The present study investigated the effects of nesfatin-1 on gastric distension (GD)-responsive neurons via an interaction with corticotropin-releasing factor (CRF) receptor signaling in the ventromedial hypothalamic nucleus (VMH), and the potential regulation of these effects by hippocampal projections to VMH. Extracellular single-unit discharges were recorded in VHM following administration of nesfatin-1. The projection of nerve fibers and expression of nesfatin-1 were assessed by retrograde tracing and fluoro-immunohistochemical staining, respectively. Results showed that there were GD-responsive neurons in VMH; Nesfatin-1 administration and electrical stimulation of hippocampal CA1 sub-region altered the firing rate of these neurons. These changes could be partially blocked by pretreatment with the non-selective CRF antagonist astressin-B or an antibody to NUCB2/nesfatin-1. Electrolytic lesion of CA1 hippocampus reduced the effects of nesfatin-1 on VMH GD-responsive neuronal activity. These studies suggest that nesfatin-1 plays an important role in GD-responsive neuronal activity through interactions with CRF signaling pathways in VMH. The hippocampus may participate in the modulation of nesfatin-1-mediated effects in VMH., H. Feng, Q. Wang, F. Guo, X. Han, M. Pang, X. Sun, Y. Gong, L. Xu., and Obsahuje bibliografii
The aimof this study was to compare the levels of nesfatin-1 in healthy subjects with those in prediabetic and diabetic patients who have different glucose tolerance levels. Overall, 100 subjects were divided into
5 groups healthy control (C), impaired fasting glycemia (IFG), impaired glucose tolerance (IGT), metabolic syndrome (MS) an type 2 diabetes mellitus, (Type2 DM).Glycated hemoglobin (HbA1c) assessed the glycemic
control. Homeostasis modelassessment of insulin resistance (HOMA
-IR) was determined using computer analyses. Nesfatin-1 levels were
measured using ELISA method. IFG and IGT (prediabetic groups)from MS and Type 2 DM (diabetic groups) differed significantly in HOMA-IR. The nesfatin-1 levels were lower, although not statistically significant, in IFG
(0.937±0.03 ng/ml, p=0.07) andIGT (1.039±0.06 ng/ml, p=0.5) groups compared to healthysubjects (1.094±0.07 ng/ml). However, the nesfatin-1 levelswere lower in patients with Type 2 DM (0.867±0.02 ng/ml, p=0.007) and MS (0.885±0.01ng/ml, p=0.01) compared to healthy subjects. Nesfatin-1 levels were significantly lower in diabetic patients compared to healthy
subjects. This studysupports the role of insulin resistance in decreased nesfatin-1 levels in patients with Type 2 DM and MS.