Abstract
The metabolism of triglycerides (TGs) is regulated, among others, by the lipoprotein lipase (LPL) that hydrolyses the TGs on endothelial cells. In turn, LPL is inhibited by the ANGPTLs family of proteins, such as ANGPTL3, 4, and, 8; the latter is the least known. In this work, we have tried to establish the expression and localisation of the Angiopoietin-like 8 (ANGPTL8) protein in the visceral adipose tissue (VAT) of morbid-obese and non-obese patients. 109 subjects (66 women and 43 men) undergoing laparoscopic surgery participated in this study. A blood sample and a portion of the VAT were obtained, and the patients were classified according to their Body Mass Index (BMI) as non-obese (19.5–30 kg/m2) and morbid-obese (40–50 kg/m2). No significant changes in ANGPTL8 plasma levels were determined by EIA in obese patients. The immunocytochemistry and Western blotting showed the presence of increased ANGPTL8 in morbid-obese patients (p < 0.05). In-situ hybridisation and a real time polymerase chain reaction (RT-PCR) confirmed that the mRNA that encodes ANGPTL8 was present in adipocytes, without differences in their nutritional state (p = 0.89), and even in the endothelial cells. Our data suggests that ANGPT8 plasmatic levels do not change significantly in patients with morbid obesity, although there is a modest difference related to gender. Besides, we demonstrate that in visceral adipose tissue, ANGPTL8 is well defined in the cytoplasm of adipocytes coexisting with perilipin-1 and its mRNA, also is present in endothelial cells. These findings suggest the possibility that among other functions, ANGPTL8 could perform either a paracrine and/or an endocrine role in the adipose tissue.
Highlights
The prevalence of obesity has grown in an epidemic way, and nowadays millions of people suffer from this disease
It is unknown whether Angiopoietin-like 8 (ANGPTL8) is secreted from adipose tissue, in white adipose tissue (WAT) and brown adipose tissue (BAT) it is speculated that ANGPTL8 could function in a non-endocrine manner [35]
Our data suggests that ANGPTL8 plasmatic levels do not change significantly in patients with morbid obesity, there is a modest difference related to gender that we cannot explain with the current studies
Summary
The prevalence of obesity has grown in an epidemic way, and nowadays millions of people suffer from this disease. Excess weight is associated with other pathologies, such as type 2 diabetes, cardiovascular disease, metabolic syndrome and some types of cancer [1]. It is widely recognised by both epidemiological and controlled clinical trials, that obesity is often associated with hypertriglyceridaemia with lower levels of HDL-cholesterol and, sometimes, higher LDL-cholesterol. The disruption of the COOH–terminal in the LPL, in mice, causes remarkably higher plasma triglycerides (TGs) levels at birth, and the deaths of animals occur within the first 24 h [4]. Transgenic mice that overexpress human LPL throughout the body show a 75% reduction in plasmatic TG [5]. LPL activity is carefully regulated to ensure that the rate of the uptake of fatty acids matches local energy demands
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