Roadie_scum said:If all you want to do is burn fat - sit still. Everyone falls about laughing at my joke regarding the high rate of lipolysis at rest. Guffaw.
Extract from the citrus fruit Garcinia found in Asia and India. HCA has been used in weight loss since 1969.
Inhibits enzyme known as ATP-citrate lyase, which is the major enzyme responsible for the production of fatty acids. Because of the inhibition a build-up of citrate occurs. That buildup may cause the cell to inhibit the breakdown of stored sugar. It also may increase glucogen storage resulting in a feeling of fullness as gluco-receptors in liver activate vegas nerve.
Animal research, suggests that HCA may be a useful weight loss aid. HCA has been demonstrated in the laboratory to reduce the conversion of carbohydrates into stored fat by inhibiting certain enzymes processes.
Animal research indicates that HCA suppresses appetite and induces weight loss.
One case report found that eating 1 gram of the fruit containing HCA before each meal resulted in the loss of 1 pound per day. potent inhibitor of ATP citrate-lyase, was tested in Hep G2 cells for effects on cholesterol homoeostasis. After 2.5 h and 18 h incubations with (-)-hydroxycitrate at concentrations of 0.5 mM or higher, incorporation of [1,5-14C]citrate into fatty acids and cholesterol was strongly inhibited.
This most likely reflects an effective inhibition of ATP citrate-lyase. Cholesterol biosynthesis was decreased to 27% of the control value as measured by incorporations from 3H2O, indicating a decreased flux of carbon units through the cholesterol-synthetic pathway. After 18 h preincubation with 2 mM-(-)-hydroxycitrate, the cellular low-density-lipoprotein (LDL) receptor activity was increased by 50%, as determined by the receptor-mediated association and degradation.
Measurements of receptor-mediated binding versus LDL concentration suggests that this increase was due to an increase in the numbers of LDL receptors. Simultaneously, enzyme levels of 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase as determined by activity measurements increased 30-fold. Results suggest that the increases in HMG-CoA reductase and the LDL receptor are initiated by the decreased flux of carbon units in the cholesterol-synthetic pathway, owing to inhibition of ATP citratelyase.
A similar induction of HMG-CoA reductase and LDL receptor was also found after preincubations of cells with 0.3 microM-mevinolin, suggesting that the underlying mechanism for this induction is identical for both drugs.
interhealthusa.comSuperCitriMax.aspxOpen ↗