High concentrations of calcium stearate, zinc stearate

can lead to insulin resistance. According to reports, hyperlipidemia is due to lipid metabolism disorder caused by one or more of the plasma lipid composition characterized by abnormally elevated  Barium soap  concentrations of illnesses. Hyperlipidemia and insulin resistance, diabetes mellitus have a close relationship.
However, there is a serum fatty acid profile in hyperlipidemia studies are concentrated in the fasting state, in their study investigated the postprandial state is still blank stage. As we all know, three meals a day, the body most of the time in a postprandial state, so research postprandial serum fatty acid profile and metabolic changes impact on the body has more practical significance.
By postprandial hyperlipidemia population  PVC heat stabilizer for window changes of serum fatty acid, a fatty acid for the first time found that only calcium stearate, zinc stearate in the postprandial state levels were significantly increased in high concentrations of calcium stearate zinc can lead to insulin resistance, and reduce expression of SREBP-1c to reduce calcium stearate, zinc levels, thereby improving insulin resistance.
Researchers crowd postprandial hyperlipidemia serum calcium stearate, zinc stearate, elevated levels of  PVC window stabilizer the molecular mechanism of high concentrations of calcium stearate, zinc stearate implications for insulin resistance and how to reduce postprandial rise high calcium stearate, zinc stearate level of in-depth research, eventually found increased calcium stearate, zinc stearate, postprandial serum insulin concentration is due to the increase of stimulated calcium stearate, hard de novo synthesis of fat and zinc palmitate direct extension (ELOVL6). By in vivo, in vitro small RNA interference techniques, the researchers confirmed that reduces SREBP-1c or ELOVL6 expression could reduce calcium stearate, zinc levels, thereby improving insulin resistance. Further comparison of the interference in the difference after two targets, they found that inhibition of expression of SREBP-1c can more effectively improve insulin resistance.