The risk of endocrinopathic laminitis is the pivotal reason that veterinarians should recognise horses affected with equine metabolic syndrome (Harris et al, 2020). Laminitis is often debilitating and, when severe, may lead to euthanasia. Therefore, laminitis should be prevented where possible through the institution of effective management as soon as equine metabolic syndrome is first identified. Diagnosis of equine metabolic syndrome is based on review of the medical history, management, physical examination and laboratory testing (Durham et al, 2019). Management approaches to reduce laminitis risk in horses with equine metabolic syndrome include exercise, nutritional advice, weight loss and, if needed, laminitis management. Pharmacological options are available for the treatment of severe or refractory cases, which will be discussed in Part 2 of this series.
Equine metabolic syndrome and obesity
The relationship between obesity and insulin dysregulation (in which obesity promotes insulin dysregulation), as has been well documented in the human medical context (Wondmkun, 2020). This is less clear in equine metabolic syndrome. However, degrees of obesity commonly alert veterinarians to consider equine meta-bolic syndrome. Obesity is also a risk factor for worsening laminitis by virtue of the additional physical weight force acting on the hoof–lamellar interface. Insulin is a pleiotropic hormone and one of its actions is to stimulate adipogenesis. Therefore, an obese phenotype may, in part, be promoted directly through elevated insulin influence, especially in the face of a positive energy balance.
In addition to insulin dysregulation, equine obesity is also associated with several other detrimental health concerns (Pratt-Phillips and Munjizun, 2023). Examples include risk of colic (mesenteric lipoma), asthma, poor wound healing, exercise intolerance, heat stress, reduced mare reproductive performance, deteriorating gait quality and arthritis (Thomas et al, 2021; Hallman et al, 2023; Pratt-Phillips and Munjizun, 2023). Equine obesity is common, with incidence reported between 23% and 54% (Giles et al, 2014; Robin et al, 2015; Potter et al, 2016; Golding et al, 2023). Insulin dysregulation is not demonstrable in all horses with obesity, and hyperinsulinaemia-associated laminitis may arise in relatively lean horses with insulin dysregulation (Pratt-Phillips and Munjizun, 2023).
Severe adipocyte hypertrophy and increased expression of leptin and some inflammatory cytokines (TNFα, IL1β and CCL2) have been reported in (peri-renal and retroperitoneal) adipose tissues obtained from horses with equine metabolic syndrome (Reynolds et al, 2019). These authors concluded that adipose tissue from horses with obesity and equine metabolic syndrome is markedly dysfunctional with a hypertrophic-inflammatory phenotype. Therefore, the presence of excessive (dysfunctional) adipose tissue in horses with equine metabolic syndrome is itself an important contributor to insulin dysregulation in these horses.
Adipokines are hormones that are produced by adipocytes. Abnormal circulating levels of adipokines exert pleiotropic actions in obese states. Evidence that hyperleptinaemia and hypoadiponectinaemia may play important direct roles in the pathogenesis of hyperinsulinaemia-associated laminitis is emerging (Burns et al, 2019; Elliott and Bailey, 2023).
Leptin is a proinflammatory adipokine; hyperleptinaemia contributes to obesity-associated adipose tissue dysfunction and may promote inflammatory processes in the hoof–lamellar interface (Burns et al, 2019; Reynolds et al, 2019). However, sustained inflammation also inhibits leptin receptor signalling in the hypothalamus (leptin resistance), resulting in impairment of leptinmediated weight control, a normal function of leptin, thus further promoting obesity. The role of leptin in the pathogenesis of hyperinsulinaemia-associated laminitis deserves further investigation. Leptin exerts mitogenic effects, regulates the pro-inflammatory response of epidermal keratinocytes and promotes epithelial-to-mesenchymal transition, all of which are reported components of hyperinsulinaemia-associated laminitis pathophysiology. Lamellar epidermal cells are invested with leptin receptors, suggesting that these cells are responsive to circulating leptin (Burns et al, 2019).
There has been increasing interest in the role of adiponectin in equine metabolic syndrome. Adiponectin is an adipokine with both insulin-sensitising and anti-inflammatory properties (Elliott and Bailey, 2023). Low adiponectin status (adiponectin deficiency), another consequence of adipose tissue dysfunction, has been demonstrated in equine obesity, insulin dysregulation and hyperinsulinaemia-associated laminitis. Hypoadiponectinaemia has been associated with increased epidermal cell apoptosis and proliferation, endoplasmic reticulum stress and reduced cellular protection against oxidative stress, all of which contribute to the pathogenesis of hyperinsulinaemia-associated laminitis. Pharmaceutical options are potentially available to reverse adiponectin deficiency.
Nutritional considerations in equine metabolic syndrome
Horses evolved with healthy adaptations to the consumption of native prairie grassland species with relatively low sugar and starch content. Consumption of modern rations with high non-structural carbohydrate content, coupled with low levels of physical activity, are an important driving force for both obesity and hyperinsulinaemia. One of the first principles for both prevention of hyperinsulinaemia-associated laminitis and obesity reversal is the provision of a ration with relatively low non-structural carbohydrate content (<10%) (Durham et al, 2019).
Equine metabolic syndrome is commonly first encountered when horses develop acute hyperinsulinaemia-associated laminitis at times of the year when the non-structural carbohydrate content of field grass is relatively high. Discussion of the factors that contribute to high field grass non-structural carbohydrate content and how to minimise their influence is beyond the scope of this article; further valuable information is available elsewhere (Watts, 2010; Fitzgerald et al, 2019). High field grass non-structural carbohydrate content especially arises when overnight ambient temperatures do not exceed 5°C for 2–3 weeks (Watts, 2010). Owners should be cautioned to restrict access to pasture for horses with insulin dysregulation in these conditions. Although grazing muzzles, reduced time at grass and strip grazing approaches can help limit non-structural carbohydrate consumption for horses with controlled insulin dysregulation, severely compromised horses with insulin dysregulation should never be allowed access to freerange grazing. The most common recommendation for both prevention and treatment of hyperinsulinaemia-associated laminitis is that the individual's dietary non-structural carbohydrate content should not exceed 10–12%, based on dry matter.
Fructan content contributes to the measured non-structural carbohydrate value, but does not contribute to post-prandial hyperinsulinaemia. This suggests that when making decisions about the suitability of hay for horses with equine metabolic syndrome, restriction thresholds based on combined ethanol-soluble carbohydrates (fructose, sucrose, glucose and short-chain fructans) and starch (combined ethanol-soluble carbohydrates plus starch) percentages would be more practical (Kellon, 2022). Therefore, it may be better to recommend that horses with insulin dysregulation should be provided forage with a combined ethanol-soluble carbohydrate plus starch content of <10%.
Several excellent reviews regarding nutritional management strategies intended to prevent equine metabolic syndrome, addressing active hyperinsulinaemia-associated laminitis and reverse obesity have been published (Geor, 2009; Watts, 2010; Durham et al, 2019; Shepherd et al, 2021). If available, input from specialist nutritional consultants may be considered. Broadly speaking, most affected individuals respond to the provision of rations characterised by low non-structural carbohydrate content (<10%). Pasture grazing, grain and (excessive) treats should not be provided (supplements are typically constituted with starch and sugar). Provision of a mixed species grass hay-based diet of 1.25–1.5% of bodyweight (dry matter intake) or 1.4–1.7% of bodyweight (as fed) is recommended (Durham et al, 2019). The non-structural or ethanolsoluble carbohydrate content of grass or preserved forage cannot be estimated based on gross inspection, and forage analysis laboratory testing is essential for this purpose. Both acquisition of nutrient analysis and careful weighing of provided forage to horses with equine metabolic syndrome (based on bodyweight) should be emphasised.
Additional strategies may be needed for some refractory (weight loss resistant) cases. When needed, additional levels of restriction (1.0% of bodyweight (dry matter) or 1.15% actual bodyweight) may be considered, but patients must be carefully observed. Soaking the hay may lessen its water-soluble carbohydrate content and reduce post-prandial hyperinsulinaemia. It is recommended that the effectiveness of soaking for a given batch of hay should be objectively tested by measuring the non-structural carbohydrate content before and after soaking. Soaking can result in loss of other important nutrients and a balancer containing protein, vitamins and minerals should be used. In hot, humid conditions, soaked hay rapidly becomes mouldy, so any leftover hay should be removed after 2–3 hours. Straw is a safe, cost-effective, low energy fibre source characterised by low water-soluble carbohydrate content and may be added to forage rations to further reduce non-structural carbohydrate intake (Dosi et al, 2020). Proprietary commercial feedstuffs with guaranteed low non-structural carbohydrate content are also available in some locations.
Non-structural carbohydrates
The consumption of rations high in non-structural carbohydrates by horses with insulin dysregulation is crucially important for the development of obesity, hyperinsulinaemia and hyperinsulinaemia-associated laminitis. Non-structural carbohydrate-induced hyperinsulinaemia is much more common in horses with equine metabolic syndrome (Carter et al, 2009a). Products of small intestinal digestion of the sugar and starch components of non-structural carbohydrate are the primary drivers of post-prandial hyperglycaemia and hyperinsulinaemia, with implications for the risk of hyperinsulinaemia-associated laminitis in equine meta-bolic syndrome.
Fructans – chains of fructose molecules with a terminal glucose – are accumulated by cool-season grasses (such as tall fescue and ryegrass) for energy storage and contribute to the measured non-structural carbohydrate content of grass (Longland and Byrd, 2006). Fructans do not directly provoke an insulinaemic response and are likely not a risk factor for hyperinsulinaemia-associated laminitis (Kellon, 2022). The extent to which fructan ingestion contributes to naturally occurring hyperinsulinaemia-associated laminitis in grazing horses has been overstated and is much debated.
Predicting body fat composition based on assessment of body morphology
Characterisation of patients regarding total body fat content is usually based on subjective assessment during a physical examination. Indeed, evaluation of the patient's body condition represents an important component of every examination. Identifying generalised obesity or regional adiposity should trigger consideration of underlying insulin dysregulation and may lead to expanded diagnostic testing. Obesity is define as a body fat composition exceeding 20% (Dugdale et al, 2012). The gold standard for measurement of body fat percentage is deuterium oxide dilution, a technique that has been validated for use in horses (Dugdale et al, 2012). Ideally, subjective methods of obesity scoring should be compared to this standard.
The 9-point Henneke body condition score and cresty neck score are the most frequently employed subjective clinical assessments for obesity or adiposity in equine veterinary practice (Henneke et al, 1983; Carter et al, 2009b) (Figure 1). Although the body condition score works reasonably well to predict body fat percentage in the hands of experienced investigators, it is unreliable when used by horse owners, even following specific training (Potter et al, 2016; Golding et al, 2023). Moreover, body condition score does not lessen in parallel with weight reduction following dietary restriction in obese horses with a body condition score >7 (consequent to adipose tissue redistribution) (Dugdale et al, 2012). Other body condition scoring methods include the EQUI-FAT system, Kohnke-modified Henneke system and the 6-point Carroll and Huntingdon system (Morrison et al, 2017). In some of those reports, results were based on small numbers of horses and ponies. Body condition scoring and other morphometric measures of obesity failed to reflect adiponectin levels and were not reliable for predicting insulin dysregulation or hyperinsulinaemia-associated laminitis in a recent study involving 734 native-breed ponies in England (Barnabé et al, 2024).
A novel body condition index was introduced using specific morphometric measurements and validated using the deuterium dilution method (Potter et al, 2024). Objective measurements included body length, mid-neck circumference, belly girth circumference, heart girth circumference and height at the withers. This body condition index was superior to subjective methods used for the purpose of tracking patients' weight loss or weight gain (such as body condition scoring), and minimised subjectivity errors when used by horse owners. Best results were obtained for equids within the 3–8 range of the Henneke body condition score scale. The body condition index approach did not work well for Shetland ponies and Miniature horses as a result of their different body shape. Overall consistency and repeatability of the body condition index as an indicator of body fat content was very good, even when used by inexperienced assessors (Potter et al, 2024). Other methods to facilitate objective assessment of body fat composition have been investigated with variable results, including bioelectrical impedance spectroscopy and ultrasonography (Martin-Giminez et al, 2016; Greco-Otto and Léguillette, 2018).
Laboratory testing for insulin dysregulation and equine metabolic syndrome
Diagnostic testing for insulin dysregulation is recommended for individuals with obesity to positively support a diagnosis of equine metabolic syndrome, but also for individuals without obesity(exhibiting laminitis) before ruling out equine metabolic syndrome based on lean body morphology (Durham et al, 2019). Testing for insulin dysregulation is also recommended for horses with pituitary pars intermedia dysfunction (a common co-morbidity), before the prescription of corticosteroid treatments. For the assessment of responses to hyperinsulinaemia-associated laminitis and insulin dysregulation treatments, diabetic horse candidates (rare), during a prepurchase examination and to provide guidance for nutritional decision making. Principal diagnostic tests to support diagnosis of insulin dysregulation include demonstration of:
- Resting (basal) hyperinsulinaemia
- Post-prandial hyperinsulinaemia
- Tissue insulin resistance.
Any or all of those three criteria may be present in horses with equine metabolic syndrome. Older horses (>10 years old) commonly develop both equine metabolic syndrome and pituitary pars intermedia dysfunction. The co-existence of equine metabolic syndrome and pituitary pars intermedia dysfunction is associated with worsening insulin dysregulation, severe laminitis and poorer clinical outcomes. Therefore, testing for pituitary pars intermedia dysfunction is also recommended for older equids.
Serum insulin concentration
Basal hyperinsulinaemia is evidence of underlying insulin dysregulation. Confounding factors that should be considered include:
- Stress (including severe laminitis pain) that may cause hyperinsulinaemia because of increased influence of cortisol, catecholamines or both
- Transport
- Severe systemic illness
- Starvation and the imposition of fasting (~6 hours) activate stress responses potentially resulting in hyperinsulinamia
- Recent ingestion of grain.
Breed differences and seasonality are becoming increasingly recognised as sources of variability in basal serum insulin levels. Preliminary data suggest that resting (basal) serum insulin (and glucose) concentrations are higher in the winter, possibly reflecting a seasonal state of insulin resistance that may benefit survival (Potier and Durham, 2020). However, Macon et al (2022) found that serum insulin concentrations in horses with insulin dysregulation were higher in spring. These variances are important considerations when basal serum insulin concentrations are used for the assessment of treatment effectiveness.
Different assays are used for the laboratory measurement of serum insulin concentrations, including radioimmunoassay, ELISA and chemiluminescent assays. Point-of-care insulin testing is also becoming available, but further research for stronger validation is needed for this test methodology. Reference values vary significantly depending on specific methodologies, which must be considered when evaluating results from different research groups in the literature.
During the management of equine metabolic syndrome, it is essential to consistently use the same laboratory methodology and testing conditions (eg time of day, feeding arrangements before sampling). The most current information regarding the cut-off values for serum insulin thresholds (level of hyperinsulinaemia supporting a diagnosis of insulin dysregulation) is provided by the Equine Endocrinology Group (2024). New information based on current research is regularly reviewed by the Equine Endocrinology Group and adjustments to specific recommendations for diagnosis and management of equine metabolic syndrome are also provided.
Diagnostic cut-offs for hyperinsulinaemia are based on different assay methodologies and whether the tested individual has been consuming hay or has been grazing at pasture. Horses should be removed from pasture 2 hours before blood sampling. High variability between different pastures and hay sources regarding non-structural carbohydrate content affects basal insulin concentration and somewhat precludes the establishment of a universally reliable cut-off for diagnostic corroboration under different conditions. Blood obtained for insulin determination should not be sampled within 5 hours of grain feeding.
Given the aforementioned limitations, diagnosis of insulin dysregulation is supported by serum insulin concentrations >50 µU/mL (via radioimmunoassay and Immulite 1000 methods) and >75 µU/mL (Immulite 2000 xpi method). Serum insulin concentrations between 20 µU/mL and 50 µU/mL (radioimmunoassay and Immulite 1000 methods) or 30 µU/mL and 75 µU/mL (Immulite 2000 xpi method) should be interpreted as being suspicious for insulin dysregulation, but dynamic testing should be undertaken for confirmation. Low values for insulin concentration are non-diagnostic and do not reliably rule out diagnosis of insulin dysregulation.
Although acquisition of a single blood sample to screen for insulin dysregulation in either hayor pasture-fed horses is commonly undertaken, convenient, non-invasive and extremely practical, this diagnostic approach lacks sensitivity (many false negatives; horse with mild insulin dysregulation may not be hyperinsulinaemic at the time of testing). However, this approach enables detection of more severely affected horses with equine metabolic syndrome. Overall, dynamic testing is a superior diagnostic approach, with improved sensitivity.
Dynamic testing for insulin dysregulation
Dynamic tests fall into two broad categories: tests that evaluate insulin production in response to food, sugar or glucose that has been introduced into the gastrointestinal tract (true tests of the entero–insular axis), and tests that evaluate tissue sensitivity to insulin (looking for evidence of peripheral insulin resistance). Comprehensive endocrine characterisation of equine metabolic syndrome entails the use of both approaches.
Oral sugar test
The oral sugar test evaluates the insulinaemic response to a standardised dose of orally administered sugar, mimicking the enteroendocrine response to ingested food. This test protocol entails administration of sugar, typically as Karo Light Corn Syrup, using a dose syringe. Alternative syrups have been successfully used with similar results in other countries; for example, a Scandinavian glucose syrup (Dan Sukker, Nordic Sugar A/S, Copenhagen, Denmark) (Lindåse et al, 2016; Durham et al, 2019). Serum insulin concentration is measured before and at 60–90 minutes afterwards. Higher-than-normal serum insulin responses during the oral sugar test in horses with insulin dysregulation are associated with a risk of hyperinsulinaemia-associated laminitis, but are also influenced by gastrointestinal transit time, enzymatic degradation of sugars, intestinal glucose absorption, incretin hormone response, degree of pancreatic insulin release and the extent to which the liver removes secreted insulin from the circulation. Test results may be influenced by individual variations at each of these discrete steps in the entero–insular axis.
Up-to-date recommendations to help with assessment of oral sugar test outcomes are provided by the Equine Endocrinology Group and should be consulted. Different feeding/fasting, dosing and sampling protocols have been used since the oral sugar test was originally introduced. Evidence is emerging that outcomes of the oral sugar test differ between breeds, and breed-specific reference guidelines may eventually be needed (Bamford et al, 2014).
Typically, a small hay feeding (0.2–0.4 kg per 100 kg of body-weight) is provided for the horse in the evening and the test is undertaken on a relatively empty stomach the next morning following a brief 3–6-hour overnight fast. Serum insulin concentration is determined at 60 minutes following oral administration of the syrup (0.45 ml/kg of bodyweight). Using this protocol, elevated insulin concentrations >65 µIU/mL (radioimmunoassay method) or >63 µIU/mL (Immulite 2000 xpi method) are consistent with insulin dysregulation. Results of the oral sugar test are influenced somewhat by season but, overall, they are reliable in all seasons for confirmation of insulin dysregulation; reliance on only serum insulin concentration is less so (Macon et al, 2022).
Oral glucose test
The in-feed oral glucose (dextrose powder) test is a useful alternative to the oral sugar test, especially if commercial syrup products are unavailable. The patient is briefly fasted (as for an oral sugar test), improving the acceptance of the test dose and standardising gastric transit time. Glucose powder (0.5–1.0 g/kg of bodyweight) is mixed with a small quantity of a low-glycaemic meal such as chaff. Blood is sampled for insulin determination at 120 minutes following ingestion of glucose. Diagnosis of insulin dysregulation is supported by serum insulin concentration >68 µIU/mL (following glucose 0.5 g/kg dose) or >80–90 µIU/mL (following glucose 1.0 g/kg dose) (Immulite 1000 method). If the patient is compliant and does not require sedation (minimising stress), the dose of glucose (1.0 g/kg of bodyweight in 2 litres of water) may be administered via nasogastric intubation. The diagnostic cut off for this method is a serum insulin concentration >110 µIU/mL at 120 minutes (equine-optimised insulin ELISA method).
Insulin response test
This test provides direct information about peripheral tissue sensitivity to insulin, but does not directly address aspects of equine metabolic syndrome that involve the entero–insular axis. Tissue insulin insensitivity is generally referred to as ‘insulin resistance’ and is an important contributor to hyperinsulinaemia in some cases. Reduced tissue sensitivity to insulin develops gradually with age and may be worsened by the following comorbidities:
- Genetics/epigenetics
- Obesity
- Insufficient exercise
- Dietary factors (including starvation)
- Stress (hypercortisolism)
- Corticosteroid drugs (such as dexamethasone)
- Pregnancy
- Chronic disease states (inflammatory and neoplastic).
Tissue insensitivity to insulin also arises secondary to sufficiently protracted hyperinsulinaemia (any cause). This paradoxical change is a result of peripheral insulin receptor withdrawal and tissue desensitisation to insulin that results from increased insulin stimulation (Carpentier, 1994). Laboratory test approaches to measure insulin sensitivity include the euglycaemic hyperinsulinaemic clamp and the frequently sampled intravenous glucose tolerance test, neither of which are practical in the field. Therefore, a simplified, practical, test has been developed for this purpose: the 2-step insulin response test (Bertin and Sojka-Kritchevsky, 2013).
Pre-test fasting is not needed, and glucose measurements can be made using a glucometer at the premises, boosting test practicality. Blood glucose concentration is determined immediately before and at 30 minutes following administration of regular (human recombinant) insulin (Humulin, 0.1 U/kg of bodyweight intravenously). If used in insulin-sensitive individuals, signs of hypoglycaemia may arise during the protocol, so close monitoring is needed and a grain meal with hay is provided on conclusion of the test. Positive evidence of insulin insensitivity is inferred if the blood glucose concentration fails to decrease to <50% of the resting baseline level.
It cannot be overlooked that, for purposes of diagnostic testing, the administration of exogenous insulin or glucose to a potentially insulin-dysregulated individual could result in aggravation of underlying laminitis. The author's experience and anecdotal reports suggest that this complication is unlikely when testing is performed in stable patients (not exhibiting laminitis pain at the time of testing). However, albeit unlikely, this risk should be addressed with the patient's owner prior to testing.
Other diagnostic tests
Parallel testing for pituitary pars intermedia dysfunction should also be undertaken in older horses and ponies (>10 years of age) because treatment of pituitary pars intermedia dysfunction using pergolide mesylate should help offset hyperinsulinaemia and reduce the impact of insulin dysregulation in horses with both endocrinopathies. Measurement of the basal blood glucose concentration rarely provides useful information, as most horses with equine metabolic syndrome have hyperinsulinaemia with euglycaemia. Hyperglycaemia not explained by excitement at the time of sampling could indicate type 2 diabetes mellitus, a rare complication of equine metabolic syndrome (Durham et al, 2009).
Hypertriglyceridaemia may be evident, usually mildly, in some cases of equine metabolic syndrome. Marked hypertriglyceridaemia (>500 mg/dl) may arise in Miniature horses, Shetland ponies and donkeys affected with hyperlipemia syndrome (hepatic lipidosis), a potentially fatal complication of insulin dysregulation. Hyperleptinaemia and hypoadiponectinaemia may be present in horses with insulin dysregulation. Rather than being directly implicative for insulin dysregulation, hyperleptinaemia is more reflective of obesity. Both hyperleptinaemia and hypoadiponectinaemia likely promote and exacerbate hyperinsulinaemia-associated laminitis. Plasma concentrations of glucagon-like peptide-1 (activated form) and glucagon-like peptide-2 are elevated in some cases of equine metabolic syndrome. Accentuated incretin responses to ingested food may contribute to hyperinsulinaemia (de Laat and Fitzgerald, 2023). Commercially available laboratory tests for incretin hormones are not presently available. Used in the research setting, the combined glucose insulin tolerance test, frequently sampled intravenous glucose tolerance test and euglycaemic hyperinsulinaemic clamp methods are not typically used in clinical practice. Similarly, proxy measures of insulin sensitivity or the glucose:insulin ratio are not recommended for diagnosis of insulin dysregulation in individual horses.
There is increasing interest in evaluating the post-prandial insulin response to various types of provided feed instead of using oral sugar and glucose tests. Such an approach might prove to be both very practical and facilitate useful follow-up evaluations in response to treatments given (Macon et al, 2023).
Conclusions
There has been an explosion of new information regarding the pathophysiology, treatment and prevention of hyperinsulinaemia-associated laminitis throughout the antecedent decade. Research leading to much of this new information was provoked by the sentinel finding that insulin itself causes endocrinopathic laminitis, which is the most common form of laminitis. There have been remarkable advances in veterinary understanding regarding how insulin acts in order to cause laminitis, including the nutritional and endocrine mechanisms that lead to hyperinsulinaemia, information about how nutritional factors can be assessed and usefully adjusted to reduce the risk of hyperinsulinaemia-associated laminitis and in the treatment of acute laminitis. Diagnostic tests for equine metabolic syndrome are based on the demonstration of an insulin dysregulated state and optimisation of these testing approaches is an active area of investigation. Equine obesity is being reported at alarming rates, and failure to recognise, prevent and reverse obesity is a significant welfare issue for horses. Moreover, recognition that abnormal adipokine levels (a dysadipokinaemic state) are associated with both obesity and insulin dysregulation has led to novel diagnostic approaches to better characterise the extent of this common endocrine disease.
KEY POINTS
- Equine metabolic syndrome and obesity are being increasingly recognised in horses and ponies.
- Insulin dysregulation represents the underlying endocrinological abnormality and may be manifest by basal hyperinsulinaemia, post-prandial hyperinsulinaemia and/or tissue insulin resistance.
- Endocrinopathic laminitis, the most common type of laminitis, is a direct consequence of elevated insulin in susceptible (insulin dysregulated) horses and ponies.
- Practical and inexpensive diagnostic tests are available for the diagnostic corroboration of insulin dysregulation.