Insulin may be an important regulator of serum apolipoprotein A-V (apoA-V) levels in obese people and may contribute to the development of obesity-associated dyslipidemia, say Japanese researchers.
"The proposed mechanism is that, in obesity, hyperinsulinemia might induce a decrease in apoA-V level, and a decrease of LPL [lipoprotein lipase] activity following increased TG [triglyceride] level," say Tomoo Okada (Nihon University School of Medicine, Tokyo) and team.
LPL, which is made primarily in adipose and muscle tissue, catalyses the hydrolysis of the triacylglycerol component of circulating chylomicrons and very-low-density lipoproteins.
In an analysis of 17 children with obesity, which was defined as more than 20% overweight, the prevalence of hypertriglyceridemia, low high-density lipoprotein (HDL) cholesterol, and hyperinsulinemia was 41.2%, 11.8%, and 41.2%, respectively.
The median apoA-V level was 198.1 ng/mL and the LPL mass (LPLm) level was 284.2 µg/ml.
Analysis showed that apoA-V levels were negatively correlated with TG and insulin levels and with the homeostasis model of assessment ratio (HOMA-R), while they were positively correlated with HDL cholesterol and LPLm.
However, obese children who had hyperinsulinemia had a higher waist-to-hip ratio, higher TG, lower HDL cholesterol, lower apoA-V, and a higher HOMA-R than obese children without hyperinsulinemia. The LPLm level was also lower, although this did not reach significance.
As reported in Obesity Research and Clinical Practice, insulin level was the only independent predictor for TG level after apoA-V and LPLm were accounted for, whereas apoA-V independently predicted HDL cholesterol level after adjusting for insulin level.
"Our results suggest that insulin is a determinant of the apoA-V level in obesity," say Okada et al.
"The apoa-V level may partly contribute to the development of obesity-associated dyslipidemia, both hypertiglyceridemia and a reduced HDL cholesterol level," they conclude.
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