“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 email@example.com
“Endocrinopathic laminitis has been defined as laminitis developing from hormonal influences” (rather than in association with pro-inflammatory and intestinal conditions)
– 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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