Postprandial dyslipidemia in insulin resistant states in adolescent populations

Abstract

Obesity and the metabolic syndrome are becoming increasingly prevalent not only in adults, but also in adolescents. The metabolic syndrome, a complex cluster of metabolic abnormalities, increases one's risk of developing type 2 diabetes and cardiovascular disease (CVD). Dyslipidemia, a key component of the metabolic syndrome, is highly associated with insulin resistance and contributes to increased CVD risk. Dyslipidemia has traditionally been assessed using a fasting lipid profile [ i.e . fasting triglycerides, total cholesterol, low-density lipoprotein cholesterol (LDL-C), and high-density lipoprotein cholesterol (HDL-C)]. However, the postprandial state predominates over the course of a day and non-fasting triglycerides independently predict CVD risk. In insulin resistant states, the intestine overproduces triglyceride-rich lipoprotein (TRL) particles, termed chylomicrons (CMs), following ingestion of a fat-containing meal, as well as in the fasting state. Along with elevated hepatic TRLs ( i.e . very-low density lipoproteins), CMs contribute to remnant lipoprotein accumulation, small dense LDL particles, and reduced HDL-C, which collectively increase CVD risk. Given the early genesis of atherosclerosis and physiological metabolic changes during adolescence, studying postprandial dyslipidemia in the adolescent population is an important area of study. Postprandial dyslipidemia in the pediatric population poses a significant public health concern, warranting a better understanding of its pathogenesis and association with insulin resistance and CVD. This review discusses the metabolic syndrome, focusing on the link between insulin resistance, postprandial dyslipidemia, and CVD risk. Furthermore, the clinical significance and functional assessment of postprandial dyslipidemia, specifically in the adolescent population, is discussed in more detail.

Determinants of the postprandial triglyceride response to a high-fat meal in healthy overweight and obese adults

“…In turn, the liver secretes more TG-rich VLDL and may exhibit fat accumulation, pushing a feedforward loop advancing insulin resistance. Insulin resistance also promotes increased chylomicron secretion from the intestine and the general postprandial accumulation of TRLs from the liver and intestine [ 49 – 51 ]. Improved insulin sensitivity through physical activity may not only improve glucose transport [ 52 ] but may additionally prevent the accumulation of TRLs and reduce the overall TG response in the postprandial period.…”

The chylomicron saga: time to focus on postprandial metabolism

“…When insulin (+glucose) was infused into healthy men, a reduction in apoB48 -containing lipoprotein synthesis of 50–52% compared to saline infusion, and a reduction of 16–21% when the insulin-induced lowering of FA was avoided by concurrent intralipid infusion. These findings imply that insulin has a direct effect, in addition to lowering plasma FA levels, in reducing the formation of intestinal lipoproteins ( 65 , 66 , 70 ).…”

Determinants of the Postprandial Triglyceride Response to a High-fat Meal in Healthy Overweight and Obese Adults.

“…In turn, the liver secretes more TG-rich VLDL and may exhibit fat accumulation, pushing a feedforward loop advancing insulin resistance. Insulin resistance also promotes increased chylomicron secretion from the intestine and the general postprandial accumulation of TRLs from the liver and intestine (45)(46)(47). Improved insulin sensitivity through physical activity may not only improve glucose transport (48) but may additionally prevent the accumulation of TRLs and reduce the overall TG response in the postprandial period.…”