38.8+/-181.7 vs
357.1+/-181.7 pmol/L), K(G)-value (Delta K(G) 0.14+/-0.15 vs
0.12+/-0.11; -0.32+/-0.16 vs 0.15+/-0.15) or disposition index (Delta
disposition index 1465.4+/-830.4 vs 953.8+/-690.0; -1641.6+/-1034.3 vs
446.6+/-905.1). Considering the 75th percentile of n-6/n-3 ratio (5.82) the
results on insulin sensitivity, insulin secretion and disposition index were
confirmed, while, in this more extreme situation, n-3 fatty acid
supplementation induced a significant deterioration of K(G)-value (p=0.02).
CONCLUSIONS: In healthy individuals a moderate supplementation of fish oil
does not affect insulin sensitivity, insulin secretion, beta-cell function
or glucose tolerance. The same is true even when the habitual dietary intake
of n-6 and n-3 fatty acids is taken into account.
PMID: 17127043

Diabetes. 2003 Jan;52(1):29-37.
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

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