| Background: Motilin, a 22-amino acid brain-gut peptide, is released by the endocrine cell in the mucosa of the upper part of the small intestine during the intergestive state. Its peripheral distrinution and mechanism has been established extensively. The peripheral function of motilin mainly involved in the regulation of gastrointestinal motility and migrating motor complex (MMC)-phrase III of the gastrointestinal tract in interdigestive state. But effects of motilin in brain on the central modulation of the gastric motility and food intake is still unclear. Nowadays, the motilin and its receptors have been found in central nervous system (CNS), cerebellum, cerebral cortex, amygdala, hypothalamic nuclei, hypophysis and pineal body. Injections of motilin intravenously (i.v.) and intracerebroventricularly (i.c.v.) stimulate gastric motor activity and food intake in rats and mice. Motilin also regulate the secretion of pituitary and reduce the levels of anxiety in mice.Somatostatin (SS),a 14-amino acid, brain-gut peptide. It distributed extensively in CNS and peripheral organs. The main effects of SS included regulating the secretion of growth hormone (GH) and the function of pancreatic island and inhibiting the motility of gastrointestinal tract peripherally. However, it was showed that microinjection of SS into CNS stimulates gastric motility and food intake.It was reported that motilin (MT) and somatostatin (SS) participate in the physiologyic mechanisms of regulating gastrointestinal motility and affecting energy homeostasis. Diabetic gastroparasis mellitus (DGP) was found in the cases of diabetes as one of the complications. It was identifided that the plasma levels of these two peptides increased in diabetic mellitus. However, the contribution of MT and SS in the brain under the conditions of fasting and diabetes remains to be revealed.Objective: The aim of the present study was to investigate whether MT and SS cells in brain participate in the integration of gastrointestinal function under fasting and diabetes conditions. Material and Methods:1 Establishment of diabetic mellitus (DM) model rats:1.1 Diabetic mellitus were induced by injected 2.5% Alloxan (120mg/kg, ip) and repeated one more time after 24h.1.2 Weight, food intake, water intake, urine sugar concentration, blood sugar concentration and urine volume of the rats were recorded after drug was given.2 ImmunohistochemistryStudy were undertaken to investigate the expression and distribution of MT or SS immunoreactive (IR) neurons in different brain regions in three groups: Normal diet group, fasting group, diabetic mellitus group. Results :1 Indexes recorded from Diabetic mellitus (DM) rats:Food intake, water intake, urine volume, blood sugar concentration and urine sugar concentration of DM rats increased obviously compared with thoses taken from before DM model set. Criteria for DM model are (1) urine sugar concentration more than one" +" (2) blood sugar concentration on an empty stomach ^ 13.6mmol/L, sustained more than then days.2 Expression of MT-immunoreactive (IR) cells and SS- immunoreactive (IR) cells in different brain regions2.1 Normal diet rats (control group)MT-IR and SS-IR cells were detected in the paraventricular nucleus (PVN), superoptic nuclei (SON), ventromedial nucleus (VMH), lateral area (LHA), arcuate nucleus (Arc.n.), median emidence (ME) of hypothalamus and hippocampus (Hip).2.2 Fasting and DM groups:(1) Expressions of MT-IR cells: Compared with control group, the numbers of MT-IR cells showed a significant increase in PVN and SON of fasting and diabetes group, especially in PVN. (control 4.0+0.7; fasted: 31.4+2.1**; Diabetes: 53.4+1.6**; increased 8- fold and 12- fold separately compared with control group ). There was 1.6- fold and 0.2- fold increase of MT-IR cells in SON and Hip separately in fasting group (P<0.05). Numbers of MT-IR cells in SON are increased by 1.5 -fold in DM rats (P<0.05); There was no difference of MT-IR cells... |