“endocrinopathic laminitis has been defined as laminitis developing from hormonal influences” (rather than in association with pro-inflammatory and intestinal conditions)

Endocrinopathic laminitis
Notes from powerpoint slides – Sweden (Tidaholm), 18th May 2010
Melody de Laat BVSc (Hons)
Australian Equine Laminitis Research Unit
The University of Queensland
Gatton, Qld, Australia

“Endocrinopathic laminitis has been defined as laminitis developing from hormonal
influences” (rather than in association with pro-inflammatory and intestinal
– iatrogenic corticosteroid administration – Equine Cushing’s Syndrome – Insulin resistance (Equine metabolic syndrome and pasture • Cortisol is the main glucocorticoid • Maintains blood glucose • Important functions are – gluconeogenesis – protein catabolism – mobilisation of fatty acids • Limits glucose utilisation by peripheral tissue • Opposing effect to insulin • Corticosteroids inhibit insulin-mediated glucose uptake by a direct mechanism that limits the movement of glucose transporters to the cell surface • Thus during hypercortisolaemia the brain has more glucose while peripheral • Insulin and glucose remain within a narrow physiological range in the fasted • Persistent deviation from normal is diagnostic of abnormal insulin metabolism • Insulin maintains normal blood glucose by stimulating glucose uptake by • Glucose uptake is regulated by specific transport proteins • Most tissues rely on insulin to regulate glucose uptake via GLUT-4 • The brain does not rely on insulin for glucose uptake = GLUT-1 – freely permeable to glucose – starved or overloaded if not euglycaemic • Occurs when transport proteins fail or become over-used – Human type 2 diabetes – Equine metabolic syndrome • Increased production of insulin results • Hyperinsulinaemia clears excess glucose • Thus glucose intolerance → insulin resistance • Excessive glucocorticoids (ECD, iatrogenic), obesity (EMS/IRS) and over- eating (pasture-associated) all lead to glucose intolerance • Glucose intolerance leads to increased insulin secretion • So the common link between the causes of endocrinopathic laminitis is IR Insulin resistance IR is defined as the failure of tissues to respond appropriately to insulin (Frank, 2006) Mechanisms • Failure of GLUT-4 proteins • Decreased density of insulin receptors • Malfunction of insulin receptors • Defects in internal signalling pathways • In the horse, IR leads to persistent hyperinsulinaemia which maintains • IR has been linked to laminitis in many studies • Serum insulin concentration is a good predictive and prognostic factor for – 50% of cases of laminitis (USDA) – Pony breeds not included in this study! • Summer months – lush pasture • Risk factors are – Obesity – Genetic predisposition – Insulin insensitivity • Easy keepers → BCS (1-9) • Abnormal fat distribution – rump, tail base, sheath, supra-orbital, neck → • Laminitis may not have occurred • Most common from 8-18 years • Insulin resistance – elevated serum insulin concentration – usually normal blood glucose concentration Basal serum insulin • Normal range (10-30 µIU/ml) • Can be unreliable (diet composition, stress, diurnal, seasonal) • Best to use a standardised laboratory • Fasted (8h) samples (pasture fed ok?) • Best between 7am-10am before am feed • Not during an episode of laminitis • In some EMS horses basal insulin is normal – need dynamic testing • The equine digit is well vascularised and has counter current heat exchange • Sophisticated thermoregulation - cold tolerant • The distal phalanx has a tertiary blood supply • Vascular shunts exists between arteries and veins (AVAs) to help control • There are no vessels in the lamellae of the inner hoof wall • Blood supply comes from the adjacent dermis • The lamellae depend on the vasculature for supply of nutrients such as oxygen • Compromise of the lamellar circulation can cause damage to the lamellae • Hoof wall surface temperature (HWST) is a reasonable reflection of underlying perfusion if measured under conditions of controlled ambient temperature and minimal movement • Normal horse HWST varies between a large range of temperatures over time • Conflicting opinions and proposed theories include: – Increased blood flow delivering a laminitis trigger factor – Decreased blood flow causing lamellar ischaemia – Increased blood flow with diversion through AVA shunts causing • Insulin is an important vasomediator – Main action is vasodilation (through nitric oxide (NO) synthesis and – Also capable of vasoconstriction (through release of endothelin-1 (ET- • Hyperinsulinaemia has been linked with elevated HWST – In experimentally-induced laminitis (de Laat 10) – Also in cases of P-A laminitis (Carter 09) • This is probably caused by vasodilation • NO mediated vasodilation may be impaired in IR horses • Does IR tip the balance towards vasoconstriction? • Major nutrient requirement = glucose • Glucose consumption reflects glycolysis and oxidation • Most glucose is metabolised to lactate • Anaerobic tissues: glucose to lactate via glycolytic pathway • The foot of a horse at rest produces more lactate and consumes more glucose • Blood vessels and lamellar epidermal basal cells are rich in LDH (Wattle • In resting horses hoof lamellae are net lactate producers that seem to depend on anaerobic energy metabolism (Wattle 2004). • The epidermal/dermal interface may be quite indifferent to the oxygen (but not the glucose) status of its blood supply. Prevention of endocrinopathic laminitis • Crucial when dealing with endocrinopathic laminitis • Will help in all forms of laminitis • 2 main aims: • Want serum insulin < 50-60 µIU/ml • Slowly and carefully! • Carefully controlled exercise in pain free horses • Improved fitness • Gradual weight loss • Monitor with weight tapes, BCS, CNS • Difficult in chronically laminitic horses • Plant carbohydrates include structural (cell wall) and non-structural elements • NSC originate from plant cell content • NSC contents = sugar, starch and fructans • Cereal grains and pastures with forage species are high in NSC content • Such foods are associated with marked blood glucose and serum insulin • Reduce non-structural carbohydrate intake, especially fructans • Important – get the owner to accept their animal is overweight! • Evaluate current feeding plan and housing • Assess weekly workload • Set realistic weight loss goals • Monitor progress (girth and neck circumference, BCS, CNS) every 2-4 wks • Make diet and exercise changes gradual • Develop maintenance program • Carefully controlled exercise in pain free horses • Improved fitness = prolonged benefit • Start 20-30 mins 1-2/wk then daily • Swimming, hand walking, lungeing • Gradual ↑ duration and intensity • Difficult in chronically laminitic horses • Feed hay with lower NSC content (<10%) • Divide ration into 3-4 smaller feeds/day • Prolong feeding times • Haynets with small holes • Provide protein, vitamin and mineral requirements with supplements • Avoid excessive treats (apples etc) • Limit access to pasture – Limit/prevent access to pasture – 1-2 hrs/day (ponies can consume 40% daily DMI in 3 hrs (Ince 2005) ) – dry yards/ indoor schools – grazing muzzles (ensure able to consume enough water, watch herd – Strip grazing behind other horses – Wood chip layer – Mow prior to access (remove clippings) • Avoid overgrazing (plant stems = fructans) • Pasture weeds also contain fructans • Winter and autumn pasture is not necessarily safer • Fructans can accumulate at temps below what is required for plant growth • Cold bright days can result in significant photosynthesis and minimal plant growth which promotes fructan accumulation • 50% cases due to inappropriate dietary intake……. • Less food • More exercise • Better client/owner education • Discipline

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Source: http://www.gyllenhov.se/tidaholm.pdf

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