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  Discussion on Research Summary: Insulinemia and Laminitis
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DrO

Posted on Tuesday, Feb 12, 2013 - 3:28 pm:

It has been long recognized that prolonged increases in serum insulin concentration (insulinemia), has a predisposing role in some types of laminitis. Cushing's and Metabolic SynDrOme related laminitis are possible examples. The currently proposed thought is the insulinemic state suggests the tissues are not responding normally with increased glucose uptake and this impaired glucose absorption caused the problems. Here is another possibility: insulin induction of a growth factor with inappropriate lamellar cell proliferation weaking the laminae.
DrO

Vet J. 2013 Feb 8.
A potential role for lamellar insulin-like growth factor-1 receptor in the pathogenesis of hyperinsulinaemic laminitis.
de Laat MA, Pollitt CC, Kyaw-Tanner MT, McGowan CM, Sillence MN.

Australian Equine Laminitis Research Unit, School of Veterinary Science, The University of Queensland, Gatton, Queensland 4343, Australia. Electronic address: melody.de_Laat@okstate.edu.
Abstract

The reason why a sustained high concentration of insulin induces laminitis in horses remains unclear. Cell proliferation occurs in the lamellae during insulin-induced laminitis and in other species high concentrations of insulin can activate receptors for the powerful cell mitogen, insulin-like growth factor (IGF)-1. The first aim of this study was to determine if IGF-1 receptors (IGF-1R) are activated in the hoof during insulin-induced laminitis. Gene expression for IGF-1R and the insulin receptor (InsR) was measured using qRT-PCR, in lamellar tissue from control horses and from horses undergoing a prolonged euglycaemic, hyperinsulinaemic clamp (p-EHC), during the mid-developmental (24h) and acute (46h) phases of insulin-induced laminitis. Gene expression for both receptors was decreased 13-32-fold (P<0.05) at both time-points in the insulin-treated horses. A second aim was to determine if the down-regulation of the receptor genes could be accounted for by an increase in circulating IGF-1. Serum IGF-1 was measured at 0, 10, 25 and 46h post-treatment in horses given a p-EHC for approximately 46h, and in matched controls administered a balanced, electrolyte solution. There was no increase in serum IGF-1 concentrations during the p-EHC, consistent with down-regulation of both receptors by insulin. Stimulation of the IGF-1R by insulin may lead to inappropriate lamellar epidermal cell proliferation and lamellar weakening, a potential mechanism for hyperinsulinaemic laminitis. Targeting this receptor may provide insights into the pathogenesis or identify a novel therapy for hyperinsulinaemic laminitis.
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