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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^sup 2^). 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 < 0.0001) 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
Body weight regulation critically depends on the interplay between the central nervous system and endocrine messengers from the periphery, adipokines like leptin and adiponectin in partic- ular (1). Visfatin is a recently described peptide, previously identified as pre-B-cell colony- enhancing factor (PBEF) or nicotinamide phosphoribosyltransferase (Nampt), that is produced by adipose tissue as well as skeletal muscle, liver, and immune cells (2). The initial assumption that visfatin acts directly on the insulin receptor and displays insulin-mimetic properties has been recently cast into doubt, and still little is known about the role of this adipokine in energy homeostasis (3-5). Observations of acutely increased plasma visfatin concentrations during hyperglycemia have linked visfatin release with regulation of glucose metabolism (6). Moreover, circulating visfatin levels...