Abstract
Anorexigenic protein, nesfatin/nucleobindin-2 (NUCB2) is ubiquitously expressed in peripheral tissues including white adipose tissue. Nesfatin/NUCB2 is selectively expressed in pancreatic β-cell, but not α-cells, δ-cells, PPcells. Starvation significantly increased circulating nesfatin-1 concentrations, and refeeding restores the increase by starvation. There is an obvious dissociation in changes between nesfatin-1 releases from pancreatic β-cells and circulating nesfatin-1, and an increase of nesfatin-1 from pancreatic islets may not be reflected to circulating concentrations of nesfatin-1.Nesfatin-1 may be a novel insulinotropic peptide, since endogenous pancreatic islet NUCB2/nesfatin is altered in diabetes and diet-induced obesity. Nesfatin-1 may also contribute to the improvement of insulin sensitivity in hyperglycemic state. An increase of circulating nesfatin-1may shift glucose uptake to peripheral organs from skeletal muscles to adipocytes. Nesfatin-1 may involve the feedback system from adipocytes to the hypothalamus via general circulation, and from the hypothalamus to adipocytes via sympathetic nervous system. The details of those molecular mechanisms should be clarified by future studies including the analysis of gene targeted animals.
Keywords: Diabetes mellitus, insulin, nesfatin, nucleobindin-2.
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