Diabetes is characterized by hyperphagia, and polydypsia. However, the mechanisms by which diabetes produces these effects are not clear. This study was conducted to examine changes in serum insulin and leptin levels in induced-type 1 diabetes mellitus in relation to concomitant changes in body weight, glycemic state and lipid profiles in rats. Moreover, we aimed to clarify that the treatment with lipoic acid (LA) is capable of reversing these effects or not. Ninety-six male rats were divided into 3 groups, control group (32 rats) was considered as normal non-diabetic, 64 rats were subcutaneously injected with alloxan (120 mg/kg.b.wt) for induction of diabetes. Then the diabetic rats were divided into two equal subgroups, the first is diabetic group that was not treated with LA, and the other is LA-treated diabetic group that was treated with LA at a dose 100 mg/kg b.wt / day for four weeks. Body weight, serum lipid profile, glucose, insulin, homeostasis model assessment– insulin resistance (HOMA-IR) and leptin were measured. The data showed significant increase in serum triacylglycerol, total cholesterol and glucose levels as well as HOMA-IR while significant decrease in the mean body weight gain, serum insulin and leptin levels in diabetic group in comparison with control group. The treatment with lipoic acid led to significant decrease in serum fasting and postprandial glucose, triacylglycerol and total cholesterol levels as well as slight decreased HOMA-IR with significant increased levels of serum insulin and leptin in comparison with diabetic group. It could be concluded that alloxan-induced diabetes led to hyperglycaemia, insulin resistance, hyperlipideamia and hypoleptinamia. Moreover, treatment with lipoic acid ameliorates these changes and improves insulin sensitivity.

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 identify signs of tissue-specific cortisol activity in samples of suspensory ligament (SL) and neck skin tissue from horses with and without pituitary pars intermedia dysfunction (PPID). SAMPLE Suspensory ligament and neck skin tissue samples obtained from 26 euthanized horses with and without PPID. PROCEDURES Tissue samples were collected from 12 horses with and 14 horses without PPID (controls). Two control horses had received treatment with dexamethasone; data from those horses were not used in statistical analyses. The other 12 control horses were classified as old horses (≥ 14 years old) and young horses (≤ 9 years old). Standard histologic staining, staining for proteoglycan accumulation, and immunostaining of SL and neck skin tissue sections for glucocorticoid receptors, insulin, 11β hydroxysteroid dehydrogenase type 1, and 11β hydroxysteroid dehydrogenase type 2 were performed. Findings for horses with PPID were compared with findings for young and old horses without PPID. RESULTS Compared with findings for old and young control horses, there were significantly more cells stained for glucocorticoid receptors in SL samples and for 11 β hydroxysteroid dehydrogenase type 1 in SL and skin tissue samples from horses with PPID. Insulin could not be detected in any of the SL or skin tissue samples. Horses with PPID had evidence of SL degeneration with significantly increased proteoglycan accumulation. Neck skin tissue was found to be significantly thinner in PPID-affected horses than in young control horses. CONCLUSIONS AND CLINICAL RELEVANCE Results suggested that tissue-specific dysregulation of cortisol metabolism may contribute to the SL degeneration associated with PPID in horses.