Vitamin B3 (niacin) is an important cofactor of the LPL enzyme, which catalyzes a key step in the removal of triglycerides from the blood. It also contributes to cardiovascular health by raising HDL-Cholesterol (the “good” cholesterol) levels.
Individuals carrying the LPL variants must consume adequate amount of dietary niacin. This common genetic predisposition, along with low consumption of niacin, triples the risk for the Metabolic Syndrome (dyslipidemia, obesity and diabetes).
Niacin (vitamin B3) is essential for digestion, energy storage, cardiovascular health, skin health and nerves.
Niacin deficiency may lead to cardiovascular disease and diabetes. An acute deficiency lead to pellagra, a life threatening disease.
Niacin interact with the LPL enzyme to catalyze a key step in the removal of triglycerides from the blood, generating fatty acids for storage in the adipose tissue or for oxidation in the skeletal muscle. Other then removing triglycerides, LPL also contribute to cardiovascular health by raising HDL-Cholesterol (the “good” cholesterol) levels.
Gene: LIPOPROTEIN LIPASE; LPL
Genomic coordinates (GRCh38): 8:19,939,070-19,967,258
The P2 variant form of LPL is associated with higher triglycerides and lower HDL cholesterol levels. The P2 allele is also positively correlated with body mass index, increasing the risk for obesity.
The P2/P2 genotype (homozygousity for the variant allele) is more common among individuals with the Metabolic Syndrome. This syndrome is characterized by co-occurance of high triglyceridesand low HDL levels, hypertension, obesity and insulin resistance. It increases the chances for type II diabetes and cardiovascular disease. However, P2/P2 individuals who consumed adequate amount of vitamin B3 were not in risk.
To sum it up, low levels of Niacin consumption result in high risk for the Metabolic Syndrome, but only among homozygotes who consume less than 14.8 mg/day niacin.