Relationship of Cerebrospinal Fluid Visfatin (PBEF/Nampt) Levels to Adiposity in Humans
- Manfred Hallschmid, PhD (hallschmid{at}kfg.uni-luebeck.de)1,
- Harpal Randeva, MD, PhD2,
- Bee K Tan, PhD2,
- Werner Kern, MD3 and
- Hendrik Lehnert, MD2,3
- From the Departments of 1Neuroendocrinology and
- 3Internal Medicine I, University of Luebeck, Luebeck, Germany, and
- 2Warwick Medical School, University of Warwick, Coventry, UK
Abstract
Objective: Observations of elevated circulating concentrations of visfatin in obesity and diabetes suggest that this recently described adipokine is involved in the regulation of body weight and metabolism. We examined in humans whether visfatin is found in cerebrospinal fluid (CSF) and, if so, how CSF visfatin concentrations relate to adiposity and metabolic parameters.
Research Design and Methods: We measured visfatin concentrations in plasma and CSF of 38 subjects (18 men, 20 women; age: 19-80 yrs) with a wide range of body weight (body mass index, BMI: 16.24-38.10 kg/m2). In addition, anthropometric parameters and endocrine markers were assessed. Bivariate correlation coefficients were determined and stepwise multiple regression analyses were performed to detect associations between CSF and plasma visfatin levels and relevant parameters.
Results: Plasma visfatin levels increased with rising BMI (P <0.0001) and body fat mass (P <0.0001). In contrast, CSF visfatin levels decreased with increasing plasma visfatin concentrations (P <0.03), BMI (P <0.001), body fat mass (P <0.0001) and insulin resistance (P <0.05). Body fat was the only factor independently associated with CSF visfatin, explaining 58% of the variation of CSF visfatin levels (P <0.0001). Neither plasma (P >0.13) nor CSF (P >0.61) visfatin concentrations differed between men and women.
Conclusions: Our data indicate that visfatin concentrations in human CSF decrease with rising body fat, supporting the assumption that visfatin transport across the blood-brain barrier is impaired in obesity and that central nervous visfatin insufficiency or resistance are linked to pathogenetic mechanisms of obesity.
Footnotes
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- Received August 27, 2008.
- Accepted December 12, 2008.
- Copyright © American Diabetes Association














