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Decreased GPIHBP1 protein levels in visceral adipose tissue partly underlie the hypertriglyceridemic phenotype in insulin resistance.

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Date

2018-11-08

Authors

Surendran, R Preethi
Udayyapan, Shanti D
Clemente-Postigo, Mercedes
Havik, Stefan R
Schimmel, Alinda W M
Tinahones, Francisco J
Nieuwdorp, Max
Dallinga-Thie, Geesje M

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Abstract

GPIHBP1 is a protein localized at the endothelial cell surface that facilitates triglyceride (TG) lipolysis by binding lipoprotein lipase (LPL). Whether Glycosyl Phosphatidyl Inositol high density lipoprotein binding protein 1 (GPIHBP1) function is impaired and may underlie the hyperTG phenotype observed in type 2 diabetes is not yet established. To elucidate the mechanism underlying impaired TG homeostasis in insulin resistance state we studied the effect of insulin on GPIHBP1 protein expression in human microvascular endothelial cells (HMVEC) under flow conditions. Next, we assessed visceral adipose tissue GPIHBP1 protein expression in type 2 diabetes Lepr db/db mouse model as well as in subjects with ranging levels of insulin resistance. We report that insulin reduces the expression of GPIHBP1 protein in HMVECs. Furthermore, GPIHBP1 protein expression in visceral adipose tissue in Lepr db/db mice is significantly reduced as is the active monomeric form of GPIHBP1 as compared to Leprdb/m mice. A similar decrease in GPIHBP1 protein was observed in subjects with increased body weight. GPIHBP1 protein expression was negatively associated with insulin and HOMA-IR. In conclusion, our data suggest that decreased GPIHBP1 availability in insulin resistant state may hamper peripheral lipolysis capacity.

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Animals
Diabetes Mellitus, Type 2
Disease Models, Animal
Endothelial Cells
Gene Expression Regulation
Humans
Hypertriglyceridemia
Insulin
Insulin Resistance
Intra-Abdominal Fat
Lipolysis
Lipoprotein Lipase
Mice

DeCS Terms

Insulina
Grasa Intraabdominal
Lipólisis
Resistencia a la Insulina
Células Endoteliales

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Keywords

Mice, Inbred NOD, Microvessels, Receptors, Lipoprotein, Triglycerides

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