PloS one, 2018-11, Vol.13 (11), p.e0205858-e0205858
2018
Details
- Autor(en) / Beteiligte
- Titel
- Decreased GPIHBP1 protein levels in visceral adipose tissue partly underlie the hypertriglyceridemic phenotype in insulin resistance
- Ist Teil von
- PloS one, 2018-11, Vol.13 (11), p.e0205858-e0205858
- Ort / Verlag
- United States: Public Library of Science
- Erscheinungsjahr
- 2018
- Link zum Volltext
- Quelle
- MEDLINE
- Beschreibungen/Notizen
- 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.
- Sprache
- Englisch
- Identifikatoren
- ISSN: 1932-6203eISSN: 1932-6203DOI: 10.1371/journal.pone.0205858Titel-ID: cdi_plos_journals_2131222595
- Format
- –
- Schlagworte
- Adipocytes, Adipose tissue, Adipose tissues, Animals, Binding sites, Biology and Life Sciences, Body weight, Cell surface, Diabetes, Diabetes mellitus, Diabetes mellitus (non-insulin dependent), Diabetes Mellitus, Type 2 - genetics, Diabetes Mellitus, Type 2 - metabolism, Diabetes Mellitus, Type 2 - pathology, Disease Models, Animal, Endothelial cells, Endothelial Cells - metabolism, Endothelium, Fatty acids, Gene expression, Gene Expression Regulation, Genetic aspects, Glycosylphosphatidylinositol, Health aspects, Heparan sulfate, Homeostasis, Humans, Hypertriglyceridemia - genetics, Hypertriglyceridemia - metabolism, Hypertriglyceridemia - pathology, Inositol, Insulin, Insulin - genetics, Insulin - metabolism, Insulin resistance, Insulin Resistance - genetics, Intra-Abdominal Fat - metabolism, Lipase, Lipids, Lipolysis, Lipolysis - genetics, Lipoprotein lipase, Lipoprotein Lipase - genetics, Lipoproteins, Medicine, Medicine and Health Sciences, Metabolic syndrome, Mice, Mice, Inbred NOD, Microvasculature, Microvessels - metabolism, Musculoskeletal system, Mutation, Phenotypes, Physical Sciences, Protein binding, Proteins, Receptors, Lipoprotein - genetics, Research and Analysis Methods, Rodents, Triglycerides - genetics, Triglycerides - metabolism, Type 2 diabetes