Objective: The objective of this research was to study the histological structures of proventriculus by light and scanning electron microscope and to investigate the localization of glucagon immunoreactive cells within the turkey proventriculus.Materials and methods: Ten adult healthy turkeys were used in this study. The specimens were fixed in 10% buffered neutral formalin. The tissue samples were studied through routine histological and immunohistochemical techniques. Other samples were used for scanning microscope. Results: This study confirmed that the turkey proventriculus was formed from four tunics; tunica mucosa, tunica submucosa, tunica muscularis and tunica serosa. The lamina epithelialis was simple columnar and gave positive reaction in Periodic Acid Schiff (PAS) stain. The lamina propria contained simple tubular glands lined with columnar cells with lymphocyte infiltration. The submucosa contained proventricular glands formed with many round lobules. Each lobule was consisted of secretory tubules radiating from the central lumen of the lobule. The lining epithelium of the central lumen was columnar epithelium. The epithelium of the secretory tubules was cuboidal. Scanning electron microscopic observations showed the mucous membrane was consisted of many macroscopic papillae that formed from many folds which separated by furrows. Immunohistochemical observations revealed that glucagon immunoreactive cells were mainly determined inside the proventricular glands than within the surface epithelium mainly in the basal portion of the lobules and in the epithelium of central lumen of gland lobules. Conclusion: The structure of proventriculus structure in turkey has some variations as compared to other species of birds, and this may be attributed to the diet and its nutritious behavior. [J Adv Vet Anim Res 2018; 5(3.000): 290-298]

The regional distributions and relative frequencies of the gastrointestinal endocrine cells inthe gean goose (Anser fabalisLatham) were investigated by immunohistochemical methods using bovineSp-1/chromogranin (CG), serotonin, gastrin, cholecystokinin (CCK)-8, somatostatin and glucagon antisera. BCG-immunoreactive cells were widespread throughout the gastrointestinal tract (GIT) with moderated frequencies except for the gizzard and proventriculus which were a few frequencies. Serotonin-immunoreactive cells were detected throughout the GIT except for the proventriculus and gizzard. These cells wer observed inthe pylorus with rare frequencies but numerous cells wee cetected in the intestinal tract. Gastrin-immunoreactive cells were restricted to the gizzard, pylorus and duodenum. These cells were most predominant in the pylorus and a few or rare in the gizzard and duodenum, respectively. CCK-8-immunoreactive cells were observed from the gizzard to ileum. the highest frequencies of endocrine cells were observed in the duodenum. These cells were increased from the gizzard to duodenum but thereafter decreased. Somatostatin-immunoreactive cells were detected in the GIT except for the large intestine. In the proventriculus and pylorus, numerous immunoreactive cells were demonstrated but a few cells were present in the other regions. Glucagon cells were observed in the gizzard, pylorus, ileum, colon and rectum with a few or moderated numbers.

Effects of Ostertagia ostertagi infection on secretion of insulin, pancreatic glucagon, cortisol, gastrin, and pepsinogen were studied in calves inoculated with 100,000 (group 1) or 10,000 (group 2) O. ostertagi infective larvae weekly for 14 weeks. Plasma insulin concentrations in both inoculated groups were lower than those in a noninfected (group 3) control group. The differences between group 1 and group 3 were significant (P < 0.05) at 2 and 12 weeks after initial inoculation. Plasma pancreatic glucagon and cortisol concentrations of groups 1 and 2 did not differ significantly from those of the control group, although plasma pancreatic glucagon concentration was consistently lower in group-1 calves from 4 weeks to the end of the study. Plasma pepsinogen and serum gastrin concentrations also increased significantly (P < 0.05) in both groups that received inoculations. We concluded that decreased plasma insulin concentrations are contributory to changes in postabsorptive protein metabolism, and that serum gastrin concentrations are more representative of the pathologic changes in the abomasum than are plasma pepsinogen concentrations.

Glucose tolerance and insulin response were evaluated in 9 normal-weight and 6 obese cats after IV administration of 0.5 g of glucose/kg of body weight. Blood samples for glucose and insulin determinations were collected immediately prior to and 2.5, 5, 7.5, 10, 15, 30, 45, 60, 90, and 120 minutes after glucose infusion. Baseline glucose concentrations were not significantly different between normal-weight and obese cats; however, mean +/- SEM glucose tolerance was significantly impaired in obese vs normal-weight cats after glucose infusion (half time for glucose disappearance in serum--77 +/- 7 vs 51 +/- 4 minutes, P < 0.01; glucose disappearance coefficient--0.95 +/- 0.10 vs 1.44 +/- 0.10%/min, P < 0.01; insulinogenic index--0.20 +/- 0.02 vs 0.12 +/- 0.01, P < 0.005, respectively). Baseline serum insulin concentrations were not significantly different between obese and normal-weight cats. Insulin peak response after glucose infusion was significantly (P < 0.005) greater in obese than in normal-weight cats. Insulin secretion during the first 60 minutes (P < 0.02), second 60 minutes (P < 0.001), and total 120 minutes (P < 0.0003) after glucose infusion was also significantly greater in obese than in normal-weight cats. Most insulin was secreted during the first hour after glucose infusion in normal-weight cats and during the second hour in obese cats. The impaired glucose tolerance and altered insulin response to glucose infusion in the obese cats was believed to be attributable to deleterious effects of obesity on insulin action and cell responsiveness to stimuli (ie, glucose).

OBJECTIVE To assess insulin, glucagon, and somatostatin expression within pancreatic islets of horses with and without insulin resistance. ANIMALS 10 insulin-resistant horses and 13 insulin-sensitive horses. PROCEDURES For each horse, food was withheld for at least 10 hours before a blood sample was collected for determination of serum insulin concentration. Horses with a serum insulin concentration < 20 μU/mL were assigned to the insulin-sensitive group, whereas horses with a serum insulin concentration > 20 μU/mL underwent a frequently sampled IV glucose tolerance test to determine sensitivity to insulin by minimal model analysis. Horses with a sensitivity to insulin < 1.0 × 10(−4) L•min−1•mU−1 were assigned to the insulin-resistant group. All horses were euthanized with a barbiturate overdose, and pancreatic specimens were harvested and immunohistochemically stained for determination of insulin, glucagon, and somatostatin expression in pancreatic islets. Islet hormone expression was compared between insulin-resistant and insulin-sensitive horses. RESULTS Cells expressing insulin, glucagon, and somatostatin made up approximately 62%, 12%, and 7%, respectively, of pancreatic islet cells in insulin-resistant horses and 64%, 18%, and 9%, respectively, of pancreatic islet cells in insulin-sensitive horses. Expression of insulin and somatostatin did not differ between insulin-resistant and insulin-sensitive horses, but the median percentage of glucagon-expressing cells in the islets of insulin-resistant horses was significantly less than that in insulin-sensitive horses. CONCLUSIONS AND CLINICAL RELEVANCE Results suggested that, in insulin-resistant horses, insulin secretion was not increased but glucagon production might be downregulated as a compensatory response to hyperinsulinemia.

Objective-To evaluate whether immunosuppressive doses of cyclosporine (CsA) have an adverse effect on the liver, kidney, and pancreatic beta cells of pigs. Animals-8 juvenile 8-week-old Landrace X Large White crossbred pigs. Procedure-CsA (100 to 140 mg/kg) was administered orally to euglycemic pigs to reach whole blood trough concentrations of approximately 1500 ng/mL. To determine pancreatic beta cell function, plasma Cpeptide and insulin concentrations were measured in response to IV administration of glucose, glucagon, arginine, and oral administration of glucose. Effects on liver and kidney were determined by monitoring serum measurements of liver function and serum creatinine concentrations, respectively. Results-Plasma concentrations of C-peptide were significantly lower in euglycemic CsA-treated pigs, compared with control pigs, following IV administration of glucose, glucagon, arginine, and oral administration of glucose. Furthermore, the glucose clearance rate was decreased in euglycemic CsA-treated pigs, compared with control pigs. Serum creatinine concentrations and 4 of 7 serum measurements of liver function were not adversely affected by CsA administration. Serum concentrations of bilirubin and albumin were significantly increased, and serum alanine aminotransferase activity was significantly decreased in CsA-treated pigs, compared with control pigs. Histologic evaluation of liver and kidney sections revealed no pathologic findings in CsA-treated or control pigs. Conclusions and Clinical Relevance-In our study, immunosuppressive doses of CsA caused an impairment of porcine pancreatic beta cell function, but did not have toxic effects on the kidney. However, on the basis of changes in serum bilirubin and albumin concentrations and alanine aminotransferase activity, subclinical toxic effects on the liver did occur when immunosuppressive doses of CsA were administered.

After IV administration of 0.5 mg of glucagon/cat, glucose tolerance and insulin secretory response were evaluated in 10 lean cats, 10 obese cats, and 30 cats with diabetes mellitus. Blood samples for glucose and insulin determinations were collected immediately before and at 5, 10, 15, 30, 45, and 60 minutes after IV administration of glucagon. Baseline serum insulin concentration and insulin secretory response were used to classify diabetes mellitus in the 30 cats as type I or type II. Mean (+/- SEM) baseline and 30-minute serum glucose concentrations in obese cats were significantly (P < 0.05) decreased, compared with values in lean cats, but were similar at all other blood sample collection times. Serum glucose concentration in diabetic cats was significantly (P < 0.05) greater than values in obese and lean cats at all blood sample collection times. Two statistically different insulin responses to IV administration of glucagon were seen in diabetic cats. Of the 30 diabetic cats, 23 had minimal insulin secretory response after glucagon administration (ie, serum insulin concentration was at or below sensitivity of the insulin assay). Seven diabetic cats had baseline serum insulin concentration similar to that of obese cats and significantly (P < 0.05) greater than that of lean cats and of the other 23 diabetic cats. In these 7 diabetic cats, serum insulin concentration increased after glucagon administration. Total insulin secretion was not significantly different between these 7 diabetic cats and the lean and obese cats, and was significantly (P < 0.05) greater than total insulin secretion in the other 23 diabetic cats. Results support existence of type-I and type-II diabetes mellitus in cats.

Modification of gastroduodenal motility has been proposed to aid endoscopic examination of the duodenum in dogs. The objective of this study was to evaluate the use of the following pharmacologic agents for facilitation of endoscopic intubation of the duodenum in 6 clinically normal dogs: metoclopramide HCl (0.2 mg/kg of body weight), atropine sulfate (0.045 mg/kg), glucagon (0.06 mg/kg), and isotonic saline solution. In a randomized, blinded, crossover design, the ease of endoscopic duodenal intubation was qualitatively scored by 3 endoscopists (in random order), using the following scale: immediate entry; rapid entry-moderate manipulation; difficult entry-multiple attempts; and no entry after 2 minutes. Anesthesia was induced with thiopental and maintained with halothane. The 4 agents were diluted to a fixed volume and randomly administered. Duodenal intubation was attempted 2 minutes after IV injection of 1 of the agents. Four endoscopic procedures (1 for each agent) were performed on each dog with a minimum of 5 days between each procedure. In this study, no agent facilitated endoscopic duodenal intubation at the dose used. Instead, atropine and metoclopramide made duodenal intubation significantly more difficult, compared with use of saline solution. Difference between intubation after administration of glucagon and saline solution was not seen. On the basis of our findings, the use of these agents for facilitating endoscopic duodenal intubation is not recommended. In addition, in this study, we found that experience in endoscopic intubation is an important factor in determining the ease of duodenal intubation.