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Cholesterol/Hypercholesterolemia/Hyperlipidemia
Published in Charles Theisler, Adjuvant Medical Care, 2023
Pantethene: Evidence indicates that taking pantethine, a product of panthothenic acid (vitamin B5), by mouth can modestly lower triglycerides, total cholesterol, and low-density lipoprotein (LDL) cholesterol as well as triglycerides and can raise high-density lipoprotein (HDL) cholesterol levels.21
Naturopathic Medicine and the Prevention and Treatment of Cardiovascular Disease
Published in Stephen T. Sinatra, Mark C. Houston, Nutritional and Integrative Strategies in Cardiovascular Medicine, 2022
Pantethine is the stable form of pantetheine, the active form of vitamin B5 or pantothenic acid. Pantothenic acid is the most important component of coenzyme A (CoA). This enzyme is involved in the transport of fats to and from cells, as well as to the energy-producing compartments within the cell. Without coenzyme A, the cell’s fats cannot be metabolized to energy.
Micronutrient Supplementation and Ergogenesis — Vitamins
Published in Luke Bucci, Nutrients as Ergogenic Aids for Sports and Exercise, 2020
Pantethine (the disulfide of pantetheine) consists of pantothenate bound to cysteamine and is a direct precursor of coenzyme A. Coenzyme A levels in perfused rat livers after pantethine administration were significantly elevated compared to control or pantothenate perfusion.238 Pantethine administration has been shown to have antiarrhythmic actions on rodent and canine hearts, with increases in intracellular ATP hypothesized to account for these actions.239–241 Pantethine supplementation significantly reduces elevated blood lipids and increases HDL cholesterol and apolipoprotein A in human subjects,242–245 with a postulated mechanism of accelerated coenzyme A synthesis. Oral pantetheine administration (1 g/d) increased peak serum pantothenate levels tenfold.246 Possible effects of increased pantothenate levels arising from pantetheine administration on athletes have not been reported, however. Since large doses of thiamine and pantothenate appeared to have ergogenic properties (see Table 2),206,228,230 studies using congeners of these two vitamins to explore potential ergogenic effects are indicated.
Efficacy and safety of coenzyme A versus fenofibrate in patients with hyperlipidemia: a multicenter, double-blind, double-mimic, randomized clinical trial
Published in Current Medical Research and Opinion, 2020
Ya-Qin Chen, Shui-ping Zhao, Hui-Jun Ye
Statin therapy has long been the cornerstone of cardiovascular disease (CVD) prevention for reducing levels of atherogenic LDL-C12. However, the residual risk in statin treated patients remains significant, despite reaching LDL-C goals. Increasing studies focus on atherogenic dyslipidemia, which includes increased TG, prevalence of smaller and denser LDL particles and low HDL-C13,14. Based on current knowledge, nutraceuticals might exert significant lipid-lowering, and their use has several advantages – they have natural origins and are mainly extracted from natural products, they are mostly safe and very well tolerated and their use is supported by the findings from randomized controlled trials and meta-analyses; finally, the lipid-lowering effect of most nutraceuticals is multimechanistic, which makes them potential candidates for improving the effects of current lipid-lowering drugs when used in combination15,16. CoA is a naturally occurring physiological compound which is proved to be effective in accelerating the clearance of TG from plasma17. Our previous data shows that oral CoA 400 U/d effectively lowered serum TG in hypertriglyceridemic patients9. In our more recent study, the lipid lowering effect of CoA is better than that of pantethine which is a commonly used lipid lowering agent in China and Japan10. In line with these results, the present study supported the TG lowering effect of both fenofibrate and CoA although the extent of lipid lowering effect is relatively weaker in CoA group. Moreover, we demonstrate TC and non-HDL-C are slightly lowered and HDL-C is mildly increased in patients treated with CoA. However, CoA is less effective than fenofibrate in HDL-C modifying. While definitive support for therapeutic options targeting atherogenic dyslipidemia to reduce residual cardiovascular risk remains awaited, the newly developed oral CoA may be an additional agent as an adjunct to improving diet and other non-pharmacological treatments (e.g. exercise, weight reduction) for the treatment.