Current understanding of insulin dysregulation and its relationship with carbohydrate and protein metabolism in horses

Abstract

Insulin dysregulation (ID) is a common metabolic disorder in horses, characterized by hyperinsulinemia and/or peripheral insulin resistance. The critical role of hyperinsulinemia in endocrinopathic laminitis has driven research into the insulinotropic effects of dietary nutrients and the reciprocal impact of ID on nutrient metabolism. The relationship between ID and carbohydrate metabolism has been extensively studied; however, the effects of ID on protein metabolism in horses remain largely unexplored. This review begins with an overview of the importance of insulin in the regulation of muscle protein synthesis and degradation and then examines the current understanding of the interplay between ID and protein and carbohydrate metabolism in horses. Horses with ID exhibit altered resting plasma amino acid concentrations and shifts in postprandial amino acid dynamics. Recent work illustrated that ID horses had higher levels of plasma amino acids following a protein meal and delayed postprandial clearance from the blood compared to non-ID horses. The postprandial muscle synthetic response does not seem to be diminished in ID horses, but alterations in key cellular signaling molecules have been reported. ID horses display a pronounced hyperinsulinemic response following the consumption of feeds providing a range of protein, non-structural carbohydrate, starch and water-soluble carbohydrate intakes. Recent studies have shown that ID horses have an increased postprandial incretin response, contributing to the observed hyperinsulinemia. To minimize the postprandial insulin response, thresholds for carbohydrate consumption have recently been proposed. Similar thresholds should be established for protein to aid in the refinement of nutritional strategies to manage ID horses.

Keywords: Hyperinsulinemia; Insulin dysregulation; Muscle protein synthesis; Non-structural carbohydrates; Postprandial response; incretins.