Immunohistochemical expression of insulin, glucagon, and somatostatin in pancreatic islets of horses with and without insulin resistance.

This research aimed to explore the expression of insulin, glucagon, and somatostatin in pancreatic islets of horses, comparing those with insulin resistance to insulin-sensitive ones. It found no difference in insulin or somatostatin expression between the groups, but noted fewer glucagon-expressing cells in insulin-resistant horses, suggesting a potential compensatory response to hyperinsulinemia.

Objective and Animals

• The research’s primary objective was to evaluate the expression of three hormones – insulin, glucagon, and somatostatin – within the pancreatic islets of horses affected by insulin resistance and compare them with insulin sensitive horses.
• The study involved 23 horses in total, with 10 being insulin-resistant and 13 being insulin-sensitive.

Procedure

• The researchers first required each horse to fast for a minimum of 10 hours before taking a blood sample to determine serum insulin concentration.
• Horses with a serum insulin concentration less than 20 μU/mL were marked as insulin-sensitive, while those with a concentration above 20 μU/mL were subjected to a frequently sampled IV glucose tolerance test.
• The glucose tolerance test was used to ascertain insulin sensitivity via minimal model analysis, with horses demonstrating a sensitivity to insulin less than 1.0 × 10 L•min•mU categorized as insulin-resistant.
• All horses were then euthanized, and pancreatic specimens were collected for study. The collected specimens were immunohistochemically stained to help determine the expression levels of insulin, glucagon, and somatostatin in the pancreatic islets.

Results

• The cells expressing insulin, glucagon, and somatostatin formed roughly 62%, 12%, and 7%, respectively, of pancreatic islet cells in insulin-resistant horses.
• In contrast, insulin-sensitive horses had about 64%, 18%, and 9% of the corresponding pancreatic islet cells.
• There was no statistical difference in insulin and somatostatin expression between insulin-resistant and insulin-sensitive horses.
• However, the median percentage of glucagon-expressing cells was significantly lower in insulin-resistant horses than in insulin-sensitive horses.

Conclusions and Clinical Relevance

• The study’s results indicate that insulin secretion wasn’t elevated in insulin-resistant horses, contradicting expectations.
• Interestingly, glucagon production appeared to be downregulated in insulin-resistant horses, potentially serving as a compensatory response to hyperinsulinemia.
• This finding may suggest novel insights into the response mechanisms of insulin-resistant horses and open new avenues for therapeutic interventions for insulin resistance in horses and potentially other animals.