Acetic Acid Inhibits Malonyl-coa

we know about all the glycogen, lpwer insulin output, better insulin sensivity and etc features of acetic acid but it´s allso shown to inhibit malonyl-coa in the liver inhibiting FA synthesis and enhancing its oxidation.....making a aswome adition for cutting...( i loved in my experience) i think some people said that it would inhibit ffa oxidation but this study show oposite ......inhibiting malony-coa makes it a good fat partishioner speacially when bulking probably preventing fat gains....that´s why so many people tha take regularly vinegar don´t gain much weight on hypercaloric and loose tons when hypo or eucaloric.......

i don´t know if this has been posted before...if it was i am sorry for any annoiance...

peace!!

Quote

Effect of acetic acid feeding on the circadian changes in glycogen and metabolites of glucose and lipid in liver and skeletal muscle of rats.

Fushimi T, Sato Y.

Central Research Institute, Mizkan Group Corporation, 2-6 Nakamura-cho, Handa, Aichi 475-8585, Japan. tfushimi@mizkan.co.jp

The aim of the present study is to investigate the effect of acetic acid feeding on the circadian changes in glycogen concentration in liver and skeletal muscle. Rats were provided meal once daily (09.00-13.00 hours) for 10 d. On the 11th day, they were either killed immediately or given 9 g diet containing either 0 (control) or 0.7 g/kg-diet acetic acid beginning at 09.00 hours for 4 h, as in the previous regimen. Rats in the fed group were killed at 4, 8 or 24 h after the start of feeding. At 4 h after the start of feeding, the acetic acid group had significantly greater liver and gastrocnemius muscle glycogen concentrations (P<0.05). Also, at this same point, liver xylulose-5-phosphate, a key stimulator of glycolysis, the ratio of fructose-1,6-bisphosphate to fructose-6-phosphate in skeletal muscle, which reflects phosphofructokinase-1 activity, and liver malonyl-CoA, an allosteric inhibitor of carnitine palmitoyl-transferase, were significantly lower in the acetic acid group than in the control group (P<0.05). In addition, the acetic acid group had a significantly lower serum lactate concentration and lower ratio of insulin to glucagon than the control group at the same point (P<0.05). We conclude that a diet containing acetic acid may enhance glycogen repletion but not induce supercompensation, a large increase in the glycogen level that is beneficial in improving performance, in liver and skeletal muscle by transitory inhibition of glycolysis. Further, we indicate the possibility of a transient enhancement of fatty acid oxidation in liver by acetic acid feeding.