INSERTED OBESOGENIC DIET IN PONIES, INITIATION OF INSULIN DYSREGULATION

Abstract

Insulin is the hormone which regulates glucose homeostasis. It is responsible for the uptake of glucose from circulation to tissue. Therefore, sensitivity of tissues to insulin secretion is important to manage glucose levels in the blood. When the uptake of glucose gets disrupted, insulin dysregulation can be a cause of this default. Insulin dysregulation refers to hyperinsulinemia, insulin resistance and normo- or hyperglycemia. As an underlying cause, a diet related extensive offer of energy can dysregulate the uptake of glucose. It is known that there are relations among (morbid) obesity of dietary cause and insulin dysregulation as a main part of Equine Metabolic Syndrome, although specific relations are still unclear. In this longitudinal study eight Shetland ponies were followed for two years, feeding a 200% maintenance feed, including an in-between period of 100% maintenance diet during winter. The ponies were non-randomly divided into two groups; the experimental and control group. By performing oral glucose tolerance tests (OGTT), the glucose homeostasis was registered and later analyzed. Gaining weight of the experimental group was registered every week by measuring weight and body condition score (BCS). With statistical analyses it was determined whether the experimental group showed insulin dysregulation during gain of bodyweight. It was found that a significant increase of insulin levels was seen in the experimental group at the end of year 1 and during year 2, showing a significant difference compared to the control group. Also, the experimental group gained more than 20% of their bodyweight within 24 weeks, becoming obese in year 1. The study showed that insulin dysregulation in Shetland ponies is related to obesity induced by dietary energy overfeeding and is partial reversible during a period of dietary normalization. Furthermore, it has been found that the obese experimental group experienced earlier and increased onset of insulin dysregulation in the second year compared to the first year of the study, after a period of normalization during winter.