hyperinsulinism/triglyceride

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Acute hyperinsulinism modulates plasma apolipoprotein B-48 triglyceride-rich lipoproteins in healthy subjects during the postprandial period.

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The role of postprandial insulin in the regulation of postprandial lipid metabolism is still poorly understood. The roles of hyperinsulinemia and insulin resistance in the alteration of postprandial lipid metabolism are not clear either. To improve knowledge in this area, we submitted healthy men to

VLDL-triglyceride kinetics during hyperglycemia-hyperinsulinemia: effects of sex and obesity.

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We have previously shown that sex and obesity independently affect basal very low density lipoprotein (VLDL)-triglyceride (TG) kinetics. In the present study, we investigated the effect of hyperglycemia-hyperinsulinemia on VLDL-TG kinetics in lean and obese men and women (n = 6 in each group).

Changes in blood pressure, plasma triglyceride and aldosterone concentration, and red cell cation concentration in patients with hyperinsulinemia.

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Blood pressure, plasma concentration of triglyceride, aldosterone, renin activity (PRA), and atrial naturietic peptide (ANP), and red blood cell, urine, and plasma sodium and potassium concentration were determined in 24 healthy individuals divided into two groups defined as being either

Contributions of de novo synthesis of fatty acids to total VLDL-triglyceride secretion during prolonged hyperglycemia/hyperinsulinemia in normal man.

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Triglycerides (TG) are synthesized in the liver principally from two sources of fatty acids (FA): FA synthesized de novo in the liver and preformed FA. We have measured the rate of secretion of de novo synthesized FA and total secretion of FA bound to VLDL-TG in healthy men (n = 5) in the basal

Hyperinsulinemia and triglyceride-rich lipoproteins.

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Hypertriglyceridemia is the most frequent form of hyperlipidemia seen in diabetes. Because hypertriglyceridemia and hyperinsulinemia often coexist in the general population and because patients with NIDDM generally are hyperinsulinemic, we have undertaken a series of in vivo studies to examine the

Hyperinsulinemia and in vivo very-low-density lipoprotein-triglyceride kinetics.

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The effect of hyperinsulinemia (2 wk of twice daily NPH insulin) on the kinetics of very-low-density lipoprotein (VLDL)-triglyceride (TG) was studied in rats. To avoid profound hypoglycemia the rats were allowed sucrose ad libitum. Two control groups were needed: chow only and ad libitum

Acute hyperinsulinemia inhibits intramyocellular triglyceride synthesis in high-fat-fed obese rats.

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Hyperinsulinemia is common in obesity, but whether it plays a role in intramyocellular triglyceride (imcTG) buildup is unknown. In this study, hyperinsulinemic-euglycemic clamp experiments were performed in overnight-fasted lean and high-fat-fed obese rats, awake, to determine the effect of insulin

Triglyceride-rich lipoprotein metabolism during acute hyperinsulinemia in hypertriglyceridemic humans.

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Chronic endogenous hyperinsulinemia is associated with increased rates of triglyceride production in humans. The effect of acute exogenous hyperinsulinemia on triglyceride production was studied in seven hypertriglyceridemic men before and during six hours of hyperinsulinemic-euglycemic clamping,

Triglyceride kinetics: effects of dietary glucose, sucrose, or fructose alone or with hyperinsulinemia.

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The effects of different dietary sugars, with or without exogenously induced hyperinsulinemia, on rat plasma triglyceride kinetics have been studied. Glucose, sucrose, or fructose were supplied as 10% drinking solutions. The sugar-supplemented groups were each divided into subgroups, one receiving 6

Effect of long-term exogenous hyperinsulinemia and fructose or glucose supplementation on triglyceride turnover in rats.

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We examined the effect of long-term (6 months) hyperinsulinemia on VLDL-triglyceride turnover in male Wistar rats. Hyperinsulinemia was induced in rats by daily s.c. injection of Ultralente insulin (6 U/day at 19:00). Fructose (F) or glucose (G) was supplied in the drinking water (10%) in order to

Visceral obesity and hyperinsulinemia modulate the impact of the microsomal triglyceride transfer protein -493G/T polymorphism on plasma lipoprotein levels in men.

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The dyslipidemic state of visceral obesity is characterized by increased plasma triglyceride levels, low high-density lipoprotein-cholesterol concentration and alterations in low-density lipoprotein (LDL) composition and concentration. A functional, non-coding microsomal triglyceride transfer

Tissue triglycerides, insulin resistance, and insulin production: implications for hyperinsulinemia of obesity.

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Obesity is associated with both insulin resistance and hyperinsulinemia. Initially hyperinsulinemia compensates for the insulin resistance and thereby maintains normal glucose homeostasis. Obesity is also associated with increased tissue triglyceride (TG) content. To determine whether both insulin

Effects of acute hyperinsulinemia on VLDL triglyceride and VLDL apoB production in normal weight and obese individuals.

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The effects of short-term hyperinsulinemia on the production of both VLDL triglyceride and VLDL apoB were determined semiquantitatively before and during a 6-h euglycemic hyperinsulinemic clamp (40 mU.m-2 x min-1) in 17 women (8 chronically hyperinsulinemic obese, BMI = 35.7 kg/m2; 9 normal weight,

Hyperinsulinemia in patients with low fractional catabolic rate of triglycerides.

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In non-diabetic persons whose serum triglyceride (TG) concentrations ranged from normal to very high levels, endogenous TG turnover was measured using the radioglycerol method of Farquhar and coworkers. Insulin, FFA, and glucose concentrations were estimated during an oral glucose tolerance test.

Acute hyperinsulinemia and reduced plasma free fatty acid levels decrease intramuscular triglyceride synthesis.

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OBJECTIVE To investigate the effect of acute hyperinsulinemia and the resulting decrease in plasma free fatty acid (FFA) concentrations on intramuscular TG synthesis. METHODS U-(13)C(16)-palmitate was infused for 3 h in anesthetized rabbits after overnight food deprivation. Arterial blood and leg

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