metforim is used to regulate glycemia in type-II diabete.
is well known MET regulates glycemia ruducing endogenus glucose production:" Metformin lowered the rate of glucose production in these patients through a reduction in gluconeogenesis."(2)
the reduction of gluconeogenesis seems to be a good thing for dieting bbers, because it could have a spanning effect on muscles, that during diet are used to produce glucose.
it's interesting that, while MET reduces gluconeogenesis, increases FFA in skeletal muscle and liver. "The metabolic actions of the anti-diabetic agent, metformin, which include stimulation of fatty acid oxidation, are believed to occur in part via activation of AMP-activated protein kinase (AMPK) in liver and skeletal muscle"(1)
a)could produce a faster fat-loss, and
b)could avoid the problem of very low blood glucose, because glucose is spanned increasing FFA oxidation.
METFORMIN can increases FFA oxidation. this should reduce glucose oxidation, producing a more stable glycemia. a more stable glycemia could reduce gluconeogenesis, spanning muscles.
by the other side, metformin reduces gluconoegenesis by its self, and this could be another factor to figure a muscle-spanning-effect of metformin.
we can figure that using met during cutting can speed fat loss, while preserving muscles.
this model could explain why so may bber report good resault using met during cutting.
(1)METFORMIN STIMULATES MYOCARDIAL FATTY ACID OXIDATION INDEPENDENT OF CHANGES IN AMP-ACTIVATED PROTEIN KINASE ACTIVITY.
H Parsons, R Wambolt, R Saeedi, M Allard
Vancouver, British Columbia
(2)Effects of Metformin on Hepatic Glycogenolysis and Gluconeogenesis in Type 2 Diabetes.
Diabetes, May, 2000, by Ripudaman S. Hundal, Martin Krassak, Didier Laurent, Vincent Lebon, Visvanathan Chandramouli, Silvio Inzucchi, William C. Schumann, Bernard R. Landau, Kitt F. Petersen