[b said:
Quote[/b] (tai4ji2x @ Mar. 12 2003,4:15)]blade:
whoa, where did that come from?
I wasn't directing my post at anyone in particular, I just remember someone saying after the FAQ section was up that "now no one will ask questions anymore". But then you see a multitude of posts asking the same questions over and over again - even to the point where you have three-four threads in succession in the same forum related to the same topic, so I was just suggesting that people do their homework first...
Virtualcyber, I'll look into that thread on Avant, but a quick search revealed a study related to the one in the FAQ section demonstrating the effects of CLA on insulin sensitivity in muscle:
Am J Physiol Endocrinol Metab 2003 Mar 4; [epub ahead of print]
Isomer-specific Actions of Conjugated Linoleic Acid on Muscle Glucose Transport in the Obese Zucker Rat.
Henriksen EJ, Teachey MK, Taylor ZC, Jacob S, Ptock A, Kramer K, Hasselwander O.
Department of Physiology, University of Arizona, Tucson, AZ, USA.
The fatty acid conjugated linoleic acid (CLA) enhances glucose tolerance and insulin action on skeletal muscle glucose transport in rodent models of insulin resistance. However, no study has directly compared the metabolic effects of the two primary CLA isomers, cis-9,trans-11-CLA (c9,t11-CLA) and trans-10,cis 12-CLA (t10,c12-CLA). Therefore, we assessed the effects of a 50:50 mixture of these two CLA isomers (M-CLA) and of preparations enriched in either c9,t11-CLA (76% enriched) or t10,c12-CLA (90% enriched), on glucose tolerance and insulin-stimulated glucose transport in skeletal muscle of the insulin-resistant obese Zucker (fa/fa) rat. Animals were treated daily by gavage with either vehicle (corn oil), M-CLA, c9,t11-CLA, or t10,c12-CLA (all CLA treatments at 1.5 g total CLA/kg body wt) for 21 consecutive days. During an oral glucose tolerance test, glucose responses were reduced (P<0.05) by 10% and 16%, respectively, in the M-CLA and t10,c12-CLA animals, while insulin responses were diminished by 21% and 19% in these same groups. There were no significant alterations in these responses in the c9,t11-CLA group. Insulin-mediated glucose transport activity was enhanced by M-CLA treatment in both type I soleus (32%) and type IIb epitrochlearis (58%) muscles, and by 36% and 48%, respectively, with t10,c12-CLA. In the soleus these increases were associated with decreases in protein carbonyls (index of oxidative stress, r=-0.616, P=0.0038) and intramuscular triglycerides (r=-0.631, P=0.0028). Treatment with c9,t11-CLA was without effect on these variables. These results suggest that the ability of CLA treatment to improve glucose tolerance and insulin-stimulated glucose transport activity in insulin-resistant skeletal muscle of the obese Zucker rat are associated with a reduction in oxidative stress and muscle lipid levels, and can be specifically ascribed to the actions of the t10,c12 isomer. In the obese Zucker rat, the c9,t11 isomer of CLA is metabolically neutral.