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Published on: January 7, 2018
Postprandial VLDL-TG metabolism in type 2 diabetes
Esben Søndergaard1, Rakel Fuglsang Johansen2, Michael D Jensen3
1Department of Endocrinology and Internal Medicine, Aarhus University Hospital, Nørrebrogade 44, 8000 Aarhus C, Denmark; Danish Diabetes Academy, Odense University Hospital, Kløvervænget 10, Entrance 112, 3rd floor, 5000 Odense C, Denmark; Endocrine Research Unit, Mayo Clinic, 1216 2nd St SW, Rochester, MN 55902, USA.
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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