Insulin and non-esterified fatty acid relations to alimentary lipaemia and plasma concentrations of postprandial triglyceride-rich lipoproteins in healthy middle-aged men

Abstract

A cluster of risk factors for Type II (non-insulin-dependent) diabetes mellitus and cardiovascular disease, called the metabolic syndrome, is a common feature of otherwise healthy people living in industrialised countries. Increased visceral adipose tissue depots, insulin resistance with ensuing hyperinsulinaemia and dyslipoproteinaemia including hypertriglyceridaemia, a low HDL cholesterol concentration and a preponderance of small, dense LDL particles are central components of this syndrome [1]. The links between glucose-insulin homeostasis and lipoprotein metabolism have received particular atten- Abstract Aims/hypothesis. Enhanced and prolonged postprandial lipaemia is related to cardiovascular disease but how postprandial lipaemia is regulated is poorly known. We therefore determined the relations of fasting insulin concentrations to fasting and postprandial lipids, lipoproteins and non-esterified fatty acids in middle-aged men. Methods. The subjects, 99 healthy 50-year-old men with an apolipoprotein E3/3 genotype, ate a mixed meal. The apolipoprotein B-48 and B-100 contents were determined in triglyceride-rich lipoproteins as a measure of chylomicron remnant and very low density lipoprotein particle concentrations. Results. Fasting plasma insulin was associated with the triglyceride response to the test meal, independently of body mass index, waist-to-hip circumference ratio, blood glucose and the insulin effect on fasting plasma triglycerides. Exaggerated and prolonged postprandial lipaemia in subjects in the upper quartile of the plasma insulin distribution was largely accounted for by large (Svedberg flotation rate > 60) very low density lipoproteins and chylomicron remnants. Insulin relations to large postprandial triglyceride-rich lipoproteins exclusively reflected the association between plasma insulin and the fasting plasma concentrations of these lipoprotein species, whereas plasma insulin and late postprandial plasma concentrations of small (Svedberg flotation rate 20±60) chylomicron remnants were related, independently of insulin influences on fasting concentrations. Strong positive relations were found between the late increases in large triglyceride-rich lipoproteins and plasma non-esterified fatty acid concentrations after 6 h. Conclusion/interpretation. The degree of insulin sensitivity is a major determinant of postprandial lipaemia in healthy middle-aged men and could add to the regulation of the basal production of large triglyceride-rich lipoproteins. [Diabetologia (2000)

Acute Hyperinsulinism Modulates Plasma Apolipoprotein B-48 Triglyceride--Rich Lipoproteins in Healthy Subjects During the Postprandial Period

“…In the vast majority of studies already conducted in the field of postprandial lipid metabolism, both insulin resistance and related hyperinsulinism took part in the abnormal metabolic syndrome exhibited by the subjects (5,12,14,15). Thus, although key data showing a positive association between insulin resistance/hyperinsulinism and exaggerated postprandial lipemia have been obtained, it has not yet been possible to discriminate between the respective roles of insulin resistance or hyperinsulinism on postprandial lipid metabolism.…”

“…Because these patients display both hyperinsulinism and insulin resistance, it is difficult to evaluate the respective role of hyperinsulinism and insulin resistance in the abnormalities of the postprandial lipemia observed. Several studies have shown that the observed accumulation of exogenous triglyceride-rich lipoproteins (TRLs) after a fat-containing test meal positively correlates with both fasting and postprandial plasma insulin levels in normal or obese subjects (5,12,14,15). Some reports, on the basis of indirect arguments, have suggested that insulin resistance is the main factor in this phenomenon (5,12,14,15), and that the amplitude of postprandial lipemia correlates with the severity of insulin resistance (14).…”

“…Several studies have shown that the observed accumulation of exogenous triglyceride-rich lipoproteins (TRLs) after a fat-containing test meal positively correlates with both fasting and postprandial plasma insulin levels in normal or obese subjects (5,12,14,15). Some reports, on the basis of indirect arguments, have suggested that insulin resistance is the main factor in this phenomenon (5,12,14,15), and that the amplitude of postprandial lipemia correlates with the severity of insulin resistance (14). Thus, even if a clear consensus can be derived from these studies that hyperinsulinemia and insulin resistance are associated with exacerbated postprandial lipid accumulation, the causal relationship is not yet established.…”

Nateglinide Suppresses Postprandial Hypertriglyceridemia in Zucker Fatty Rats and Goto-Kakizaki Rats: Comparison with Voglibose and Glibenclamide.

“…The role of early phase insulin has not been clarified since insulin has pleiotropic effects (both directly and indirectly) on exogenous lipoprotein metabolism and endogenous lipoprotein synthesis. 19,20) One of the well-defined molecules that influence the levels of triglycerides is lipoprotein lipase (LPL), which hydrolyzes the triglyceride component of circulating lipoprotein, and decreases the blood triglyceride levels. Insulin is a major stimulator of the postprandial increase of LPL activity, but other reports have suggested that decreased LPL gene expression is mediated by the increase of insulin in rats with postprandial hyperlipidemia.…”

Energy replacement attenuates the effects of prior moderate exercise on postprandial metabolism in overweight/obese men

“…Postprandial lipoproteins and their remnants may deposit into arterial walls accelerating the development of atheromatous plaques 1 and the postprandial elevation in circulating triglyceride (TG)-rich lipoproteins contributes to the accumulation of small, dense low-density lipoproteins (LDL) and a decrease in cardio-protective high-density lipoproteins (HDL); a combination known as the atherogenic phenotype. 2 In addition, postprandial hyperinsulinaemia, together with the transient postprandial increase in insulin resistance may also contribute to atherogenic progression [3][4][5] and the development of chronic insulin resistance and type 2 diabetes. 6 As humans spend the majority of the day in the postprandial state, interventions which alter postprandial metabolism may have implications for the prevention and management of metabolic diseases.…”