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Weight loss partially restores glucose-driven betatrophin response in humans

Item Type:Article
Title:Weight loss partially restores glucose-driven betatrophin response in humans
Creators Name:Maurer, L. and Brachs, S. and Decker, A.M. and Brachs, M. and Leupelt, V. and Jumpertz von Schwartzenberg, R. and Ernert, A. and Bobbert, T. and Krude, H. and Spranger, J. and Mai, K.
Abstract:Context: Recently a potential role of betatrophin was shown in the postprandial switch from lipid to glucose metabolism. Objective: To analyse whether obesity is associated with altered postprandial betatrophin response and whether this could be restored by weight loss. Design, Setting, Participants, Intervention: Oral glucose load was performed in 12 lean individuals at baseline as well as in 20 obese subjects before and after a 12-week structured weight loss program at an endocrinology research center. Euglycemic hyperinsulinemic clamps were performed in the obese cohort. Effect of insulin and different glucose concentrations on betatrophin expression were analysed in 3T3-L1 adipocytes. Main Outcome Measure: Circulating betatrophin levels during glucose challenge. Results: Betatrophin level decreases after an oral glucose intake (p<0.001). This correlates with the increase of glucose levels (r=-0.396; p<0.05). Hyperinsulinemia results in an increase of betatrophin. In vitro experiments in 3T3-L1 adipocytes confirmed that insulin and low glucose concentration increases betatrophin expression, whereas further elevation of glucose levels blunts this effect. Obese subjects are characterized by lower fasting betatrophin (600.6±364.4 vs. 759.5±197.9 pg/ml; p<0.05) and a more pronounced betatrophin suppression during the glucose challenge. The impaired betatrophin response in obese subjects is restored after weight loss and comparable to lean individuals. Conclusions: Obesity is associated with increased betatrophin suppression after an oral glucose load, which is driven by increased hyperglycemia. Given the metabolic properties of betatrophin, this may indicate that betatrophin is tightly linked to obesity-associated metabolic disturbances. In line with such an assumption weight loss almost completely eliminated this phenomenon. Obesity is associated with altered postprandial betatrophin response, which seems to be driven by increased hyperglycemia. Weight loss almost completely eliminates this phenomenon.
Keywords:3T3-L1 Cells, Adiposity, Blood Glucose, Body Mass Index, Cohort Studies, Glucose Clamp Technique, Hyperglycemia, Hyperinsulinism, Hypoglycemia, Insulin, Obesity, Overweight, Peptide Hormones, Postprandial Period, Weight Loss, Weight Reduction Programs, White Adipocytes, Animals, Mice
Source:Journal of Clinical Endocrinology and Metabolism
ISSN:0021-972X
Publisher:Endocrine Society (U.S.A.)
Volume:101
Number:11
Page Range:4014-4020
Date:November 2016
Official Publication:https://doi.org/10.1210/jc.2016-1788
PubMed:View item in PubMed

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