Endocrine disorders and laminitis

Abstract

SummaryTwo common endocrine disorders, pituitary pars intermedia dysfunction and equine metabolic syndrome, predispose horses and ponies to laminitis and may even induce the condition. The exact mechanisms involved in endocrinopathic laminitis have not been elucidated but hyperinsulinaemia and insulin resistance are currently being investigated. Obesity and regional adiposity may also contribute to laminitis susceptibility through the release of inflammatory cytokines and adipokines. In the case of pituitary pars intermedia dysfunction, glucocorticoid excess is likely to weaken hoof structures, alter vascular dynamics within the foot and induce or exacerbate insulin resistance. This review will summarise current theories regarding the pathophysiology of endocrinopathic laminitis and provide recommendations for the diagnosis and management of these common equine endocrine disorders.

Insulin resistance in the horse: a review

“…Obesity-related IR is probably caused by the thrifty genotype; while such genes provided an advantage over other animals living in the wild and buffered seasonal food shortages, under domestication conditions the high energy efficiency becomes a burden, especially when combined with improper practices (Johnson et al 2009;Tinworth et al 2010;Tadros & Frank 2013). Evolutionarily adapted to living in a food-poor environment, horses and ponies are more predisposed to obesity and IR where food is available throughout the year (Johnson et al 2009;Frank & Tadros 2014).…”

“…Other diseases accompanying equine obesity and IR have been rarely described (Wylie & Collins 2010;Johnson et al 2012;Tadros & Frank 2013). Type 1 diabetes mellitus (T1DM) is characterized by the lack of insulin secretion by beta cells of the pancreas as a result of their destruction (due to viral or immune-mediated disease), whereas type 2 diabetes mellitus (T2DM), characterized by relatively reduced insulin secretion, is a complex metabolic disorder that develops due to chronic hyperinsulinemia.…”

“…There are two basic theories linking obesity to IR: the down-regulation of signalling pathways induced by adipokines and cytokines produced in adipose tissue, and the accumulation of intracellular lipids in insulin-sensitive tissue such as skeletal muscle (lipotoxicity) (Tadros & Frank 2013). Along with muscle and liver glycogen, triglycerides stored in adipose tissue are the body's most important sources of energy.…”

“…Post-receptor activity involves inhibiting insulin signalling at the level of phosphatidylinositol 3-kinase and translocating GLUT-4 protein into the cell membrane, thus impairing the uptake of glucose by the cell and causing IR (Draznin 2006;Olszanecka-Glininowicz & Zahorska-Markiewicz 2008). Equine obesity is associated with quantity changes in adiponectins release -the studies reported an elevated concentration of leptin and a lowered level of adiponectin, which increases tissues' sensitivity to insulin (Tadros & Frank 2013).…”

“…NO is generated by NO synthase vascular endothelial cells and undergoes local diffusion, causing the vessels to dilate slowly. NO is secreted when the PI3K pathway is activated, whereas activation of the MAPK pathway leads to the release of ET-1 (Venugopal et al 2011;Tadros & Frank 2013). During IR, the regulatory action of insulin on blood vessels is disturbed and the PI3K pathway is blocked, whereas the mitogen-activated pathway functions normally, which causes the blood vessels to contract.…”