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ECEIM consensus statements > EMS > Flashcards

EMS Flashcards

1
Q

What is EMS?

A

EMS stands for Equine Metabolic Syndrome, which is a collection of risk factors for endocrinopathic laminitis in horses.

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2
Q

What is insulin dysregulation in the context of EMS?

A

Insulin dysregulation refers to a disturbance in the balanced interrelationship between plasma concentrations of insulin, glucose, and lipids in horses.

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3
Q

What are the manifestations of insulin dysregulation?

A

Basal hyperinsulinaemia, excessive or prolonged hyperinsulinaemia in response to glucose challenge, glucose intolerance, and tissue insulin resistance.

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4
Q

What serum biochemistry changes can tissue insulin resistance lead to?

A

Hypertriglyceridemia

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5
Q

What is obesity in the context of EMS?

A

Obesity refers to increased adiposity that negatively impacts the health of the individual horse.

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6
Q

What are the features of obesity in EMS?

A

Generalized or regional fat accumulation, predisposition to weight gain, and resistance to weight loss.

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7
Q

How does obesity affect cardiovascular parameters in EMS?

A

Increased blood pressure (BP), heart rate (HR), and cardiac dimensions are observed in horses with obesity-related EMS.

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8
Q

What are the cardiovascular features associated with EMS?

A

Increased BP, HR, and cardiac dimensions.

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9
Q

What are the abnormal plasma adipokine concentrations in EMS?

A

Hypoadiponectinaemia and hyperleptinaemia are observed in horses with EMS.

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10
Q

What are some clinical consequences of EMS, besides laminitis?

A

Hyperlipaemia, critical care-associated metabolic derangements, preputial and mammary oedema, mesenteric lipoma, inappropriate lactation, and subfertility.

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11
Q

What breeds are primarily affected by EMS?

A

Primarily British native breeds, with differences in insulin sensitivity observed in ponies and Andalusian horses compared to standardbreds.

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12
Q

What is the prevalence of obesity in the UK horse population?

A

The prevalence of obesity in the UK ranges from 21-45%, with regional adiposity observed in 33% of horses in SW England.

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13
Q

How does exercise affect insulin sensitivity in EMS?

A

Exercise has a beneficial effect on insulin sensitivity and reduced adiposity in physically inactive animals with EMS.

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14
Q

Are insulin concentrations higher in older or younger horses with EMS?

A

Insulin concentrations are higher in older horses compared to younger ones, with lower adiponectin levels in older horses.

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15
Q

What is the effect of sex on EMS prevalence?

A

There is no influence of sex on EMS prevalence in horses.

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16
Q

What are the potential risk factors for EMS related to endocrine disrupting chemicals (EDCs)?

A

Preliminary data suggest that horses from farms near EDC disposal sites are more likely to have had laminitis, indicating EDC exposure as a potential risk factor for EMS.

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17
Q

What is the primary consequence of hyperinsulinaemia in EMS?

A

Hyperinsulinaemia in EMS is linked to the development of laminitis.

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18
Q

What changes occur in the secondary epidermal lamella due to hyperinsulinaemia?

A

Lengthening, narrowing, tapered tips, and acute angulation to the primary epidermal lamellar axis are observed in the secondary epidermal lamella.

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19
Q

How does hyperinsulinaemia cause laminitis?

A

Changes in intracellular insulin signaling leading to endothelial dysfunction and mechanisms involving insulin-like growth factor 1 (IGF-1).

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20
Q

What is the role of genetics in EMS?

A

There is evidence of a genetic component, with some horses being “good doers,” and prevalence of laminitis consistent with dominantly expressed genes.

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21
Q

How does dietary energy restriction contribute to EMS management?

A

Limiting total dry matter intake, avoiding high NSC (non-structural carbohydrate) feeds, and considering progressive BMI losses by energy restriction can improve insulin sensitivity in obese horses.

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22
Q

What is the recommended NSC content in forage for EMS management?

A

Forage with NSC (non-structural carbohydrate) content below 10% is recommended to limit postprandial insulin responses.

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23
Q

What are the potential risks associated with soaking hay?

A

Soaking hay can reduce glycaemic and insulinemic responses but may lead to nutrient leaching, microbial growth concerns, and potential loss of essential nutrients.

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24
Q

How does pasture access affect hyperinsulinaemia in ponies with EMS?

A

High NSC pasture exacerbates hyperinsulinaemia in ponies, and restricting grazing time has a limited effect on total dry matter intake.

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25
Q

How does exercise contribute to EMS management?

A

Exercise improves insulin sensitivity, even in the absence of weight loss, and has an anti-inflammatory effect in horses with EMS.

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26
Q

What are the key exercise recommendations for horses with EMS?

A

Gradual increase in exercise based on the horse’s baseline fitness level, careful monitoring for signs of lameness, and avoidance of high-intensity exercise in horses with lamellar instability.

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27
Q

What is metformin, and how is it used in EMS?

A

Metformin is a commonly prescribed drug, although not licensed for use in horses. It is used to blunt postprandial increases in blood glucose and insulin in severe cases of insulin dysregulation.

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28
Q

How does levothyroxine contribute to EMS management?

A

Levothyroxine may be prescribed to accelerate weight loss by increasing the metabolic rate in horses with increased adiposity.

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29
Q

What is the role of pioglitazone in EMS management?

A

Pioglitazone, a thiazolidinedione antidiabetic drug, is not routinely used for managing insulin dysregulation in horses, but recent studies have shown more encouraging results.

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30
Q

What is pergolide, and how is it used in EMS management?

A

Pergolide is a dopamine receptor agonist licensed for the treatment of PPID. It may improve insulin regulation in horses with EMS.

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31
Q

What are SGLT2 inhibitors, and how are they used in EMS?

A

Sodium-glucose co-transporter 2 (SGLT2) inhibitors target receptors in the kidney to increase glucose loss in the urine. Preliminary studies in horses have been conducted, but further research is needed.

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32
Q

What are T1R2/3 inhibitors, and how do they affect EMS?

A

Sweet taste receptor (T1R2/3) inhibitors have been used to reduce insulin and glucose responses to oral carbohydrates in horses, with some minor beneficial effects observed.

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33
Q

How should you monitor for the development of laminitis in horses with EMS?

A

Frequent monitoring for the earliest signs of laminitis, such as divergent hoof rings, widened white line, and P3 remodelling, is crucial for timely intervention.

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34
Q

How can obesity control be challenging in EMS management?

A

Compliance may be poor, and owners may underestimate their horse’s condition, leading to difficulties in tailoring individualized weight loss plans.

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35
Q

Why is body mass monitoring important in EMS?

A

Regular monitoring of body mass using a weigh bridge or tape, along with body condition scoring, is crucial to assess progress and tailor the weight loss plan.

36
Q

What are some key considerations for endocrine monitoring in EMS?

A

Monitoring should be based on the degree of insulin dysregulation and the desire for a return to pasture, including oral carbohydrate challenge tests and regular assessments.

37
Q

What are the key recommendations for drug treatment in EMS?

A

Drug treatment should never replace diet and exercise interventions. Metformin may be useful for severe insulin dysregulation, levothyroxine for weight loss resistance, and pergolide if PPID is diagnosed.

38
Q

Why is monitoring serum triglyceride concentrations important during weight loss in EMS?

A

Regular monitoring of serum triglyceride concentrations helps detect hyperlipaemia owing to negative energy balance, especially in pregnant animals or miniature breeds.

39
Q

What is the recommended frequency for veterinary re-examinations during EMS management?

A

Initial veterinary re-examinations should be performed monthly after starting dietary restriction and less frequently (3-12 monthly intervals) once good progress is made.

40
Q

What should be the basis for judging success in EMS management?

A

Success should be judged based on retesting for insulin dysregulation, especially using oral carbohydrate challenge tests, rather than solely on body mass losses.

41
Q

What is the role of the gut microbiota in EMS?

A

The gut microbiota has been suggested as a driving force in the pathogenesis of metabolic disease and obesity in horses, with studies showing less diversity in EMS horses.

42
Q

How does carbohydrate content in hay affect hindgut streptococci in horses?

A

Small changes in carbohydrate content in different cuttings of hay elicit measurable changes in equine hindgut streptococci, indicating the importance of hay quality.

43
Q

What is the impact of obesity on adipokines and inflammatory mediators in EMS?

A

Increased fat mass in obesity leads to dysregulation of adipokines (leptin, adiponectin) and inflammatory mediators, affecting glycaemic control, inflammation, and cardiovascular function.

44
Q

How does leptin resistance relate to obesity in EMS?

A

Obesity-related leptin resistance has been observed in horses, resulting in higher-than-normal concentrations, correlating with hyperinsulinaemia in ponies.

45
Q

What is the role of genetics in EMS?

A

Genes contributing to the “good doer” phenotype are likely advantageous for survival during periods of starvation, and prevalence of laminitis is consistent with dominantly expressed genes.

46
Q

What are the dietary recommendations for EMS horses?

A

An ideal target for weight loss is 0.5-1.0% body mass losses weekly, achieved through a forage-based ration with NSC <10%, ensuring adequate protein, vitamins, and minerals.

47
Q

How does exercise contribute to EMS management?

A

Exercise improves insulin sensitivity, even in the absence of weight loss, and low-to-moderate intensity exercise has been shown to have beneficial effects on insulin dynamics.

48
Q

What are the key dietary recommendations for EMS horses?

A

Key dietary recommendations include limiting total dry matter intake, avoiding high NSC feeds, and carefully monitoring individual responses to dietary changes.

49
Q

How may endocrine disrupting chemicals influence EMS?

A

Preliminary data demonstrated that horses from farms within 30 miles of EDC disposal sites were more likely to have had laminitis, and had laboratory evidence of ID, suggesting EDC exposure might be an EMS risk factor

50
Q

Name the 3 known incretins in horses

A

○ GIP: Gastric inhibitory polypeptide
○ GLP-1: glucagon like peptide 1 : stimulates insulin secretion
○ GLP-2: glucagon like peptide 2:incretin. No direct effect on insulin secretion, role in EMS unclear.

51
Q

What is the relative influence on insulin secretion of glucose, GIP and GLP-1

A

an estimated influence of glucose, GLP-1 and GIP on insulin response to oral glucose administration was 76%, 23%, and 2% respectively

52
Q

What % of insulin is cleared by the liver on the first pass?

A

70%

53
Q

What are the earliest histopathological changes in laminitis and how early may they be observed?

A

in the secondary epidermal lamella (SEL)
○ Lengthening, narrowing, develop tapered tips and angled more acutely to the primary epidermal lamesllar axis.
○ Stretching of the lamellar epithelial cells occurs within 6 hours of hyperinsulinaemia= earliest histological change = cytoskeletal disruption.
Subsequent cellular changes results in accelerated apoptosis and proliferation.

54
Q

Do lamellar epithelial cells have insulin receptors?

A

No. On the vascular endothelium only

55
Q

Describe the 2 intracellular pathways normally stimulated by insulin.

A

○ Insulin receptor stimulation -> metabolic pathway (intracellular) -> NO mediated vasodilation and GLUT4 translocation
In IR horses:
○ Pathway blocked-> favours the MAP kinase (or Ras ERK 1/2) pathway (Mitogenic/ mitogen activated protein)
Results in
□ endothelin 1 mediated vasoconstriction
□ Upregulation of cellular adhesion molecules
□ Mitogenesis

56
Q

Which pathway is preferentially activated in IR?

A

MAP kinase (or Ras ERK 1/2)

57
Q

What are the consequesnces of activation of the MAP Kinase pathway in lamellar cells?

A

endothelin 1 mediated vasoconstriction
Upregulation of cellular adhesion molecules
Mitogenesis

58
Q

What is the role of the IGF-1 receptor in laminitis?

A

has a similarity with the insulin receptor and may be activated by high concentrations of insulin -> signalling through the MAP kinase pathway
§ Is found on lamellar epithelial cells and endothelial cells
□ c.f. insulin receptors- on endothelial cells only
§ Studies of horses have shown clear evidence of upregulation of intracellular signalling downstream from the IGF-1 receptor both in response to dietary carbohydrate challenge and insulin infusion.
Observed activation of the downstream molecule RPS6, which disrupts cytoskeletal regulation resulting in a loss of cell stiffness or integrity that might explain the observed cellular elongation or stretching

59
Q

What is a function of RPS6 molecule?

A

Disrupts cytoskeletal regulation. Loss of cell stiffness. Activated by IGF-1 receptor signalling.

60
Q

T/F The faecal microbiota is more diverse in EMS horses

A

F: less diverse

61
Q

What phylum of bacteria is increased in the faeces of horses with EMS?

A

Verrucomicrobia

62
Q

Is adiponectin associated with systemic inflammation?

A

○ Decreased adiponectin associated with mildly increased SAA and the development of ID I horses fed a cereal based diet (horses on a fat based diet showed no evidence of ID and had normal adiponectin concentrations).

63
Q

Which adipokine is positively correlated with hyperinsulinaemia in ponies?

A

leptin

64
Q

What is the primary determinant of leptin concentration?

A

Fat mass

65
Q

What is the proposed mode of inheritance for the propensity for EMS?

A

dominant, reduced penetrance

66
Q

What test gives an accurate assessment of pancreatic insulin secretion?

A

C- peptide: Is unaffected by hepatic first pass metabolism so gives a more accurate assessment of pancreatic secretion of insulin.

67
Q

Should you fast before sampling basal insulin?

A

No: low sensitivity and possible confounding effects of secondary IR induced by fasting.

68
Q

What is the procedure for an OGT?

A
  • Fast overnight
  • 0.5-1g/kg glucose powder in low glycaemic feed.
  • Peak plasma glucose 60-120 minutes after the meal.
    (alt. 1g/kg in 2l water via NGT)
69
Q

Do OGT results correlate with laminitis risk?

A

In a study where 14 of 37 ponies developed laminitis while receiving a high-NSC diet, no pony developed laminitis that had resting insulin <8.5μIU/mL and insulin <65.5μIU/mL at 120 minutes following 1.0 g/kg glucose

70
Q

What is the procedure for an OST?

A
  • Fast 3-12 hours
  • 0.15ml/kg or 0.45ml/kg Karo lite syrup.
    Sample between 60-90 mins
71
Q

What is the procedure for an IRT?

A
  • No fasting (hypoglycaemia)
    Admin exogenous insulin (0.02-0.125IU/kg)
72
Q

Give a limitation of the IRT

A

Omits influence of enteroinsular axis and incretins
hypoglycaemia

73
Q

Give the protocol for CGIT

A
  • 150 mg/kg BM glucose IV, directly followed by 0.1 IU/kg BM neutral(regular) insulin IV
    both insulin and glucoseare measured in the basal sample and after 45 and 75 minutes
74
Q

What is a normal response to a CGIT?

A
  • Healthy: biphasic blood glucose curve starting with hyperglycaemia, followed by a negative phase in which glucose drops below the initial baseline value. Glucose should normally then increase back to baseline concentrations within 45 minutes.
    Insulin concentration should be < 20μIU/mL both at baseline and at 75 minutes, andr emain<100μIU/mL at 45 minutes
75
Q

What is the gold standard test for assessing peripheral insulin sensitivity?

A

Euglycaemic hyperinsulinaemic clamp:
* Basal glucose and insulin
* CRI glucose and insulin (3 mIU/kg/min)- maintain glucose at 5mmol/l (variable)
* Blood glucose every 5-10 mins

76
Q

Give the 4 key testing recommendations

A

Ø The specific methodology used to quantify analytes such as insulin has a marked effect on results and should always be considered, especially when considering diagnostic criteria from published studies

Ø The most useful and practical tests for routine assessment of the various manifestations of ID include resting (not fasting) insulin, the OGT or OST, and the IRT or CGIT.

Ø Interpretation of the test results requires a good understanding of the test selected.

A subset of animals with PPID have ID, and EMS and PPID can coexist, thus concurrent testing for PPID should be considered in all horses over 10 years of age.

77
Q

What is the opitmal degree of forage restriction?

A

Mixed species grass 1.25-1.5% actual BM as DMI, or 1.4-1.7% BM as fed.
corresponding to a digestible energy (DE) intake of 64%-94% of maintenance requirements.

78
Q

Why is restricting grazing time not recommended?

A

Restricting grazing time has a limited effect on DMI- rapid consumption of over 0.9% BM can occur in 3 hours.

79
Q

What are the effects of a grazing muzzle?

A

reduced DMI to 77-83% of grazing without muzzle. Increase foraging time and exercise.

80
Q

What is the maximum recommended loss of BM?

A

0.5-1% BM/ week

81
Q

What % of the forage can be made up of straw?

A

30% Monitor for impactions!

82
Q

Give the 4 Key Dietary Recommendations

A

An ideal target for weight loss in obese horses is between 0.5%and 1.0% BM losses weekly.

This may be achieved with a forage-based ration totaling 1.4%-1.7% BM as fed, or in exceptional cases that appear weight loss resistant, as little as 1.15% BM as fed.

Forage with NSC <10% is recommended to limit postprandial insulin responses in horses with ID and soaking may be required to achieve this in many instances.

Ensuring adequate protein, vitamins, and minerals is important via a ration balancer supplement.

83
Q

What are the specific exercise recommendations for non-laminitic horses with ID?

A

minimum recommendations are low-to moderate-intensity exercise (canter to fast canter, ridden or unridden; or HRs 130-170 bpm) for >30 minutes, >5 times per week.

84
Q

What are the specific exercise recommendations for previously laminitic horses?

A

low-intensity exercise on a soft surface (fast trot to canter unridden; or HRs110-150 bpm) for >30 minutes, >3 times per week, while carefully monitoring for signs of lameness

85
Q

4 key pharmacologic recommendations

A

Drug treatment of EMS should never be used as a substitute for diet and exercise interventions.

Because metformin appears to blunt postprandial increases in blood glucose and insulin, it may be useful for horses with severe ID while management changes are implemented, and in animals that remain insulin dysregulated even when managed optimally.

Levothyroxine may be used in weight loss-resistant cases along-side dietary control and exercise.

Where PPID has been diagnosed, pergolide treatment is recommended to minimize the effects of PPID on ID

86
Q

What is a limitation of BCS monitoring?

A

non-linear association between fat and BCS when BCS >7/9

87
Q
A

ECEIM consensus statements (11 decks)

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