Post-prandial hyperinsulinemia does not affect the intravascular synthesis of HDL-apoproteins in humans

P. Lucidi, Elena Volpi, P. De Feo

Research output: Contribution to journalArticle

Abstract

This study was performed to establish whether post-prandial hyperinsulinemia affects HDL production rate in humans. For this reason, the intravascular fractional synthetic rates (IFSR)) of HDL2 and HDL3 were measured in 8 healthy volunteers, randomized in a control (CTRL) and a meal (MEAL) group matched for age (CTRL 26 ± 6, MEAL 24 ± 2 yr) and BMI (CTRL 22 ± 3, MEAL 23 ± 2 kg/m2). All subjects were studied for a period of 8 hr (0-480 min); the first study period (0-240) was used to measure HDL kinetics in the overnight post-absorptive state, the second study period (240-480 min) differed between the two groups. The subjects of the MEAL, group received an intragastric infusion of a glucose-lipid meal (~ 632 kcal) whereas those of the CTRL group only water. Plasma lipoproteins IFSR were measured after sequential ultracentrifugation and acid hydrolysis using plasma KIC specific activity (SA) as a precursor pool SA, during the continuous infusion of [1-14C] leucine. Plasma HDL-cholesterol decreased by 11% after meal ingestion (p < 0.05). In the post-absorptive state (180-240 min) the IFSR (%·h-1) of HDL2 and HDL3 apoproteins did not differ between the CTRL and the MEAL, groups (HDL2: 1.2 ± 0.4, 1.1 ± 0.2; HDL3: 0.9 ± 0.2, 1.0 ± 0.1). Meal ingestion (absorptive state, 420-480 min) increased plasma insulin but did not affect the IFSR of the HDL2 (CTRL: 1.1 ± 0.2 vs MEAL: 1.0 ± 0.3) and HDL3 apoproteins (CTRL: 0.8 ± 0.2 vs MEAL: 1.1 ± 0.2). Thus, we conclude that: 1) post-prandial hyperinsulinemia does not affect HDL production; 2) the post-prandial decrement of plasma HDL concentrations is due to increased HDL cholesterol catabolism.

Original languageEnglish (US)
Pages (from-to)289-295
Number of pages7
JournalDiabetes, Nutrition and Metabolism - Clinical and Experimental
Volume11
Issue number5
StatePublished - Oct 1998
Externally publishedYes

Fingerprint

apoproteins
Apoproteins
hyperinsulinemia
Hyperinsulinism
high density lipoprotein cholesterol
Meals
ingestion
synthesis
ultracentrifugation
acid hydrolysis
lipoproteins
leucine
volunteers
insulin
kinetics
glucose
metabolism
HDL Cholesterol
lipids
Eating

Keywords

  • Fed state
  • HDL lipoproteins
  • Leucine kinetics

ASJC Scopus subject areas

  • Medicine (miscellaneous)
  • Internal Medicine
  • Endocrinology
  • Food Science
  • Endocrinology, Diabetes and Metabolism

Cite this

Post-prandial hyperinsulinemia does not affect the intravascular synthesis of HDL-apoproteins in humans. / Lucidi, P.; Volpi, Elena; De Feo, P.

In: Diabetes, Nutrition and Metabolism - Clinical and Experimental, Vol. 11, No. 5, 10.1998, p. 289-295.

Research output: Contribution to journalArticle

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abstract = "This study was performed to establish whether post-prandial hyperinsulinemia affects HDL production rate in humans. For this reason, the intravascular fractional synthetic rates (IFSR)) of HDL2 and HDL3 were measured in 8 healthy volunteers, randomized in a control (CTRL) and a meal (MEAL) group matched for age (CTRL 26 ± 6, MEAL 24 ± 2 yr) and BMI (CTRL 22 ± 3, MEAL 23 ± 2 kg/m2). All subjects were studied for a period of 8 hr (0-480 min); the first study period (0-240) was used to measure HDL kinetics in the overnight post-absorptive state, the second study period (240-480 min) differed between the two groups. The subjects of the MEAL, group received an intragastric infusion of a glucose-lipid meal (~ 632 kcal) whereas those of the CTRL group only water. Plasma lipoproteins IFSR were measured after sequential ultracentrifugation and acid hydrolysis using plasma KIC specific activity (SA) as a precursor pool SA, during the continuous infusion of [1-14C] leucine. Plasma HDL-cholesterol decreased by 11{\%} after meal ingestion (p < 0.05). In the post-absorptive state (180-240 min) the IFSR ({\%}·h-1) of HDL2 and HDL3 apoproteins did not differ between the CTRL and the MEAL, groups (HDL2: 1.2 ± 0.4, 1.1 ± 0.2; HDL3: 0.9 ± 0.2, 1.0 ± 0.1). Meal ingestion (absorptive state, 420-480 min) increased plasma insulin but did not affect the IFSR of the HDL2 (CTRL: 1.1 ± 0.2 vs MEAL: 1.0 ± 0.3) and HDL3 apoproteins (CTRL: 0.8 ± 0.2 vs MEAL: 1.1 ± 0.2). Thus, we conclude that: 1) post-prandial hyperinsulinemia does not affect HDL production; 2) the post-prandial decrement of plasma HDL concentrations is due to increased HDL cholesterol catabolism.",
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N2 - This study was performed to establish whether post-prandial hyperinsulinemia affects HDL production rate in humans. For this reason, the intravascular fractional synthetic rates (IFSR)) of HDL2 and HDL3 were measured in 8 healthy volunteers, randomized in a control (CTRL) and a meal (MEAL) group matched for age (CTRL 26 ± 6, MEAL 24 ± 2 yr) and BMI (CTRL 22 ± 3, MEAL 23 ± 2 kg/m2). All subjects were studied for a period of 8 hr (0-480 min); the first study period (0-240) was used to measure HDL kinetics in the overnight post-absorptive state, the second study period (240-480 min) differed between the two groups. The subjects of the MEAL, group received an intragastric infusion of a glucose-lipid meal (~ 632 kcal) whereas those of the CTRL group only water. Plasma lipoproteins IFSR were measured after sequential ultracentrifugation and acid hydrolysis using plasma KIC specific activity (SA) as a precursor pool SA, during the continuous infusion of [1-14C] leucine. Plasma HDL-cholesterol decreased by 11% after meal ingestion (p < 0.05). In the post-absorptive state (180-240 min) the IFSR (%·h-1) of HDL2 and HDL3 apoproteins did not differ between the CTRL and the MEAL, groups (HDL2: 1.2 ± 0.4, 1.1 ± 0.2; HDL3: 0.9 ± 0.2, 1.0 ± 0.1). Meal ingestion (absorptive state, 420-480 min) increased plasma insulin but did not affect the IFSR of the HDL2 (CTRL: 1.1 ± 0.2 vs MEAL: 1.0 ± 0.3) and HDL3 apoproteins (CTRL: 0.8 ± 0.2 vs MEAL: 1.1 ± 0.2). Thus, we conclude that: 1) post-prandial hyperinsulinemia does not affect HDL production; 2) the post-prandial decrement of plasma HDL concentrations is due to increased HDL cholesterol catabolism.

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