The association of lipoprotein lipase PvuII polymorphism and niacin intake in the prevalence of metabolic syndrome: a KMSRI-Seoul study

Abstract

Lipoprotein lipase (LPL) polymorphism correlated with LPL activity is associated with plasma lipid and lipoprotein levels. We aimed to investigate the frequency of LPL PvuII polymorphism and effects of LPL PvuII polymorphism and niacin intake on the prevalence of metabolic syndrome (MetSyn) in Koreans. Lifestyle questionnaires, anthropometry, and dietary records were completed, and LPL PvuII polymorphism, LPL mass, and lipid profiles were determined in 548 Koreans (MetSyn: 278, Non-MetSyn: 270). The MetSyn group showed a significantly lower frequency of P1P1 (wild type) and a higher frequency of P1P2 (hetero type) than the non-MetSyn group. The P2P2 (mutant type) group significantly showed lower levels of HDLc and LPL mass and a higher level of TG than the P1P1 group. As niacin intake increased, LPL mass decreased in the P2P2 group (r 2 = 0.07). In particular, the lowest niacin intake group (B14.82 mg/day) increased more than 3 times with regard to a higher risk of MetSyn than the others in the P2P2 mutant groups. However, the MetSyn risk declined 74% at the optimal levels of niacin intake (14.83-17.80 mg/day) in the P2P2 group compared to those of the P1 allele group. The findings indicate that optimal levels of niacin intake effectively decreased Korean MetSyn prevalence in the P2P2 mutant group.

Link of dietary patterns with metabolic syndrome: analysis of the National Health and Nutrition Examination Survey

“…Our findings also suggest that the higher intake of the nutrients loaded in the second PC including dietary fiber, folate, vitamins-A, -Bs, -E, magnesium, iron and copper was associated with lower odds of MetS and its HDL, blood pressure, glucose, and central obesity components. These findings are in agreement with earlier studies reported salutary effects of dietary fiber, 29 vitamin A, 30 vitamin B12, 7, 30 niacin, 31 magnesium 32 and copper 9 on the rate of MetS. Possible mechanisms may partially be explained by improvement of insulin resistance and glucose intolerance 33 by folate, vitamin A, -E, -B6, -B12, thiamine, magnesium and copper; improvement of endothelial function 33, 34 by magnesium, folate, niacin and vitamin E; decrease in blood pressure 34, 35 by niacin, thiamine, riboflavin, vitamin B12, Iron and magnesium; increased HDL and decreased oxidative stress 36, 37 by niacin, vitamin E, magnesium and copper; and decrease in triglycerides 38 by vitamin E, and magnesium, altogether translate to lower likelihood of MetS components and eventually lower likelihood of MetS.…”

Dietary nutrient intake and metabolic syndrome risk in Chinese adults: a case–control study

“…In addition, several studies have found that niacin supplementation has beneficial effects on lipid levels in patients with MetS, diabetes, and atherosclerosis, and the pharmacological level of niacin required can treat lipid disorders and cardiovascular disease (CVD) [43]. A Korean study concluded that adequate daily intake of niacin reduced the risk of MetS, whereas inadequate intake increased the risk [44]. Riboflavin is unique among the water-soluble vitamins in that cereals, meat, and fish are good sources of riboflavin, and certain fruits and vegetables, especially dark-green vegetables, contain reasonably high concentrations [45].…”

Age Stratification in Genetic Variation of Lipoprotein Lipase in Metabolic Syndrome Javanese Ethnics of Indonesia

“…In this study, TT frequencies were more common in controls compared to cases. Lipoprotein Lipase Pvu II C > T gene variation in this research was the same as research conducted in the populations in Turkey, Saudi Arabia, Korea and Egypt [6], [8], [19], [20]. [19].…”

“…Mature LPL is a 448 amino acid glycoprotein with chromosomal location 8p22, consisting of 10 exons and 9 introns [4]. LPL hydrolyses triglycerides in circulation from chylomicrons and very-low-density lipoproteins and generates fatty acids for storage in the adipose tissue or oxidation in the skeletal muscle [5], [6]. Several mutations and variations have been described in the LPL gene in humans, most of which lead to decreased LPL-activity.…”