Scientific publications

Altered Concentrations in Dyslipidemia Evidence a Role for ANGPTL8/Betatrophin in Lipid Metabolism in Humans

Jul 29, 2016 | Magazine: The Journal of Clinical Endocrinology and Metabolism

Gómez-Ambrosi J (1), Pascual-Corrales E (1), Catalán V (1), Rodríguez A (1), Ramírez B (1), Romero S (1), Vila N (1), Ibáñez P (1), Margall MA (1), Silva C (1), Gil MJ (1), Salvador J (1), Frühbeck G (1).


CONTEXT:
ANGPTL8/betatrophin is a secreted protein initially involved in β-cell replication. Recent data in humans and mice models suggest that ANGPTL8/betatrophin is more related to lipid metabolism.

OBJECTIVE:
The aim of the present study was to compare the circulating concentrations of ANGPTL8/betatrophin in individuals with dyslipidemia defined as having high or low levels of HDL-cholesterol or triglycerides, respectively.

DESIGN, SETTING, AND PARTICIPANTS:
Serum concentrations of ANGPTL8/betatrophin were measured by ELISA in 177 subjects. We studied two different selected case-control dyslipidemic cohorts including individuals with high (n=43) or low (n=46) circulating concentrations of HDL-cholesterol or with low (n=48) or high (n=40) levels of triglycerides.

RESULTS:
Circulating concentrations of ANGPTL8/betatrophin were significantly lower in individuals with dyslipidemia P<0.001 in both males (C 27.8 ± 15.2 vs DL 17.0 ± 11.2 ng/mL) and females (C 50.0 ± 22.2 vs DL 27.0 ± 16.5 ng/mL). The magnitude of the differences was higher in dyslipidemic patients with low HDL-cholesterol than in those with high TG concentrations. ANGPTL8/betatrophin levels were lower in subjects with T2D (P<0.001) but the impact of T2D vanished (P=0.257) when the effect of dyslipidemia was included in the analysis.

CONCLUSIONS:
We conclude that serum ANGPTL8/betatrophin concentrations are altered in human dyslipidemia. ANGPTL8/betatrophin emerges as a potential player in dyslipidemia with a strong association with HDL-C and a potential therapeutic tool for the treatment of dyslipidemia.

CITATION  J Clin Endocrinol Metab. 2016 Jul 29:jc20162084