Pre‐laminitic metabolic syndrome in genetically predisposed ponies involves compensated insulin resistance

Treiber, K. H.; Kronfeld, D. S.; Hess, Tanja; Byrd, Bridgett M.; Splan, Rebecca K.

doi:10.1111/j.1439-0396.2005.00611_8.x

Cited by 19 publications

(10 citation statements)

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“…Although the serum insulin concentrations achieved in this study were higher than those commonly associated with equine Cushing's disease (McGowan et al. 2004), or those reported with some cases of pasture‐associated, endocrinopathic laminitis (Treiber et al. 2005), concentrations >1000 µ iu/ml have occasionally been reported in the field (Reeves et al.…”

Section: Discussioncontrasting

confidence: 61%

Equine laminitis: Induced by 48 h hyperinsulinaemia in Standardbred horses

Laat

McGowan

Sillence

et al. 2010

Equine Veterinary Journal

261

247

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SummaryReasons for performing study: Hyperinsulinaemia is known to induce laminitis experimentally in healthy ponies with no history of the condition. Horses are more insulin sensitive than ponies and whether prolonged hyperinsulinaemia and euglycaemia would have a similar laminitogenic effect requires study. Objectives: To determine if laminitis results when the prolonged euglycaemic hyperinsulinaemic clamp technique (p-EHC) is applied to clinically normal Standardbred horses, and to monitor hoof wall temperature seeking an association between vascular activity and laminitis development. Methods: Eight young, clinically normal Standardbred horses were assigned into 4 pairs and within each pair, one was assigned randomly to either treatment (n = 4) or control (n = 4) groups. Treated horses received continuous infusions of insulin and glucose until clinical signs of laminitis developed, at which point the horses were subjected to euthanasia. Control horses received an equivalent volume of a balanced electrolyte infusion for the same period. Hoof wall surface temperature (HWST) was monitored continuously throughout the experimental period. Results: All horses in the treatment group were calculated to have normal insulin sensitivity. All treated horses, and none in the control group, developed laminitis (P = 0.01). Pronounced digital pulses were a feature of the treatment group, while insignificant digital pulses occurred in control horses. HWST was higher and less variable in treated horses once hyperinsulinaemia was established. Conclusions: Healthy Standardbred horses subjected to prolonged hyperinsulinaemia develop laminitis within 48 h, demonstrating that laminitis in horses can be triggered by insulin. Potential relevance: Insulin resistance and the associated hyperinsulinaemia place horses and ponies at risk of developing laminitis. This study demonstrates a need for prompt management of the persistent hyperinsulinaemia seen in some endocrinopathies.

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Section: Discussioncontrasting

confidence: 61%

Equine laminitis: Induced by 48 h hyperinsulinaemia in Standardbred horses

Laat

McGowan

Sillence

et al. 2010

Equine Veterinary Journal

261

247

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“…Several conditions associated with laminitis in horses, such as equine Cushing's syndrome (pituitary pars intermedia dysfunction, PPID) (Johnson et al . 2004), equine metabolic syndrome (Johnson 2002; Treiber et al . 2005) and iatrogenic corticosteroid administration (Johnson et al .…”

Section: Introductionmentioning

confidence: 99%

Glucose transport in the equine hoof

Asplin

Curlewis

McGowan

et al. 2011

Equine Veterinary Journal

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SummaryReasons for performing study: Several conditions associated with laminitis in horses are also associated with insulin resistance, which represents the failure of glucose uptake via the insulin-responsive glucose transport proteins in certain tissues. Glucose starvation is a possible mechanism of laminitis, but glucose uptake mechanisms in the hoof are not well understood. Objectives: To determine whether glucose uptake in equine lamellae is dependent on insulin, to characterise the glucose transport mechanism in lamellae from healthy horses and ponies, and to compare this with ponies with laminitis. Methods: Study 1 investigated the effects of insulin (300 mU/ml; acute and 24 h) and various concentrations of glucose up to 24 mmol/l, on 2-deoxy-D-[2,6-3 H]glucose uptake in hoof lamellar explants in vitro. Study 2 measured the mRNA expression of GLUT1 and GLUT4 transport proteins by PCR analysis in coronary band and lamellar tissue from healthy horses and ponies, ponies with insulin-induced laminitis, and ponies suffering from chronic laminitis as a result of equine Cushing's syndrome. Results: Glucose uptake was not affected by insulin. Furthermore, the relationship between glucose concentration and glucose uptake was consistent with an insulinindependent glucose transport system. GLUT1 mRNA expression was strong in brain, coronary band and lamellar tissue, but was weak in skeletal muscle. Expression of GLUT4 mRNA was strong in skeletal muscle, but was either absent or barely detectable in coronary band and lamellar tissue. Conclusions:The results do not support a glucose deprivation model for laminitis, in which glucose uptake in the hoof is impaired by reduced insulin sensitivity. Hoof lamellae rely on a GLUT1-mediated glucose transport system, and it is unlikely that GLUT4 proteins play a substantial role in this tissue. Potential relevance: Laminitis associated with insulin resistance is unlikely to be due to impaired glucose uptake and subsequent glucose deprivation in lamellae.

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“…Prolonged administration of insulin to induce hyperinsulinaemia while maintaining normal glucose concentrations resulted in the development of clinical and histological laminitis in all 4 feet of healthy ponies within 72 h and of healthy Standardbred horses within 48 h suggesting that IR and the associated hyperinsulinaemia place horses and ponies at risk of developing laminitis through direct insulin toxicity. However, it must be acknowledged that the serum insulin concentrations achieved in these studies were much higher than those commonly associated with PPID and those reported in some cases of pasture‐associated, endocrinopathic laminitis and similarly high serum insulin concentrations have been documented in recurrently laminitic ponies in the absence of clinical signs of laminitis such that very high serum insulin concentrations alone are not necessarily laminitis‐inducing. In addition, subsequent histological examination of the laminitis lesions from the ponies with experimental insulin‐induced laminitis revealed a lack of widespread basement membrane disintegration and instead the predominant lesion was one of apoptosis and mitosis in the axial regions .…”

mentioning

confidence: 64%

Endocrinological aspects of the pathophysiology of equine laminitis

Menzies‐Gow

2012

Equine Veterinary Journal

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Pre‐laminitic metabolic syndrome in genetically predisposed ponies involves compensated insulin resistance

Cited by 19 publications

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Equine laminitis: Induced by 48 h hyperinsulinaemia in Standardbred horses

Equine laminitis: Induced by 48 h hyperinsulinaemia in Standardbred horses

Glucose transport in the equine hoof

Endocrinological aspects of the pathophysiology of equine laminitis

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