Obesity is a growing health concern for equids because of its increasing prevalence and association with altered metabolic function and disease.1,2,a Obesity has been associated with insulin resistance in horses and ponies,1,3,4 and insulin resistance in the presence of obesity has been associated with altered reproductive activity in mares and an increased risk of and predisposition for pasture-associated laminitis.5,6,b A socalled equine metabolic syndrome has been described as a grouping of metabolic abnormalities in equids that may include insulin resistance, obesity, dyslipidemia, and chronic laminitis.7 Additionally, increased risk for pasture-associated laminitis in ponies has been associated with generalized obesity, regional accumulation of neck crest adipose tissue, hyperinsulinemia, and hyperleptinemia.8 Although these factors are often observed simultaneously, it is unknown whether obesity is the primary cause of or contributes to metabolic abnormalities or whether these abnormalities are inherent characteristics of the animals.
In previous studies1,3,6 comparing groups of lean and obese horses, the obese horses had lower insulin sensitivity and high circulating concentrations of insulin, glucose, leptin, and NEFAs. Additionally, across a range of body conditions, percentage body fat and BCS are associated with insulin sensitivity and circulating concentrations of insulin and leptin.4,9,10 Previous studies in horses used cross-sectional analysis with regard to comparing metabolic variables of horses at different amounts of adiposity. However, induction of obesity in a longitudinal study would permit intraindividual comparison of variables before and after weight gain. Such a study design would limit the influence of inter-individual variation, to determine metabolic alterations with small changes in body condition (< 2 unit mean BCS change) and differentiate between metabolic abnormalities inherent to an individual horse from those induced by an increase in adiposity. Additionally, evaluating horses during a mean body condition change from moderate (BCS < 7 [scale, 1 to 9]) to overweight (7 ≤ BCS < 8) to obese (BCS ≥ 8) would be most appropriate to determine metabolic abnormalities during the development of obesity and most applicable to horses at risk of imminently developing obesity.
The study reported here was designed to test the hypothesis that diet-induced weight gain in horses decreases insulin sensitivity and increases plasma concentrations of insulin, glucose, NEFAs, triglyceride, and leptin. Specifically, the purpose of the study was to identify changes in adiposity, minimal model parameters of glucose and insulin dynamics, and basal concentrations of insulin, glucose, NEFAs, triglyceride, and leptin as adiposity increases and an overweight or obese state is achieved through overfeeding.
Acute insulin response to glucose
Body condition score
Cresty neck score
Frequently sampled IV glucose tolerance test
Nonesterified fatty acid
Glucose effectiveness calculated via minimal model analysis
Insulin sensitivity calculated via minimal model analysis
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Dexamethasone sodium phosphate injection, Vedco Inc, St Joseph, Mo.
Grass Plus Performer, Buckeye Nutrition, Dalton, Ohio.
Vacutainer, Becton-Dickinson Ltd, Franklin Lakes, NJ.
Dextrose 50% solution, Vedco Inc, St Joseph, Mo.
Humulin R, Eli Lilly & Co, Indianapolis, Ind.
CX5 Chemistry Analyzer, Beckman Coulter Inc, Fullerton, Calif.
Coat-A-Count Insulin, Diagnostic Products Corp, Los Angeles, Calif.
Multi-species Leptin RIA, Linco Research Inc, St Charles, Mo.
Coat-A-Count Cortisol, Diagnostic Products Corp, Los Angeles, Calif.
MinMod Millenium, version 5.15, University of Pennsylvania, Kennett Square, Pa.
Intercooled Stata, version 9.2, Stata Corp, College Station, Tex.
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