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Posted: Fri Jun 06, 2008 7:30 am
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PLoS ONE. 2008 Jun 4;3(6):e2328.

A combination of nutriments improves mitochondrial biogenesis and
function in skeletal muscle of type 2 diabetic Goto-Kakizaki rats.

Shen W, Hao J, Tian C, Ren J, Yang L, Li X, Luo C, Cotma CW, Liu J.

Institute for Nutritional Science, Shanghai Institutes of Biological
Sciences, Chinese Academy of Sciences, Shanghai, China.

BACKGROUND: Recent evidence indicates that insulin resistance in
skeletal muscle may be related to reduce mitochondrial number and
oxidation capacity. However, it is not known whether increasing
mitochondrial number and function improves insulin resistance. In the
present study, we investigated the effects of a combination of
nutrients on insulin resistance and mitochondrial biogenesis/function
in skeletal muscle of type 2 diabetic Goto-Kakizaki rats. METHODOLOGY/
PRINCIPAL FINDINGS: We demonstrated that defect of glucose and lipid
metabolism is associated with low mitochondrial content and reduced
mitochondrial enzyme activity in skeletal muscle of the diabetic Goto-
Kakizaki rats. The treatment of combination of R-alpha-lipoic acid,
acetyl-L-carnitine, nicotinamide, and biotin effectively improved
glucose tolerance, decreased the basal insulin secretion and the level
of circulating free fatty acid (FFA), and prevented the reduction of
mitochondrial biogenesis in skeletal muscle. The nutrients treatment
also significantly increased mRNA levels of genes involved in lipid
metabolism, including peroxisome proliferator-activated receptor-alpha
(Ppar alpha), peroxisome proliferator-activated receptor-delta (Ppar
delta), and carnitine palmitoyl transferase-1 (Mcpt-1) and activity of
mitochondrial complex I and II in skeletal muscle. All of these
effects of mitochondrial nutrients are comparable to that of the
antidiabetic drug, pioglitazone. In addition, the treatment with
nutrients, unlike pioglitazone, did not cause body weight gain.
CONCLUSIONS/SIGNIFICANCE: These data suggest that a combination of
mitochondrial targeting nutrients may improve skeletal mitochondrial
dysfunction and exert hypoglycemic effects, without causing weight
gain.

PMID: 18523557 [PubMed - in process]
 
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