Investigation of neuromedin u response to increased blood glucose in rats with experimental metabolic syndrome

Hormones that have negative effects on insulin secretion and carbohydrate metabolism and are thought to be secreted from the proximal intestines are generally called decretin. Although no decretin hormone has been identified to date, Neuromedin U (NMU) has been suggested as a possible candidate. In our study, we planned to investigate the systemic circulation NMU levels in the metabolic syndrome/hypothalamic obesity model that we will create with monosodium glutamate (MSG) and how these levels change in response to the Oral Glucose Tolerance Test (OGTT). In the MetS/HO model, we also intended to investigate the potential alteration of NMU expression in the proximal and distal gastrointestinal tract. For this purpose, newborn rats were subcutaneously injected with MSG (4 mg/g/body weight) every other day for ten days, and another group of newborn rats was given the same treatment with 0.9% isotonic injection for the Control (C) and metabolic syndrome/hypothalamic obesity (MetS/HO) groups. Following this procedure, the animals were fed at will for 5 months while the MetS/HO model was being developed. During this time, the body weight change was monitored. Blood lipid profiles, Lee's index, glucose, insulin, and NMU responses to basal and OGTT were assessed at the end of this period. The basal glucose and insulin readings were used to provide the HOMA-R score. After sacrification, abdominal obesity was examined by removing perigonadal and retroperitoneal fats, and intestinal NMU expression was evaluated by removing the duodenum jejunum and distal intestine. Our results showed a non-significant increase in the Lee index, which is an indicator of obesity, and a statistically significant increase in abdominal obesity. Diabetes mellitus, defined by hyperglycemia and hypoinsulinemia, was identified in MetS/HO group rats. Blood sugar levels increased even more in response to the OGTT, and it was found that this group was unable to produce the necessary insulin response. Basal plasma NMU levels were not different from the control group, but the lipid profiles of the MetS/HO group were abnormal. Although there was no difference in the groups' NMU responses to OGGT at baseline or at 30 minutes, it was found that the K group provided a substantially lower NMU response after 60 minutes compared to the MetS/HO group. NMU expression in the gastrointestinal tract was similarly decreased from proximal to distal in both groups. In terms of plasma levels of NMU and the distribution of NMU expression throughout the Gastrointestinal tract, we did not observe any significant differences between the MetS/HO and C groups. We believe our findings support the literature indicating that the NMU does not function like decretin.