Relationship between cerebrospinal fluid visfatin (PBEF/Nampt) levels and adiposity in humans
Hallschmid M., Randeva H., Tan BK., Kern W., Lehnert H.
Laboratory Study with a reported sample of 38 on Type 2 Diabetes, published in Diabetes (2009) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
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- Study type
- Laboratory Study
- Journal
- Diabetes (2009)
- Reported sample size
- 38
- Source database
- Europe PMC
- PMID
- 19095760
- PMCID
- PMC2646062
- DOI
- 10.2337/db08-1176
- Citations
- 49
Abstract (original English)
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/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 of CSF and plasma visfatin levels with relevant parameters. Results Plasma visfatin levels increased with rising BMI (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.
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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