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Relationship between cerebrospinal fluid visfatin (PBEF/Nampt) levels and adiposity in humans
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Hallschmid, Manfred, Randeva, Harpal S., Tan, Bee K., Kern, Werner and Lehnert, Hendrik (2009) Relationship between cerebrospinal fluid visfatin (PBEF/Nampt) levels and adiposity in humans. Diabetes, Vol.58 (No.3). pp. 637-640. doi:10.2337/db08-1176 ISSN 0012-1797.
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Official URL: http://dx.doi.org/10.2337/db08-1176
Abstract
OBJECTIVE-Observations of elevated circulating concentrations of visfatin (PBEF/Nampt) 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 the plasma and CSF of 38 subjects (18 men and 20 women; age 19-80 years) with a wide range of body weight (BMI 16.24-38.10 kg/m(2)). In addition, anthropometric parameters and endocrine markets were assessed. Bivariate correlation coefficients were determined and stepwise multiple regression analyses were performed to detect associations of CSF and plasma visfatin levels with 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. Diabetes 58:637-640, 2009
| Item Type: | Journal Article | ||||
|---|---|---|---|---|---|
| Subjects: | R Medicine > RC Internal medicine | ||||
| Divisions: | Faculty of Science, Engineering and Medicine > Medicine > Warwick Medical School > Biomedical Sciences > Translational & Experimental Medicine > Metabolic and Vascular Health (- until July 2016) Faculty of Science, Engineering and Medicine > Medicine > Warwick Medical School |
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| Journal or Publication Title: | Diabetes | ||||
| Publisher: | American Diabetes Association | ||||
| ISSN: | 0012-1797 | ||||
| Official Date: | March 2009 | ||||
| Dates: |
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| Volume: | Vol.58 | ||||
| Number: | No.3 | ||||
| Number of Pages: | 4 | ||||
| Page Range: | pp. 637-640 | ||||
| DOI: | 10.2337/db08-1176 | ||||
| Status: | Peer Reviewed | ||||
| Publication Status: | Published | ||||
| Access rights to Published version: | Restricted or Subscription Access | ||||
| Funder: | Deutsche Forschungsgemeinschaft | ||||
| Grant number: | SFB-654/B3 |
Data sourced from Thomson Reuters' Web of Knowledge
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