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Originally posted by Big Johnson:
OKAY BROS. ON SECOND WEEK OF METFORMIN WITH GOOD RESULTS. NO DIGESTIVE PROBLEMS, BUT I HAVE DROPPED ABOUT TEN POUNDS (NOT MUCH WHEN YOU START AT 250LBS) WITH AN INCREASE IN MUSCLE HARDNESS. I'VE ALSO BEEN EXPERIENCING HIGHER ENERGY LEVELS AND A SMALL STRENGTH INCREASE. I'LL KEEP YOU POSTED. I HAVE ENOUGH FOR SIX MORE WEEKS.

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Originally posted by bigrand:
Lucky fucker, i had to quit do to digestive problems.
Fonz, will ALA do for me what Met will?

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" That which does not kill me, will make me stronger"

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Originally posted by lawnsaver:
Fonz, what do you have to say about yesterday's rebutle about you ala post. Is it still worth it??

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THE TEN POUNDS I HAVE LOST I BELIEVE IS FAT, HENCE THE INCREASE IN MUSCLE HARDNESS. I'VE ACTUALLY GAINED STRENGTH, TOO, AND I KNOW ITS THE MET BECAUSE I HAVEN'T STARTED ANYTHING ELSE IN THE LAST TWO WEEKS.

I'M REALLY VERY PLEASED WITH HOW THIS STUFF MAKES ME FEEL. I HAD HEARD A LOT OF BAD STUFF ABOUT THE SIDES, BUT I HAVEN'T HAD ANYTHING BUT THE MINOR HEARTBURN. I THINK ANYONE LOOKING TO CUT CARBS WITHOUT LOSING MUSCLE MASS SHOULD GIVE IT A TRY.

"Antioxidant alpha-lipoic acid and protein turnover in insulin-resistant rat muscle."

Weinstein RB, Tritschler HJ, Henriksen EJ

Muscle Metabolism Laboratory, Department of Physiology, University of Arizona College of Medicine, Tucson, AZ, USA

We have shown previously that the antioxidant alpha-lipoic acid (ALA) can stimulate glucose transport and can enhance the stimulation of this process by insulin in skeletal muscle from insulin-resistant obese Zucker rats. As insulin can also acutely activate general protein synthesis and inhibit net protein degradation in skeletal muscle, we hypothesized that ALA could directly affect protein turnover and also increase the effect of insulin on protein turnover in isolated skeletal muscle from developing obese Zucker rats. In epitrochlearis muscles isolated from obese Zucker rats, insulin (2 mU/ml) significantly (p < 0.05) increased in vitro protein synthesis (phenylalanine incorporation into protein) and decreased net protein degradation (tyrosine release), whereas a racemic mixture of ALA (2 mM) had no effect on either process. Interestingly, rates of protein synthesis in muscle from obese Zucker rats were substantially lower compared to those values observed in age-matched insulin-sensitive Wistar rats, whereas rates of protein degradation were comparable. Obese Zucker rats were also treated chronically with either vehicle or ALA (50 mg/kg/d for 10 d). Again, insulin significantly increased net protein synthesis and decreased net protein degradation in epitrochlearis muscles isolated from vehicle-treated obese Zucker rats; however, this stimulatory effect of insulin was not improved by prior in vivo ALA treatment. These results indicate that the previously described effect of the antioxidant ALA to increase insulin-stimulated glucose transport in skeletal muscle of obese, insulin-resistant rats does not apply to another important insulin-regulatable process, protein turnover. These findings imply that the cellular mode of action for ALA is restricted to signaling factors unique to the activation of glucose transport, and does not involve the pathway of stimulation of general protein synthesis and net protein degradation.