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Equine metabolic syndrome

American College of Veterinary Internal Medicine Reprinted in the IVIS website with the permission of the ACVIM ACVIM Consensus StatementJ Vet Intern Med 2010;24:467–475 Consensus Statements of the American College of Veterinary Internal Medicine (ACVIM) provide theveterinary community with up-to-date information on the pathophysiology, diagnosis, and treatment ofclinically important animal diseases. The ACVIM Board of Regents oversees selection of relevant topics,identification of panel members with the expertise to draft the statements, and other aspects of assuring theintegrity of the process. The statements are derived from evidence-based medicine whenever possible and thepanel offers interpretive comments when such evidence is inadequate or contradictory. A draft is preparedby the panel, followed by solicitation of input by the ACVIM membership, which may be incorporated intothe statement. It is then submitted to the Journal of Veterinary Internal Medicine, where it is edited prior topublication. The authors are solely responsible for the content of the statements.
E q u i n e M e t a b o l i c S y n d r o m e N. Frank, R.J. Geor, S.R. Bailey, A.E. Durham, and P.J. Johnson Key words: Adipokines; Hyperinsulinemia; Insulin resistance; Laminitis; Obesity; Regional adiposity.
The term equine metabolic syndrome (EMS) was first characterized by expansion of subcutaneous adipose introduced to veterinary medicine in 2002 when tissues surrounding the nuchal ligament in the neck Johnson1 proposed that obesity, insulin resistance (IR), (cresty neck), development of fat pads close to the tail and laminitis were components of a clinical syndrome head, or fat accumulation behind the shoulder or in recognized in horses and ponies. The study of EMS is the prepuce or mammary gland region. Obesity is ob- therefore in its infancy, so the following consensus state- served in the majority of cases, but some affected ment reflects our current knowledge of this condition.
equids have a leaner overall body condition and re- We anticipate that defining features of the EMS pheno- gional adiposity, and others are normal in appearance.
type, approaches to diagnostic testing, and management These different phenotype variations require further options will be expanded and updated as further research  IR characterized by hyperinsulinemia or abnormal ‘‘EMS’’ was adopted as the name for this condition glycemic and insulinemic responses to oral or IV glu- because of similarities with the metabolic syndrome (MetS) in humans, which is a collection of risk factors  A predisposition toward laminitis. Clinical or subclin- assessed to predict the occurrence of coronary artery dis- ical laminitis that has developed in the absence of ease and type 2 diabetes mellitus in people.2 Despite recognized causes such as grain overload, colic, colitis, alternative nomenclature having been proposed previ- ously (eg, peripheral Cushing’s syndrome, prelaminiticmetabolic syndrome), it was the unanimous decision of Additional components of the EMS phenotype that the consensus panel to support the use of the term EMS because it has gained wide acceptance and is appropriatewhen used to define a clinical syndrome unique to equids.
 Hypertriglyceridemia or dyslipidemia as a component The panel proposed that the EMS phenotype for the ma- of EMS in some cases.3–5 Increased very low-density jority of affected equids should include: lipoprotein triglyceride concentrations have also beendetected in horses with EMS.5  Increased adiposity in specific locations (regional adi-  Hyperleptinemia resulting from increased secretion of posity) or generally (obesity). Regional adiposity is the hormone leptin by adipocytes in response to IR ora state of leptin resistance.6 Leptin is referred to as asatiety factor because it signals the hypothalamus that From the Department of Large Animal Clinical Sciences, Univer- sity of Tennessee, Knoxville, TN and School of Veterinary Medicine a state of energy excess exists within adipose tissues.7 and Science, University of Nottingham, Sutton Bonington, UK  Arterial hypertension4,8 detected in the summer in la- (Frank); and the Department of Large Animal Clinical Sciences, minitis-prone ponies,8 which is recognized as a key College of Veterinary Medicine, Michigan State University, East component of MetS related to IR in humans.9 Lansing, MI (Geor); and the Faculty of Veterinary Science, Univer-  Altered reproductive cycling in mares. Loss of the sea- sity of Melbourne, Victoria, Australia (Bailey); and the Liphook sonal anovulatory period10 and prolongation of the Equine Hospital, Forest Mere, Liphook, UK (Durham); and the De- interovulatory period11 have been described in obese partment of Veterinary Medicine and Surgery, College of VeterinaryMedicine, University of Missouri, Columbia, MO (Johnson).
Corresponding author: Nicholas Frank, Department of Large An-  Increased systemic markers of inflammation in associ- imal Clinical Sciences, University of Tennessee, Knoxville, TN; Submitted February 3, 2010; Revised February 18, 2010; Copyright r 2010 by the American College of Veterinary Internal Contributing factors for obesity should be assessed from the history, including the quantity of feed provided, size and quality of the pasture, and amount of exercise.
efficiency with respect to the utilization of dietary energy.
Horse owners sometimes refer to affected horses and po- In this context, it has been suggested that horses and po- nies as ‘‘easy keepers’’ or ‘‘good doers’’ because they nies evolutionarily adapted to survival in nutritionally require a lower plane of nutrition to maintain body sparse environments are especially predisposed to obesity and IR under modern management conditions in which Previous episodes of laminitis may be described in the plentiful feed is available year round. For example, feral history. Mild episodes of bilateral laminitis may have and native pony breeds retain strong seasonality with re- been mistakenly attributed to sole bruising, arthritis, or spect to appetite and body condition. Under ‘‘feral’’ foot soreness after trimming or shoeing. If laminitis ep- conditions these ponies gain weight during the summer isodes have been recognized in the past, it should be months when food is abundant before losing it again dur- noted whether the onset of lameness was associated with ing the winter.a Seasonal changes in insulin sensitivity also changes in the abundance or composition of pasture may occur, reflecting alterations in food availability, phys- grass, or alterations in grain feeding.
ical activity, and body condition. Season affected resting Familial patterns have been recognized for EMS,3 so serum insulin concentrations in 1 study of obese mares, relevant information about the horse’s dam and sire with higher concentrations detected in December, com- should be collected for future reference.
pared with September, October, and November.11 In thecontext of domesticated equids experiencing a chronic state of overnutrition, these seasonal changes in body con-dition and insulin sensitivity may be replaced by Clinical signs of EMS include regional adiposity, obe- progressive obesity and IR with associated adverse health sity, bilateral lameness attributable to laminitis, and/or consequences. More research is required to identify the evidence of previous laminitis such as divergent growth genetic determinants of metabolic efficiency in horses and rings on the hooves. A cresty neck score13 has been de- the effects of environmental factors such as overnutrition veloped to assess the expansion of adipose tissues within the neck region and scores range from 0 to 5. Scores 3 Adipose tissue is no longer regarded as just an energy are often detected in horses or ponies with EMS. The de- storage organ, but an endocrine organ producing many scription provided for a score of 3 is ‘‘Crest enlarged and hormones (adipokines or adipocytokines).15 Adipose tis- thickened, so fat is deposited more heavily in middle of sue dysfunction (with or without obesity) is an important the neck than toward poll and withers, giving a mounded pathophysiologic feature of MetS in humans that may appearance. Crest fills cupped hand and begins losing result in IR, systemic inflammation, hypertension, and a side-to-side flexibility.’’ Neck circumference can also be prothrombotic status. Adipokines are released from ad- measured at the midpoint of the neck with a tape mea- ipocytes and other cells within fat tissues. They include sure. This measurement is taken halfway between the leptin, resistin, adiponectin, visfatin, and apelin as well as poll and the withers when the neck is in a normal elevated inflammatory cytokines released from macrophages and position.5 The neck circumference-to-height at withers adipocytes such as tumor necrosis factor alpha (TNFa), ratio was recently used to predict the development of interleukins 1 (IL-1) and 6 (IL-6), and macrophage pasture-associated laminitis in ponies and a cut-off value chemoattractant protein 1. The inflammatory adipokines of 40.71 was established. Body weight should be mea- may then lead to a self-perpetuating cycle of enhanced sured with a scale or weight tape and body condition adipose tissue inflammation, adipokine synthesis, and scoring14 can be used to assess generalized obesity.
secondary acute phase protein synthesis by the liver.
Thus obesity in people is characterized by a state ofchronic low-grade inflammation.15 Few data are available on the pathophysiological EMS is a complex disorder for which there are more effects of obesity or regional adiposity in EMS. Obesity questions than answers at present. The principal compo- has been associated with reduced insulin sensitivity in nents of EMS are increased adiposity, IR, and laminitis, horses and ponies,3,5,10,11,16 although some obese horses but this syndrome likely encompasses a much wider spec- have normal insulin sensitivity. Whether obesity induces trum of problems that affect energy metabolism, perturb IR or the insulin-resistant horse is more predisposed to adipocyte function, promote thrombosis, induce inflam- obesity has not been determined. Further contributory mation and oxidant stress, and alter vascular endothelial factors to obesity and IR may include altered cortisol metabolism within tissues1 or leptin resistance, a situa-tion in which tissues fail to respond to leptin.7 In humans, mesenteric and omental adipose tissues are thought to play a more important role in the develop- Environmental (eg, diet, level of physical activity, sea- ment of type 2 diabetes mellitus than adipose tissues son) and intrinsic (eg, genetics) factors will affect body fat elsewhere because fatty acids and adipokines released mass. The mechanisms underlying generalized obesity or from these visceral sites enter the portal circulation regional adiposity in EMS are unknown but chronic over- and have a more profound effect on hepatic metabolism feeding in association with limited physical activity and insulin clearance.17 This situation is currently being appears to be a contributing factor. Additionally, horses examined in horses to determine whether adipose tissue and ponies with EMS appear to have enhanced metabolic from the neck crest or abdomen differs from tissues collected from other locations, but results have not yet To the panel’s knowledge, there are no published stud- ies on the epidemiology of EMS although there are a few reports on the prevalence of obesity and hyper-insulinemia in populations of ponies and horses.30,b,c,d IR involves defects of insulin signaling such as reduced Anecdotally, Welsh, Dartmoor, and Shetland ponies and insulin receptor tyrosine kinase activity and reduced Morgan Horse, Paso Fino, Arabian, Saddlebred, Span- postreceptor phosphorylation steps that impinge on met- ish Mustang, and warmblood breeds appear to be more abolic and vascular effects of insulin.18 There are two susceptible to EMS. However, the panel emphasized that primary theories linking obesity to IR: (1) the down-reg- EMS can be prevented through good management ulation of insulin signaling pathways induced by practices, so breed susceptibility should be viewed ac- adipokines and cytokines produced in adipose tissue; cordingly. EMS also occurs in other light horse breeds, and (2) the accumulation of intracellular lipids in insu- including Quarter Horses and Tennessee Walking lin-sensitive tissue such as skeletal muscle (lipotoxicity).19 Horses, but is rarer in Thoroughbreds and Standardb- The natural equine diet contains little fat, but excess glu- reds. Miniature horses, donkeys, and draft horses require cose can be converted into fat via de novo lipogenesis.
further study to determine the prevalence of EMS in Fats are used for energy or stored as triglyceride within cells. When the storage capacity of adipose tissues is ex- Susceptibility to EMS may be established from before ceeded, fats are directed toward nonadipose tissues birth, and obesity develops in some horses as soon as (repartitioning). Skeletal muscle, liver, and pancreatic they reach maturity. However, most horses with EMS tissues attempt to utilize fats by increasing b-oxidation, are between 5 and 15 years of age when veterinary or far- but lipid can accumulate within these tissues and alter rier services are first requested because of laminitis.
normal cellular functions, including insulin signaling.
A seasonal pattern has been identified for laminitis in the United States, with the highest incidence of pasture laminitis around May and June (late spring/early sum-mer).3,31 This seasonal rise in laminitis incidence has been We are limited at present to the knowledge that IR attributed to increased nonstructural carbohydrate and/or hyperinsulinemia predispose ponies to pasture- (NSC) consumption from pasture forage. In the United associated laminitis and that the condition can be exper- Kingdom, the highest incidence of pasture laminitis was during the summer (June and July), when sunshine amounts of insulin IV over 2–3 days.3,20 Potential mech- hours and presumably forage NSC content were great- anisms relating obesity, hyperinsulinemia, and IR to est.e This observation provides further circumstantial laminitis are largely extrapolated from studies in other evidence to suggest a link between grass carbohydrate species and include endothelial cell dysfunction within content and laminitis incidence. Serum insulin concen- blood vessels of the foot,21 digital vasoconstriction,22 im- trations and the reciprocal inverse square of insulin paired glucose uptake by epidermal laminar cells,23 proxy estimate of insulin sensitivity measured in ponies altered epidermal cell function or mitosis,24and matrix predisposed to laminitis suggested a decrease in insulin metalloproteinase activation by glucose deprivation or sensitivity during summer, and this was attributed to changes in pasture carbohydrate composition.8 Results Insulin has vasoregulatory actions and it was the con- suggested that aspects of the EMS phenotype in ponies sensus of the panel that this represents a plausible link may be latent under conditions of lower or restricted di- between IR and laminitis in horses. Vasodilation nor- etary water-soluble carbohydrate (WSC) content, but mally occurs in response to insulin through the increased become apparent when carbohydrate intake increases.
synthesis of nitric oxide (NO) by endothelial cells.25,26 Pasture carbohydrate content and climate/seasonal ef- However, insulin may also promote vasoconstriction by fects are inextricably linked. During periods of high stimulating the synthesis of endothelin-1 (ET-1)26 and sunshine, when sugars are produced in excess of the activating the sympathetic nervous system.27 Activation energy requirement of the pasture for growth and of the insulin receptor stimulates at least two different development, they are converted into storage, or reserve, signaling pathways within the vascular endothelial cell.28 carbohydrates, such as fructans and starches.32 NO is secreted when the phosphatidylinositol 3-kinase(PI3K) pathway is activated, whereas activation of themitogen-activated protein kinase (MAPK) pathway leads to the release of ET-1. IR states in humans havebeen found to involve selective pathway inhibition such EMS can be diagnosed by obtaining a complete that the NO synthetic PI3K pathway is inhibited whereas history, performing a physical examination, taking the MAPK pathway is unaffected and may be overstim- radiographs of the feet, and conducting laboratory tests.
ulated because of compensatory hyperinsulinemia, which Physical examination should include assessment of the results in increased ET-1 synthesis.25,29 Vasoconstriction horse for evidence of regional adiposity, including adi- may therefore be promoted in the insulin-resistant ani- pose tissue expansion within the neck crest, and body mal as NO production decreases, which might impair the condition scoring. Current screening tests for IR focus ability of vessels to respond to vascular challenges.
upon the measurement of glucose and insulin concentra- tions in single blood samples, although dynamic tests are under the curve values provide the best measure of glu- necessary to properly assess insulin sensitivity. An im- cose tolerance, although the peak concentration and time portant goal for the future is the development of a panel taken for concentrations to return to baseline can also be evaluated. The combined glucose-insulin test (CGIT) de- Hyperglycemia is rarely detected in horses with EMS veloped by Eiler et al37 can also be used to diagnose IR in because most animals maintain an effective compensa- horses.5 Insulin is injected immediately after dextrose to tory insulin secretory response in the face of IR.
lower blood glucose concentrations. Advantages of the However, blood glucose concentrations are often toward CGIT include the shorter time required for testing and the higher end of reference range indicating partial loss of information gained about both the glycemic and insulin- glycemic control. If persistent hyperglycemia is detected, emic responses. A CGIT is performed by first obtaining a a diagnosis of diabetes mellitus should be considered.
preinjection blood sample for baseline glucose and insu- Type 2 diabetes mellitus occurs in horses and may be lin measurements, and then injecting 150 mg/kg body more common than thought previously.33 This diagnosis weight (bwt) 50% dextrose solution IV, immediately fol- should be considered when hyperglycemia cannot be at- lowed by 0.10 U/kg bwt regular insulin IV.37 These tributed to other causes such as stress, recent feeding, dosages are equivalent to 150 mL of 500 mg/mL (50%) administration of a-2 agonist drugs, or inflammatory dextrose and 0.50 mL of 100 U/mL insulin for a horse weighing 500 kg. Insulin should be drawn into a tubercu- Hyperinsulinemia in the absence of confounding fac- lin syringe and then transferred into a larger syringe tors such as stress, pain, and a recent feed provides containing 1.5-mL sterile saline (0.9% NaCl) before in- evidence of IR in horses and ponies. However, resting jection. Blood glucose concentrations are measured at 1, insulin concentrations are not found to be increased in all 5, 15, 25, 35, 45, 60, 75, 90, 105, 120, 135, and 150 min- cases, so dynamic testing provides the most accurate di- agnosis of IR. It should also be recognized that reference When the CGIT is performed in healthy animals, ranges vary among laboratories, in part because of differ- blood glucose concentrations return to below the base- ences in the assay used. More research is required to line value by 45 minutes, so preliminary results are determine cut-off values for hyperinsulinemia, but a available within 1 hour if a glucometer is used. Blood value of 20 mU/mLf is suggested as a general guideline collected at 0 and 45 minutes is submitted for insulin as- for the upper limit of serum/plasma insulin concentra- say and this allows the insulin response to be evaluated.
Horses with insulin concentrations 4100 mU/mL at 45 Sampling conditions are important when diagnosing minutes are secreting more insulin than normal and/or the chronic IR associated with EMS. Cortisol and epi- clearing the hormone from the circulation at a slower nephrine released as a result of pain or stress lower tissue rate. This is interpreted as an indication of IR. The test insulin sensitivity and raise resting glucose and insulin can be abbreviated to 60 minutes when used in the field, concentrations.34,35 Insulin concentrations are likely to but it is advisable to complete all of the measurements so be higher in a horse that is currently suffering from la- that the horse’s complete response can be recorded for minitis, so testing should be delayed until after the pain future comparison. Hypoglycemia is a potential compli- and stress of this condition has subsided. Blood samples cation of testing, although this is rarely encountered in should be collected after an approximately 6-hour period the patients selected for testing. If clinical signs of hypo- of feed withholding, ideally between 8:00 and 10:00 AM.
glycemia (sweating, weakness, and muscle fasciculation) These conditions can be achieved by providing not more are recognized or if blood glucose concentrations fall be- than 1 flake of low-NSC grass hay per 500 kg bodyweight low 40 mg/dL (2.2 mmol/L), administer 60 mL of 50% no later than 10:00 PM the night before sampling. Under dextrose IV and repeat as necessary.
these conditions, hyperinsulinemia (420 mU/mL) pro- In addition to glucose, it has been found that feeding vides evidence of IR. If hyperinsulinemia is not detected, some other carbohydrates to ponies induces an exaggerated but other components of the EMS phenotype are recog- insulin response in IR individuals. These carbohydrates nized, a dynamic test of insulin sensitivity should be include inulin, a type of fructan carbohydrate.38 Further- more, the administration of dexamethasone also elicits this Dynamic testing for evaluation of insulin sensitivity is exaggerated insulin response.5 These observations may recommended because tissue insensitivity to insulin may have implications for the likely causes of hyperinsulinemia only be revealed when glycemic control is challenged by in horses or ponies with EMS that are grazing on pasture, inducing hyperglycemia. A number of tests can be used putting them at risk of laminitis. These tests require further for this purpose, and an ideal test for diagnosing IR in horses has not been established to date.36 Testing should Future directions for diagnostic testing include the de- be conducted under the same conditions as blood sam- velopment of a test panel consisting of assays that can be pling for resting glucose and insulin measurements.
performed on a single blood sample. Such a panel might Horses must be tested after the pain and stress of lamini- further include the adipokines leptin, adiponectin, and tis has subsided, and after an approximately 6-hour fast resistin, lipids such as triglyceride and nonesterified fatty to limit confounding effects of recent feed consumption.
acids, fructosamine as a reflection of blood glucose con- Oral or IV glucose tolerance tests can be performed to centrations,39 and measures of systemic inflammation raise blood glucose and insulin concentrations and deter- including TNFa, IL-1, IL-6, C-reactive protein, serum mine the height and width of the resulting curve. Area amyloid A, and plasminogen activator inhibitor-1. Red blood cell count, PCV, iron concentration, and plasma specific hormones responsible for IR in these PPID gamma glutamyl transferase (GGT) activity might also be included on the panel. Anemia is sometimes detected 3. Are the effects of PPID on insulin sensitivity depen- in EMS horses, and some affected horses have shown elevated GGT activity that has corresponded with 4. Does EMS represent a risk factor for PPID? hepatic lipidosis, detected in biopsy and necropsy speci-mens. Pancreatic insulin secretion may be assessed by The consensus panel recognized that some equids with measuring serum connecting peptide (C-peptide) concen- EMS subsequently develop PPID, so both conditions can trations. This peptide is released in equimolar amounts occur concurrently. Anecdotal reports suggest that with insulin, but is not cleared from the blood by the horses and ponies with EMS are predisposed to PPID liver.40 Approximately 60% of the insulin secreted by the and pituitary dysfunction develops at a younger age in pancreas is extracted from the portal blood by the liver in affected animals. Further research is required in this healthy humans, so hyperinsulinemia can develop as a area, but the panel recommends that equids with EMS result of reduced insulin clearance and/or increased pan- be closely monitored for clinical signs of PPID and un- creatic secretion. Serum C-peptide concentrations can dergo regular testing for the condition. If PPID is causing indicate the relative contributions of these processes. Re- and/or exacerbating IR, treatment should improve insu- cent research suggests that reduced insulin clearance lin sensitivity. Pergolide is recommended for the significantly contributes to hyperinsulinemia in horses with EMS,41 so the C-peptide-to-insulin ratio may beuseful to further characterize the hyperinsulinemia Dietary management of EMS involves reducing the amount of energy provided in the diet to induce weight loss if the horse or pony is obese and lowering the NSC content of the diet to reduce glycemic and insulinemic responses to meals. Reducing the digestible energy (DE)content of the diet is an important factor in moderating Regional adiposity and laminitis are clinical signs of obesity as a contributory factor to EMS. Limiting or PPID as well as EMS,42 so both endocrine disorders eliminating pasture grass from the diet is a key compo- should be considered when these problems are detected.
nent of this approach because pasture grazing provides DE that cannot be quantified. Obese horses and ponies should be provided a forage diet with mineral/vitamin Age of onset: The EMS phenotype is generally first supplementation. Hay with low NSC content should be recognized in younger horses, whereas PPID is more selected, which can be determined by submitting a sam- common in older horses; although these disorders may ple for analysis or by purchasing forage with a declared nutrient analysis. Simple sugars, starches, and fructans Further clinical signs suggestive of PPID, but not are NSC, whereas cellulose and hemicelluloses are struc- EMS, including delayed or failed shedding of the win- tural carbohydrates.32 It was thought previously that ter haircoat, hirsutism, excessive sweating, polyuria/ fructans undergo minimal hydrolysis until they reach polydipsia, and skeletal muscle atrophy.42 the large intestine of the horse, so they would be less Positive diagnostic test results for PPID: For example, likely to contribute to the glycemic response after a meal.
detection of an increased plasma adrenocorticotropin However, there is some evidence indicating that there hormone concentration in the absence of confounding may be appreciable microbial and acid hydrolysis of factors such as pain and stress, and outside of the late fructans before they reach the equine large intestine.32 summer/autumn period when false positive results oc- Furthermore, insulin-resistant ponies exhibit an insulin response to dietary fructans.38 It is therefore recom-mended that NSC be calculated by adding starch and Reduced glucose tolerance indicative of IR has also WSC percentages together, and this value should ideally been detected in horses with PPID.43 However, it was the fall below 10% of dry matter when feeding horses or po- consensus of the panel that normal insulin sensitivity is nies with EMS. Hay can be soaked in cold water for 60 more common in horses with PPID, which suggests that minutes to lower the WSC content if the amount of NSC the relationship between these conditions is complex.
exceeds 10%.44 However, a recent study demonstrated Discussion of this subject generated several questions that results vary markedly among different hay sam- that require further research, including: ples,45 so this strategy cannot be relied upon tocompletely address the problem of high WSC concentra- 1. Does IR only accompany PPID when the animal was tions in the hay that is being fed to a horse or pony with insulin resistant before pituitary dysfunction devel- oped? If this is the case, PPID may exacerbate IR, but Weight loss should be induced in obese horses by re- stricting the total number of calories consumed and by 2. If PPID causes IR in some horses, but not others, is increasing the individual’s level of physical activity. In this a particular manifestation of the disorder? Are horses that are being overfed, removal of all concentrates from the diet is sometimes sufficient to induce weight ration can be increased by feeding soaked beet pulp loss. An obese horse should be placed on a diet consisting shreds (nonmolassed) or vegetable oil. The latter can be of hay fed in an amount equivalent to 1.5% of ideal body mixed with beet pulp or with hay cubes that have been weight (1.5 lb hay per 100 lb bwt). Hay should be weighed soaked in water. Corn and soy oils are commonly used in on scales to ensure that correct amounts are fed. If an equine rations; 1 standard cup (225 mL or 210 g) of obese horse or pony fails to lose weight after hay has vegetable oil provides 1.7 Mcal (7.1 MJ) of DE. Depend- been fed at an amount equivalent to 1.5% of ideal body ing on energy requirements, 1/2 to 1 cup of oil can be fed weight for 30 days, this amount should be lowered to 1%.
once or twice daily. Smaller amounts (eg, 1/4 cup once However, amounts should not fall below this minimum daily) should initially be fed, with a gradual increase over of 1% and it should be noted that severe calorie restric- a 7- to 10-day period. With all of these strategies, the goal tion may lead to worsening of IR, hyperlipemia, and is to lower the glycemic and insulinemic response to the unacceptable stereotypical behaviors.
meal, which is the degree to which blood glucose and in- Pasture access should be eliminated until insulin sensi- sulin concentrations rise in response to the feed. Further tivity has improved because carbohydrates consumed on information regarding the dietary management of obe- pasture can trigger gastrointestinal events that lead to la- sity and IR in equids is provided in a recent review.49 minitis in susceptible horses.46 Mildly affected horses canreturn to pasture once obesity and IR have been ad- dressed, but care must be taken to restrict pasture accesswhen the grass is going through dynamic phases, such as Regular physical exercise is an effective therapeutic rapid growth in the spring or preparation for cold weather intervention to improve insulin sensitivity in obese in the fall. Measurement of pasture grass NSC content at insulin-resistant people. An exercise prescription of ap- different times of the day has revealed that grazing in the proximately 200 minutes per week of moderate intensity early morning is likely to be safer for horses with IR, ex- exercise results in a sustained increase in insulin sensitiv- cept after a hard frost when grasses accumulate WSC.47 ity50,51 and improvements in other risk factors (eg, lipid Other risk factors for high fructan content include regular profile) that are criteria for MetS.52 Furthermore, im- cutting, cool, and bright conditions and predominance of provements in insulin sensitivity associated with physical certain grass species such as ryegrass.32,48 Strategies for activity can occur in the absence of weight loss or change limiting grass consumption include short (o1 hour) turn- in fat distribution.53 Therefore, subject to the status of out periods (or hand-grazing), confinement in a small foot pain and structural damage, an increase in physical paddock, round pen, or area enclosed with electric fence, activity is recommended for equids with EMS in order to or use of a grazing muzzle. Horses and ponies with EMS promote weight loss and improve insulin sensitivity.54,55 can have rapid rates of grass intake, so 41–2 hours graz- More research is required to determine an optimal exer- ing may be excessive for these animals.32 Unfortunately, cise prescription for management of EMS, but a general severely insulin-resistant horses that suffer from recurrent recommendation is to start with 2–3 exercise sessions per laminitis must be kept off pasture permanently. These pa- week (riding and/or longeing), 20–30 minutes per session.
tients should be housed in dirt paddocks so that they are Subsequently, there should be a gradual increase in the able to exercise once hoof structures have stabilized. For- intensity and duration of exercise, for example, building to age only diets will not provide adequate protein, minerals, or vitamins. Supplementing the forage diet with a low-ca-lorie commercial ration balancer product that contains sources of high-quality protein and a mixture of vitaminsand minerals to balance the low vitamin E, vitamin A, Most horses and ponies with EMS can be effectively copper, zinc, selenium, and other minerals typically found managed by controlling the horse’s diet, instituting an ex- in mature grass hays is therefore recommended. These ercise program, and limiting or eliminating access to products are designed to be fed in small quantities (eg, pasture. Many studies have revealed that IR in human subjects is controlled most effectively by changes in life- Insulin-resistant horses with a thinner overall body style and diet although these strategies may fail due to lack condition are challenging to manage from a dietary of self-discipline.56 Similarly, compliance of the owner/ standpoint because hay alone may not meet energy re- manager is critical to the success of management changes quirements. Commercial low-NSC feeds are available for designed to alleviate risk factors for laminitis in EMS.
use in these situations in which digestible fibers (beet pulp Pharmaceutical products used to treat IR and type 2 or soya hulls) and/or vegetable oils are included in place diabetes mellitus in humans primarily include insulin of starch-rich ingredients. The energy density (ie, DE per sensitizers comprising metformin (a biguanide) and kg) of these feeds is variable depending on composition, so energy requirements and the severity of IR must be and insulin secretagogues comprising sulphonylureas taken into account before feed selection. It is also better (glyburide [glibenclamide], glipizide and glimepiride), to divide the daily ration into multiple small meals and to repaglinide (a benzoic acid derivative), and nateglinide feed hay beforehand as this may slow the rate of feed in- (a phenylalanine derivative).57 In horses, only levothy- take and gastric emptying and minimize postfeeding roxine sodium and metformin have thus far received any increases in the circulating concentrations of both glu- attention in the context of medical management of IR cose and insulin. Alternatively, the energy density of the b McGowan CM, Geor R, McGowan TW. Prevalence and risk fac- tors for hyperinsulinemia in ponies. J Vet Intern Med 2008; 22:734 Weight loss can be induced and insulin sensitivity im- proved by administering levothyroxine sodium to c Muno J, Gallatin L, Geor RJ, et al. Prevalence and risk factors for horses.58–60 Levothyroxine sodium is given to horses hyperinsulinemia in clinically normal horses in central Ohio. J Vet and larger (4350 kg) ponies at a dosage of 48 mg/day in the feed for 3–6 months at the same time that diet and d Thatcher C, Pleasant R, Geor R, et al. Prevalence of obesity in exercise interventions are initiated. Smaller ponies and mature horses: an equine body condition study. The American Miniature horses are given 24 mg levothyroxine sodium Academy of Veterinary Nutrition 7th Annual Clinical Nutrition per day for the same time period. Treated horses should and Research Symposium, Seattle, WA. 2007;6 (abstract) e Katz L, DeBrauwere N, Elliott J, et al. A retrospective epidemio- be weaned off levothyroxine sodium once ideal body logical study of laminitis in one region of the UK. Proceedings of weight has been attained by reducing the dosage to the 40th British Equine Veterinary Association Congress, Harro- 24 mg/day for 2 weeks and then 12 mg/day for 2 weeks.
Serum tT4 concentrations often range between 40 and f Measured by Coat-A-Count insulin radioimmunoassay (Siemens 100 ng/mL in treated horses, indicating that levothyrox- Medical Solutions Diagnostics, Los Angeles, CA), Immulite ine sodium is being given at a supraphysiological dosage.
insulin solid-phase chemiluminescent assay (Siemens Medical However, clinical signs of hyperthyroidism such as ema- Solutions Diagnostics), or DSL-1600 insulin radioimmunoassay ciation, sweating, tachycardia, or tachypnea have not (Diagnostic Systems Laboratory Inc, Webster, TX) been observed in treated horses.58,61,62 Benefits of treat- Donaldson MT, McDonnell SM, Schanbacher BJ, et al. Variation ing horses with levothyroxine at lower dosages for longer in plasma ACTH concentration and dexamethasone suppressiontest results in association with season, age, and sex in healthy po- periods have not been evaluated scientifically.
nies and horses. J Vet Intern Med 2004;18:414 (abstract) Positive responses to metformin have been reported in hyperinsulinemic horses and ponies at a dosage of15 mg/kg twice daily PO.63 Insulin sensitivity estimated by proxy measures improved in treated animals, with-out the adverse effect of hypoglycemia. Metformin is a 1. Johnson PJ. The equine metabolic syndrome peripheral Cush- biguanide drug that enhances the action of insulin ing’s syndrome. Vet Clin North Am Equine Pract 2002;18:271–293.
within tissues at the postreceptor level most likely by 2. Fulop T, Tessier D, Carpentier A. The metabolic syndrome.
promoting AMP-dependent protein kinase.64 Inhibi- Pathol Biol (Paris) 2006;54:375–386.
tion of gluconeogenesis and glycogenolysis within the 3. Treiber KH, Kronfeld DS, Hess TM, et al. Evaluation of ge- liver appears to be its main mode of action along with netic and metabolic predispositions and nutritional risk factors forpasture-associated laminitis in ponies. J Am Vet Med Assoc many other insulin- and noninsulin-related effects.65 Results of this first study look promising, but safety 4. Carter RA, Treiber KH, Geor RJ, et al. Prediction of incipient studies have not been performed to date in horses, so this must be considered before the drug is prescribed rleptinaemia and generalised and localised obesity in a cohort of long term. Results of recent pharmacokinetic studies ponies. Equine Vet J 2009;41:171–178.
indicate that oral bioavailability of metformin is lower 5. Frank N, Elliott SB, Brandt LE, et al. Physical characteristics, in horses than humans.66,67 Efficacy might therefore be blood hormone concentrations, and plasma lipid concentrations in improved by further investigation of appropriate dos- obese horses with insulin resistance. J Am Vet Med Assoc 6. Cartmill JA, Thompson DL Jr., Storer WA, et al. Endocrine responses in mares and geldings with high body condition scores grouped by high vs. low resting leptin concentrations. J Anim Sci Chromium, magnesium, cinnamon, and chasteberry (Vitex agnus-castus) are commonly recommended for the 7. Houseknecht KL, Spurlock ME. Leptin regulation of lipid homeostasis: Dietary and metabolic implications. Nutr Res Rev management of EMS. It was the consensus of the panel that there is insufficient scientific evidence to support the 8. Bailey SR, Habershon-Butcher JL, Ransom KJ, et al. Hyper- use of these supplements at this time and that results of tension and insulin resistance in a mixed-breed population of ponies controlled studies should be examined before these prod- predisposed to laminitis. Am J Vet Res 2008;69:122–129.
9. Lamounier-Zepter V, Ehrhart-Bornstein M, Bornstein SR.
Insulin resistance in hypertension and cardiovascular disease. BestPract Res Clin Endocrinol Metab 2006;20:355–367.
10. Gentry LR, Thompson DL Jr., Gentry GT Jr., et al. The re- lationship between body condition, leptin, and reproductive and hormonal characteristics of mares during the seasonal anovulatoryperiod. J Anim Sci 2002;80:2695–2703.
a Dugdale AHA, Curtis GC, Knottenbelt DC, et al. Changes in 11. Vick MM, Sessions DR, Murphy BA, et al. Obesity is asso- body condition and fat deposition in ponies offered an ad libitum ciated with altered metabolic and reproductive activity in the mare: chaff-based diet. 12th Congress on the European Society for Vet- Effects of metformin on insulin sensitivity and reproductive cyclic- erinary Clinical Nutrition, Vienna, Austria. 2008;39 (abstract) ity. Reprod Fertil Dev 2006;18:609–617.
12. Vick MM, Adams AA, Murphy BA, et al. Relationships 36. Firshman AM, Valberg SJ. Factors affecting clinical among inflammatory cytokines, obesity, and insulin sensitivity in assessment of insulin sensitivity in horses. Equine Vet J 2007;39: the horse. J Anim Sci 2007;85:1144–1155.
13. Carter RA, Geor RJ, Burton Staniar W, et al. Apparent ad- 37. Eiler H, Frank N, Andrews FM, et al. Physiologic assess- iposity assessed by standardised scoring systems and morphometric ment of blood glucose homeostasis via combined intravenous measurements in horses and ponies. Vet J 2009;179:204–210.
glucose and insulin testing in horses. Am J Vet Res 2005;66:1598– 14. Henneke DR, Potter GD, Kreider JL, et al. Relationship between condition score, physical measurements and body fat per- 38. Bailey SR, Menzies-Gow NJ, Harris PA, et al. Effect of di- centage in mares. Equine Vet J 1983;15:371–372.
etary fructans and dexamethasone administration on the insulin 15. Rasouli N, Kern PA. Adipocytokines and the metabolic response of ponies predisposed to laminitis. J Am Vet Med Assoc complications of obesity. J Clin Endocrinol Metab 2008;93:S64– 39. Murphy D, Reid SW, Graham PA, et al. Fructosamine mea- 16. Van Weyenberg S, Hesta M, Buyse J, et al. The effect of surement in ponies: Validation and response following experimental weight loss by energy restriction on metabolic profile and glucose cyathostome infection. Res Vet Sci 1997;63:113–118.
tolerance in ponies. J Anim Physiol Anim Nutr (Berlin) 2008;92: 40. Wilcox G. Insulin and insulin resistance. Clin Biochem Rev 17. Santosa S, Jensen MD. Why are we shaped differently, and 41. Toth F, Frank N, Martin-Jime´nez T, et al. Measurement why does it matter? Am J Physiol Endocrinol Metab 2008;295: of C-peptide concentrations and responses to somatostatin, glucose infusion, and insulin resistance in horses. Equine Vet J 18. Kashyap SR, Defronzo RA. The insulin resistance syn- drome: Physiological considerations. Diab Vasc Dis Res 2007;4: 42. Schott HC II. Pituitary pars intermedia dysfunction: Equine Cushing’s disease. Vet Clin North Am Equine Pract 2002;18:237– 19. Summers SA. Ceramides in insulin resistance and lipotoxic- ity. Prog Lipid Res 2006;45:42–72.
43. Garcia MC, Beech J. Equine intravenous glucose tolerance 20. Asplin KE, Sillence MN, Pollitt CC, et al. Induction of la- test: Glucose and insulin responses of healthy horses fed grain or minitis by prolonged hyperinsulinaemia in clinically normal ponies.
hay and of horses with pituitary adenoma. Am J Vet Res 21. Jansson PA. Endothelial dysfunction in insulin resistance 44. Cottrell E, Watts K, Ralston S. Soluble sugar content and and type 2 diabetes. J Intern Med 2007;262:173–183.
glucose/insulin responses can be reduced by soaking chopped hay in 22. Sarafidis PA, Bakris GL. Review: Insulin and endothelin: An water. Proceedings of the Nineteenth Equine Science Society Sym- interplay contributing to hypertension development? J Clin End- posium, Tucson, AZ. 293–298, 2005.
45. Longland AC, Barfoot C, Harris PA. The loss of water-sol- 23. French KR, Pollitt CC. Equine laminitis: Glucose depriva- uble carbohydrate and soluble protein from nine different hays tion and MMP activation induce dermo-epidermal separation in soaked in water for up to 16 hours. J Equine Vet Sci 2009;29:383– vitro. Equine Vet J 2004;36:261–266.
24. Nourian AR, Baldwin GI, van Eps AW, et al. Equine la- 46. Elliott J, Bailey SR. Gastrointestinal derived factors are po- minitis: Ultrastructural lesions detected 24–30 hours after induction tential triggers for the development of acute equine laminitis. J Nutr with oligofructose. Equine Vet J 2007;39:360–364.
25. Muniyappa R, Montagnani M, Koh KK, et al. Cardiovas- 47. Allen EM, Meyer W, Ralston SL, et al. Variation in soluble cular actions of insulin. Endocr Rev 2007;28:463–491.
sugar content of pasture and turf grasses. Proceedings of the Nineteenth 26. Muniyappa R, Iantorno M, Quon MJ. An integrated view of Equine Science Society Symposium, Tucson, AZ. 321–323, 2005.
insulin resistance and endothelial dysfunction. Endocrinol Metab 48. Harris P, Bailey SR, Elliott J, et al. Countermeasures for Clin North Am 2008;37:685–711, ix–x.
pasture-associated laminitis in ponies and horses. J Nutr 27. Mancia G, Bousquet P, Elghozi JL, et al. The sympathetic nervous system and the metabolic syndrome. J Hypertens 49. Geor RJ, Harris P. Dietary management of obesity and in- sulin resistance: Countering risk for laminitis. Vet Clin North Am 28. Leclercq IA, Da Silva Morais A, Schroyen B, et al. Insulin resistance in hepatocytes and sinusoidal liver cells: Mechanisms and 50. Houmard JA, Tanner CJ, Slentz CA, et al. Effect of the vol- consequences. J Hepatol 2007;47:142–156.
ume and intensity of exercise training on insulin sensitivity. J Appl 29. Cusi K, Maezono K, Osman A, et al. Insulin resistance differentially affects the PI 3-kinase- and MAP kinase-mediated sig- 51. Bajpeyi S, Tanner CJ, Slentz CA, et al. Effect of exercise in- naling in human muscle. J Clin Invest 2000;105:311–320.
tensity and volume on persistence of insulin sensitivity during 30. Wyse CA, McNie KA, Tannahill VJ, et al. Prevalence of training cessation. J Appl Physiol 2009;106:1079–1085.
obesity in riding horses in Scotland. Vet Rec 2008;162:590–591.
52. Johnson JL, Slentz CA, Houmard JA, et al. Exercise training 31. Treiber KH, Kronfeld DS, Geor RJ. Insulin resistance in amount and intensity effects on metabolic syndrome (from studies equids: Possible role in laminitis. J Nutr 2006;136:2094S–2098S.
of a targeted risk reduction intervention through defined exercise).
32. Longland AC, Byrd BM. Pasture nonstructural carbohy- drates and equine laminitis. J Nutr 2006;136:2099S–2102S.
53. Hawley JA. Exercise as a therapeutic intervention for the 33. Durham AE, Hughes KJ, Cottle HJ, et al. Type 2 diabetes prevention and treatment of insulin resistance. Diabetes Metab Res mellitus with pancreatic b-cell dysfunction in 3 horses confirmed with minimal model analysis. Equine Vet J 2009. In press.
54. Powell DM, Reedy SE, Sessions DR, et al. Effect of short- 34. Tiley HA, Geor RJ, McCutcheon LJ. Effects of dexametha- term exercise training on insulin sensitivity in obese and lean mares.
sone on glucose dynamics and insulin sensitivity in healthy horses.
55. Stewart-Hunt L, Geor RJ, McCutcheon LJ. Effects of 35. Geor RJ, Hinchcliff KW, McCutcheon LJ, et al. Epineph- short-term training on insulin sensitivity and skeletal muscle glu- rine inhibits exogenous glucose utilization in exercising horses. J cose metabolism in standardbred horses. Equine Vet J Suppl 56. Knowler WC, Barrett-Connor E, Fowler SE, et al. Reduc- 62. Alberts MK, McCann JP, Woods PR. Hemithyroidectomy tion in the incidence of type 2 diabetes with lifestyle intervention or in a horse with confirmed hyperthyroidism. J Am Vet Med Assoc metformin. N Engl J Med 2002;346:393–403.
57. Inzucchi SE. Oral antihyperglycemic therapy for type 2 dia- 63. Durham AE, Rendle DI, Newton JE. The effect of met- betes: Scientific review. JAMA 2002;287:360–372.
formin on measurements of insulin sensitivity and beta cell response 58. Frank N, Sommardahl CS, Eiler H, et al. Effects of oral ad- in 18 horses and ponies with insulin resistance. Equine Vet J ministration of levothyroxine sodium on concentrations of plasma lipids, concentration and composition of very-low-density lipopro- 64. Zhou G, Myers R, Li Y, et al. Role of AMP-activated pro- teins, and glucose dynamics in healthy adult mares. Am J Vet Res tein kinase in mechanism of metformin action. J Clin Invest 59. Frank N, Elliott SB, Boston RC. Effects of long-term oral 65. Del Prato S, Bianchi C, Marchetti P. Beta cell function and administration of levothyroxine sodium on glucose dynamics in anti-diabetic pharmacotherapy. Diabet Metab Res Rev 2007;23: healthy adult horses. Am J Vet Res 2008;69:76–81.
60. Frank N, Buchanan BR, Elliott SB. Effects of long-term oral 66. Hustace JL, Firshman AM, Mata JE. Pharmacokinetics and administration of levothyroxine sodium on serum thyroid hormone bioavailability of metformin in horses. Am J Vet Res 2009;70:665– concentrations, clinicopathologic variables, and echocardiographic measurements in healthy adult horses. Am J Vet Res 2008;69: 67. Tinworth KD, Edwards S, Harris PA, et al. Pharmacokinet- ics of oral metformin in insulin-resistant ponies. Am J Vet Res 2010.
61. Ramirez S, McClure JJ, Moore RM, et al. Hyperthyroidism associated with a thyroid adenocarcinoma in a 21-year-old gelding.
J Vet Intern Med 1998;12:475–477.

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