osteochondritis dissecans in yearlings

Fasting insulin status and osteochondritis dissecans in Thoroughbred yearlings

Published on: 12/30/2011
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Insulin resistance in horses is a complex pathophysiological condition that appears to underlie several chronic conditions often encompassed by the term "equine metabolic syndrome", including laminitis, obesity and hyperkalemic periodic paralysis (Geor and Frank, 2009). There is much interest in the effect of insulin on bone metabolism, as the skeleton is increasingly regarded as an endocrine organ that affects energy metabolism and has a role, through osteocalcin, in regulating insulin response (Reinhr and Roth, 2010). Another recent study has shown that leptin, produced by adipose tissue, regulates bone metabolism via the sympathetic nervous system (Confavreux et al., 2009). Furthermore, IGF-1, which acts in concert with insulin to promote bone and cartilage growth, also exerts insulin-like effects on carbohydrate metabolism. Therefore, perturbation of any of these hormones may contribute to skeletal disease.

In horses, osteochondritis dissecans (OCD) is a developmental disease caused by a defect in the normal process of bone formation and causes thickening, cracking and tearing of the joint cartilage (Jeffcott, 1996). OCD is a multi-factorial condition associated with dietary deficiencies or nutrient imbalances, biomechanical stress or trauma, rapid growth rate and genetics. The prevailing hypothesis is that an elevated post-feeding blood insulin level predisposes a growing horse to OCD (Ralston, 1996; Pagan et al., 2001). However, it is not clear whether the hyperinsulinaemia observed in these studies was a direct cause of OCD or whether it reflected the excess body weight of the rapidly growing foals. We investigated the relationship between fasting insulin status and OCD in Thoroughbred yearlings.

Yearlings were recruited in 2007 from two Thoroughbred stud farms (farm A, n = 53; farm B, n = 16) and blood samples were collected between 06:00 and 07:00 after an overnight (>12 h) fast. The following year (2008), another group of yearlings was sampled from farm A (n = 30) using the same blood sampling procedure. Plasma insulin concentrations were determined using a radioimmunoassay (Coat-ACount Insulin; Diagnostic Products Corp., Los Angeles, CA) previously validated for use with equine plasma (Sessions et al., 2004). Plasma glucose concentrations were analysed enzymatically using a hexokinasebased Olympus kit and an Olympus AU 400 analyser (Olympus Diagnostics Systems Division, Melville, NY) and skeletal abnormalities were determined using radiography.

In the 2007 farm A cohort, fasting insulin concentrations were lower in yearlings with OCD and skeletal abnormalities than in yearlings with no abnormalities (3.0 ± 0.4 mIU/L and 4.5 ± 0.3 mIU/L, respectively; P < 0.01). A similar result was obtained for the 2007 farm B cohort (P < 0.05). Neither fasting glucose concentrations nor birth weights were significantly different between the two groups across both farms. In the 2008 farm A cohort, fasting insulin concentrations were also significantly lower in yearlings with OCD and other skeletal abnormalities than in yearlings with no abnormalities (1.5 ± 0.3 mIU/L and 3.2 ± 0.6 mIU/L, respectively; P < 0.05).

The results demonstrate a relationship between low fasting plasma insulin concentration and the incidence of OCD in Thoroughbred yearlings. Perturbation of insulin metabolism during growth may be linked to the development of equine skeletal diseases.

Funding was received from the Rural Industries Research and Development Corporation, Canberra, Australia.

This paper was presented at the Recent Advances in Animal Nutrition (RAAN) - Australia Volume 18 (95-96). Engormix.com thanks the authors and the organizing committee for this contribution. 

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