Role of vaspin in human eating behaviour

PLoS One. 2013;8(1):e54140. doi: 10.1371/journal.pone.0054140. Epub 2013 Jan 14.

Abstract

Objective: The adipokine vaspin (visceral adipose tissue derived serine protease inhibitor, serpinA12) follows a meal-related diurnal variation in humans and intracerebroventricular vaspin administration leads to acutely reduced food intake in db/db mice. We therefore hypothesized that vaspin may play a role in human eating behaviour.

Materials and methods: We measured serum vaspin concentrations in 548 subjects from a self-contained population of Sorbs (Germany) who underwent detailed metabolic testing including eating behaviour assessments using the three-factor eating questionnaire. In addition, genetic variation within vaspin was assessed by genotyping 28 single nucleotide polymorphisms (SNPs) in all study subjects.

Results: Serum vaspin concentrations correlated positively with restraint, disinhibition and hunger (all P<0.05), although the correlations did not withstand further adjustments for age, gender and BMI (all P>0.05). Independent of observed correlations, genetic variants in vaspin were associated with serum vaspin levels but showed no significant association with any of the eating behaviour phenotypes after accounting for multiple testing (P≥0.05 after adjusting for age, gender and BMI).

Conclusion: Our data suggest that serum vaspin concentrations might modulate human eating behaviour, which does not seem to be affected by common genetic variation in vaspin.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Feeding Behavior / physiology*
  • Female
  • Genotype
  • Humans
  • Male
  • Middle Aged
  • Polymorphism, Single Nucleotide / genetics
  • Serpins / blood*
  • Serpins / genetics

Substances

  • SERPINA12 protein, human
  • Serpins

Grants and funding

This work was supported by grants from the Federal Ministry of Education and Research (BMBF), Boehringer Ingelheim Foundation (to P.K. and D.S.), Integrated Research and Treatment Center IFB Adiposity Diseases, K7-38, K7-39 (to Y.B.) and K7-37 and K403 (to A.T.), Deutsche Forschungsgemeinschaft (DFG), the Clinical Research Group “Atherobesity” KFO 152 (projects BL 833/1-1 to M.B., and Stu192/6-1 (MS), KO 3512/1-1 to A.K., KO 3880/1-2 to P.K., M.B. and J.B.), from the German Diabetes Association (to D.S. and P.K.), from the DDS Foundation to Y.B., DHFD (Diabetes Hilfs- und Forschungsfonds Deutschland; to M.S., P.K., M.B., A.T.), and LIFE – Leipzig Research Center for Civilization Diseases, Universität Leipzig. LIFE is funded by means of the European Union, by the European Regional Development Fund (ERDF) and by means of the Free State of Saxony within the framework of the excellence initiative. IFB Adiposity Diseases is supported by the Federal Ministry of Education and Research (BMBF), Germany, FKZ: 01EO1001. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.