Pantethine, a derivative of vitamin B5, favorably alters total, LDL and non-HDL cholesterol in low to moderate cardiovascular risk subjects eligible for statin therapy: a triple-blinded placebo and diet-controlled investigation

Abstract

High serum concentration of low-density lipoprotein cholesterol (LDL-C) is a major risk factor for coronary heart disease. The efficacy of pantethine treatment on cardiovascular risk markers was investigated in a randomized, triple-blinded, placebo-controlled study, in a low to moderate cardiovascular disease (CVD) risk North American population eligible for statin therapy, using the National Cholesterol Education Program (NCEP) guidelines. A total of 32 subjects were randomized to pantethine (600 mg/day from weeks 1 to 8 and 900 mg/day from weeks 9 to16) or placebo. Compared with placebo, the participants on pantethine showed a significant decrease in total cholesterol at 16 weeks (P=0.040) and LDL-C at 8 and 16 weeks (P=0.020 and P=0.006, respectively), and decreasing trends in non-high-density lipoprotein cholesterol at week 8 and week 12 (P=0.102 and P=0.145, respectively) that reached significance by week 16 (P=0.042). An 11% decrease in LDL-C from baseline was seen in participants on pantethine, at weeks 4, 8, 12, and 16, while participants on placebo showed a 3% increase at week 16. This decrease was significant between groups at weeks 8 (P=0.027) and 16 (P=0.010). The homocysteine levels for both groups did not change significantly from baseline to week 16. Coenzyme Q10 significantly increased from baseline to week 4 and remained elevated until week 16, in both the pantethine and placebo groups. After 16 weeks, the participants on placebo did not show significant improvement in any CVD risk end points. This study confirms that pantethine lowers cardiovascular risk markers in low to moderate CVD risk participants eligible for statins according to NCEP guidelines.

Mechanistic basis for impaired ferroptosis in cells expressing the African-centric S47 variant of p53

“…Additionally, CoA is a key regulator of lipid metabolism and has been reported to protect against the injurious effects of reactive oxygen species to inhibit lipid peroxidation, to enhance GSH levels, and to stimulate the incorporation of fatty acids into membrane phospholipids, promoting repair (49,50). Finally, it remains possible that CoA contributes to an increased abundance of acetyl-CoA, affecting epigenetic modulation and gene expression control (51).…”

Metabo groups in response to micronutrient intervention: Pilot study

“…Sex and fold change in alpha-tocopherol and fold change in pantothenic acid plasma levels explained 31% and 34% of the fold change variation in plasma LDL levels, respectively. Micronutrients, including pantothenic acid (vitamin B5), play an important role in lipid metabolism (Al-Attas et al, 2014;Evans et al, 2014;Hadjistavri et al, 2010;Heng et al, 2013;Kelishadi et al, 2014Kelishadi et al, , 2010, which supports the changes in LDL metabolism in the pool 2. This is the first study showing a possible association between American genetic ancestry and vitamin E in children and adolescents.…”

Nutrition and Nutritional Supplements in the Management of Dyslipidemia—Part 2

“…HDL-C and ApoA1 are increased by 8%. 1,[55][56][57][58][59] The effects on lipids are slow to occur and have a peak effect at four months but may take up to six to nine months. Pantethine reduces lipid peroxidation of LDL-C and decreases lipid deposition, IMT, and fatty streak formation in the aorta and coronary arteries.…”

“…Pantethine reduces lipid peroxidation of LDL-C and decreases lipid deposition, IMT, and fatty streak formation in the aorta and coronary arteries. 1,[55][56][57][58][59] Pantethine inhibits cholesterol synthesis and accelerates FA metabolism in the mitochondria by inhibiting hepatic acetyl-CoA carboxylase, increases CoA in the cytoplasm, which stimulates the oxidation of acetate at the expense of FA and cholesterol synthesis, and increases Krebs cycle activity. 1,[55][56][57][58][59] In addition, cholesterol esterase activity increases and HMG-CoA reductase activity are decreased.…”