Postprandial VLDL-TG metabolism in type 2 diabetes

Esben Søndergaard, Rakel Fuglsang Johansen, Michael Dennis Jensen, Søren Nielsen

Research output: Contribution to journalArticle

5 Citations (Scopus)

Abstract

Background Type 2 diabetes is associated with excess postprandial lipemia due to accumulation of chylomicrons and VLDL particles. This is a risk factor for development of cardiovascular disease. However, whether the excess lipemia is associated with an impaired suppression of VLDL-TG secretion and/or reduced clearance into adipose tissue is unknown. Objective We measured the postprandial VLDL-TG secretion, clearance and adipose tissue storage to test the hypothesis that impaired postprandial suppression of VLDL-TG secretion, combined with impaired VLDL-TG storage in adipose tissue, is associated with excess postprandial lipemia. Design We studied 11 men with type 2 diabetes and 10 weight-matched non-diabetic men using ex-vivo labeled VLDL-TG tracers during an oral high-fat mixed-meal tolerance test to measure postprandial VLDL-TG secretion, clearance and storage. In addition, adipose tissue biopsies were analyzed for LPL activity and cellular storage factors. Results Men with type 2 diabetes had greater postprandial VLDL-TG concentration compared to non-diabetic men. However, postprandial VLDL-TG secretion rate was similar in the two groups with equal suppression of VLDL-TG secretion rate (≈ 50%) and clearance rate. In addition, postprandial VLDL-TG storage was similar in the two groups in both upper body and lower body subcutaneous adipose tissue. Conclusions Despite greater postprandial VLDL-TG concentration, men with type 2 diabetes have similar postprandial suppression of VLDL-TG secretion and a similar ability to store VLDL-TG in adipose tissue compared to non-diabetic men. This may indicate that abnormalities in postprandial VLDL-TG metabolism are a consequence of obesity/insulin resistance more than a result of type 2 diabetes per se.

Original languageEnglish (US)
Pages (from-to)25-35
Number of pages11
JournalMetabolism: Clinical and Experimental
Volume75
DOIs
StatePublished - Oct 1 2017

Fingerprint

Type 2 Diabetes Mellitus
Adipose Tissue
Hyperlipidemias
Chylomicrons
Subcutaneous Fat
Meals
Insulin Resistance
Cardiovascular Diseases
Obesity
Fats
Biopsy
Weights and Measures

Keywords

  • Lipid metabolism
  • Postprandial period
  • Triglyceride
  • Type 2 diabetes
  • VLDL

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Endocrinology

Cite this

Postprandial VLDL-TG metabolism in type 2 diabetes. / Søndergaard, Esben; Johansen, Rakel Fuglsang; Jensen, Michael Dennis; Nielsen, Søren.

In: Metabolism: Clinical and Experimental, Vol. 75, 01.10.2017, p. 25-35.

Research output: Contribution to journalArticle

Søndergaard, Esben ; Johansen, Rakel Fuglsang ; Jensen, Michael Dennis ; Nielsen, Søren. / Postprandial VLDL-TG metabolism in type 2 diabetes. In: Metabolism: Clinical and Experimental. 2017 ; Vol. 75. pp. 25-35.
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abstract = "Background Type 2 diabetes is associated with excess postprandial lipemia due to accumulation of chylomicrons and VLDL particles. This is a risk factor for development of cardiovascular disease. However, whether the excess lipemia is associated with an impaired suppression of VLDL-TG secretion and/or reduced clearance into adipose tissue is unknown. Objective We measured the postprandial VLDL-TG secretion, clearance and adipose tissue storage to test the hypothesis that impaired postprandial suppression of VLDL-TG secretion, combined with impaired VLDL-TG storage in adipose tissue, is associated with excess postprandial lipemia. Design We studied 11 men with type 2 diabetes and 10 weight-matched non-diabetic men using ex-vivo labeled VLDL-TG tracers during an oral high-fat mixed-meal tolerance test to measure postprandial VLDL-TG secretion, clearance and storage. In addition, adipose tissue biopsies were analyzed for LPL activity and cellular storage factors. Results Men with type 2 diabetes had greater postprandial VLDL-TG concentration compared to non-diabetic men. However, postprandial VLDL-TG secretion rate was similar in the two groups with equal suppression of VLDL-TG secretion rate (≈ 50{\%}) and clearance rate. In addition, postprandial VLDL-TG storage was similar in the two groups in both upper body and lower body subcutaneous adipose tissue. Conclusions Despite greater postprandial VLDL-TG concentration, men with type 2 diabetes have similar postprandial suppression of VLDL-TG secretion and a similar ability to store VLDL-TG in adipose tissue compared to non-diabetic men. This may indicate that abnormalities in postprandial VLDL-TG metabolism are a consequence of obesity/insulin resistance more than a result of type 2 diabetes per se.",
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N2 - Background Type 2 diabetes is associated with excess postprandial lipemia due to accumulation of chylomicrons and VLDL particles. This is a risk factor for development of cardiovascular disease. However, whether the excess lipemia is associated with an impaired suppression of VLDL-TG secretion and/or reduced clearance into adipose tissue is unknown. Objective We measured the postprandial VLDL-TG secretion, clearance and adipose tissue storage to test the hypothesis that impaired postprandial suppression of VLDL-TG secretion, combined with impaired VLDL-TG storage in adipose tissue, is associated with excess postprandial lipemia. Design We studied 11 men with type 2 diabetes and 10 weight-matched non-diabetic men using ex-vivo labeled VLDL-TG tracers during an oral high-fat mixed-meal tolerance test to measure postprandial VLDL-TG secretion, clearance and storage. In addition, adipose tissue biopsies were analyzed for LPL activity and cellular storage factors. Results Men with type 2 diabetes had greater postprandial VLDL-TG concentration compared to non-diabetic men. However, postprandial VLDL-TG secretion rate was similar in the two groups with equal suppression of VLDL-TG secretion rate (≈ 50%) and clearance rate. In addition, postprandial VLDL-TG storage was similar in the two groups in both upper body and lower body subcutaneous adipose tissue. Conclusions Despite greater postprandial VLDL-TG concentration, men with type 2 diabetes have similar postprandial suppression of VLDL-TG secretion and a similar ability to store VLDL-TG in adipose tissue compared to non-diabetic men. This may indicate that abnormalities in postprandial VLDL-TG metabolism are a consequence of obesity/insulin resistance more than a result of type 2 diabetes per se.

AB - Background Type 2 diabetes is associated with excess postprandial lipemia due to accumulation of chylomicrons and VLDL particles. This is a risk factor for development of cardiovascular disease. However, whether the excess lipemia is associated with an impaired suppression of VLDL-TG secretion and/or reduced clearance into adipose tissue is unknown. Objective We measured the postprandial VLDL-TG secretion, clearance and adipose tissue storage to test the hypothesis that impaired postprandial suppression of VLDL-TG secretion, combined with impaired VLDL-TG storage in adipose tissue, is associated with excess postprandial lipemia. Design We studied 11 men with type 2 diabetes and 10 weight-matched non-diabetic men using ex-vivo labeled VLDL-TG tracers during an oral high-fat mixed-meal tolerance test to measure postprandial VLDL-TG secretion, clearance and storage. In addition, adipose tissue biopsies were analyzed for LPL activity and cellular storage factors. Results Men with type 2 diabetes had greater postprandial VLDL-TG concentration compared to non-diabetic men. However, postprandial VLDL-TG secretion rate was similar in the two groups with equal suppression of VLDL-TG secretion rate (≈ 50%) and clearance rate. In addition, postprandial VLDL-TG storage was similar in the two groups in both upper body and lower body subcutaneous adipose tissue. Conclusions Despite greater postprandial VLDL-TG concentration, men with type 2 diabetes have similar postprandial suppression of VLDL-TG secretion and a similar ability to store VLDL-TG in adipose tissue compared to non-diabetic men. This may indicate that abnormalities in postprandial VLDL-TG metabolism are a consequence of obesity/insulin resistance more than a result of type 2 diabetes per se.

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KW - VLDL

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