Obesity and Insulin Resistance (IR) in the Horse
By: Mila Bon, 12 July, 2016
Introduction
Obesity and the onset of Insulin Resistance (IR) in the horse have emerged as a growing problem among the domestic horse population in much of the western world. A recent study on the prevalence of obesity among horses in Southwest Virginia (Thatcher et al., 2012) found that 51% of the horses studied had a BCS between 7-9 on the Henneke scale. This corroborates earlier findings in Scotland by Wyse et al. (2008) where 45% of 319 horses studied were considered fat or very fat. These findings differ greatly from studies where body condition scoring was conducted by owner survey instead of using standardized assessments as was done in both studies mentioned above. This shows that horse owners overall greatly underestimate their horses’ BCS (Thatcher et al., 2012). “It seems that in the UK, the fat horse or pony is now so commonplace that it has come to represent the norm in the eyes of many owners” (Sillence, 2012).
Improved pasture with high NSC concentration, combined with little to no exercise is known to contribute to obesity and studies have shown that pasture dry matter intake may be up to 5.2 % of BW/day when pasture is available 24/7. For a 500 kg horse that would total up to 26 kg of dry matter and 10 kg of WSC of which 73% fructan at the highest measured concentration of 38.4% WSC (Longland and Byrd, 2006), although it has to be taken into account that it is difficult to measure pasture intake accurately as Glunk et al. (2013) reported years later and these numbers are at the top end of the scale as an example. Studies on pasture restriction have shown that dry matter intake rate is increased for at least the first few hours on grass when pasture access is restricted (Glunk and Siciliano, 2011; Dowler et al., 2012; Glunk et al. 2013). Dry matter intake from pasture could be as high as 55% of daily requirements in the first 4 hours on grass (Dowler et al., 2012). This makes it more difficult for horse owners to limit caloric intake and prevent horses from becoming obese.
The enormous diversity of complete horse feeds and supplements available don’t make it any easier to objectively select the best option. Sales pitch, not knowledge about equine nutrition, often seems to be a determining factor in the decision to feed concentrates, especially with labeling like ‘Performance Enhancer’ and other misleading euphemisms. Underestimating the work load may also be a factor when horses are fed more calories than they need.
Disciplines like halter classes actually award horses that are borderline obese, giving horse owners a wrong perspective of what a healthy body condition looks like.
What is Insulin Resistance (IR)
Insulin is a peptide hormone secreted by β-cells of the pancreas in response to raised blood glucose. The main function is to stimulate glucose uptake in most cells (except red cells and brain cells; Illingworth, 2010.), maintain glucose homeostasis and promote efficient glucose utilization while inhibiting hepatic gluconeogenesis (Saltiel and Kahn, 2001; Geor, 2008). Reference resting insulin range in horses is 10-30μU/mL (mU/L), but >20μU/mL could already indicate IR (Tadros and Frank, 2013)
Insulin resistance can be described as a reduced response to insulin concentrations in the blood mainly by the cells of skeletal muscle and adipose tissue. This results in reduced glucose uptake and metabolism, thereby creating an increased concentration of insulin (hyperinsulinemia) in the blood resulting in vascular and cardiovascular problems which increases the risk of laminitis (Kapper, 2004; Asplin et al., 2007; Vick et al., 2007), abnormal reproductive function (Vick et al., 2007) and (in young growing horses) altered bone metabolism (Kapper, 2004). Most insulin resistant horses maintain euglycaemia (normal blood sugar level) and hyperglycaemia would indicate that regulation and maintenance of blood glucose is dysregulated due to other failing systems (Frank, 2011)
The reduced response to insulin may have different causes, such as: a lower density or malfunction of insulin receptors; defects in signaling pathways (how cells receive, process, and respond to information from their environment); dysfunction of GLUT-4 (Frank, 2006). GLUT4 is an insulin regulating glucose transporter protein and a key factor in IR in horses (Frank, 2006). GLUT4 services skeletal muscle, adipose tissue and the heart (Illingworth, 2010).
How Does Obesity Cause Insulin Resistance (IR)?
Although there is no universally accepted definition of obesity in horses, Geor (2008) considers horses with a BCS of 8 - 9 on the Henneke scale obese and states that a BCS of 7 might also be considered obese. Geor (2008) also notes that the Henneke scale does not detect differences in regional adiposity (as seen in Equine Metabolic Syndrome).
Obese horses may show normal insulin sensitivity when tested. Tadros and Frank (2013) question whether this is a result of higher tolerance for obesity, or whether in these particular horses IR simply requires more time to develop. As body mass index increases, adipose tissues release more inflammatory cytokines in the form of tumour necrosis factor (TNF) which inhibits insulin receptor signalling and thus lowers insulin sensitivity (Saltiel and Kahn, 2001; Vick et al., 2007; Tadros and Frank, 2013). Although other inflammatory factors play a role when a horse is obese, like interleukin-1 (IL1) and interleukin-6 (IL6), TNF is the most influential and on its own able to induce IR (Vick et al., 2007). Obesity also influences the production of several hormones by adipocytes, where lower concentrations of adiponectin result in lower insulin sensitivity and impaired vasodilation Tadros and Frank, (2013).
How Does Insulin Resistance (IR) Cause Laminitis?In healthy horses, when insulin is released, slow vasodilation occurs through synthesis of nitric oxide, while at the same time stimulation of endothelin-1 causes vasoconstriction. Since insulin activates both, there is a balance. Tadros and Frank (2013) theorized that since the vasodilatory effect of insulin and the insulin-dependent stimulation of glucose uptake are both mediated by Phosphatidylinositol-3 kinase (PI3K, a signaling pathway to direct GLUT4 to the cell membrane in order to facilitate glucose transport into the cell), then, theoretically, when this PI3K pathway becomes disrupted due to IR, so would the vasodilatory effect of insulin. The stimulation of vasoconstriction would still be in tact as that pathway remains functional and would be further stimulated by hyperinsulinemia, as insulin clearance is impaired. Ischemia would be the result. Ischemia is described as one of the cascading effects causing laminitis in the Systems Theory of Orsini et al. (2009), although they theorize that “inflammation would likely be the first domino to fall that sets the cascade of failure in motion”. Inflammatory cytokines released by adipose tissue in abundance in obese horses are keeping these horses in a “mild, but chronic inflammatory state” (Vick et al., 2007). The Tadros and Frank (2013) theory above does not explain the pounding digital pulse and increased heat in the hoof wall during laminitis, but just prolonged hyperinsulinemia alone (at toxic levels) is enough to induce laminitis in healthy lean horses, independent of changes in blood glucose or insulin sensitivity and causes a prolonged vascular response, as concluded by Asplin et al. (2007). Tadros and Frank (2013) thus concluded that hyperinsulinemia induced vasodilation in the Asplin study would overcome vasoconstriction promoted by IR, but in the Asplin study the horses were not insulin resistant and neither were they infused with glucose. Asplin et al. (2007) conclusion further states that glucose uptake to hoof lamellae is not insulin dependent, while the vasculature is. However, Frank (2006) reports that GLUT4 proteins are found in keratinocytes which would suggest that hoof tissue is at least partly insulin dependent. The glucose transporter in lamellar epidermal basal cells is GLUT1, as established by Asplin et al., (2007), which, by the way, is also found in endothelium (interior lining of blood vessels) according to Illingworth, (2010). This would make blood vessels at least partly insulin independent and contrary to statements of Asplin et al. (2007) and Geor (2008) who states that insulin also regulates vascular endothelial function. Asplin et al. (2007) described increased pulse soon after insulin bolus was administered, which then returned to normal until the onset of laminitis and this can not really be explained by hyperinsulinemia alone. There does not seem to be consensus how exactly insulin resistance (which results in hyperinsulinemia) causes laminitis, but there is consensus that insulin resistance is a high risk factor for laminitis.
Managing Weight and Weight Loss
Weight loss and exercise are key components in managing obese horses with IR or at risk for developing IR (Becvarova and Pleasant, 2012; Johnson et al., 2004). Considering that horses that are used to unrestricted pasture or ad lib access to hay may have been accustomed to a much higher than recommended % of daily DM intake, McGowan et al. (2013) warn that restricting the diet to less than 1.5% of BW dry matter intake will have behavioural implications. They therefore suggest a less severe DM intake restriction by selecting hay with lower % NSC or soaking the hay to limit NSC to 10 – 12%. A balancer supplement might be needed to counter nutrient losses during soaking. Becvarova and Pleasant, (2012) use the following formula to predict optimal body weight:
Starting body weight (kg) – ((Starting BCS – Desired BCS) x 22.5 kg)
Pharmcological Intervention
Dietary Supplementation
A study to evaluate the effects of short-chain fructo-oligosaccharides that had been proven to increase insulin sensitivity in obese dogs, rodents and calves in prior studies, resulted in moderate improvement of insulin sensitivity in obese (Arabian) horses with an average BW of 523 kg at a dose of 45 g / day. Further studies are required to make findings more comprehensible. (Respondek et al., 2011)
Management of Insulin Resistance
Exercise leads to increased glucose uptake and use by skeletal muscle via insulin-independent mechanisms that persist for up to 24 hrs. (Johnson et al., 2004). Management of IR requires exercise, weight loss if overweight, a low NSC diet which means limited or no pasture access when NSC is high. Hay should be analyzed and soaked if necessary to lower NSC (McCowan et al., 2013; Tadros and Frank, 2013)
Conclusion
Prevention is always better than the cure. The numbers don’t lie, obesity has become a serious problem in the equine industry and equine professionals will have to be more vigilant when encountering over-conditioned or obese horses as research has made clear that there is imminent danger of horses developing IR when overweight, besides the strain that the extra weight already puts on a horse’s system. Horse owners hear many different perspectives and adherence to any type of counselling, whether it is management, behavioural or nutritional has always been proven difficult as many professionals have reported. Simply stating: “Your horse has to lose weight” without stressing why this is important and without looking at the management perspectives that a horse owner has to deal with will not result in an owner actively trying. No matter how easy the fix may seem, many horse owners are limited by the time they can spend with their horse as well as by the availability and cooperation of the boarding facility’s management and staff to implement any necessary changes.
Furthermore, as it seems that phenotypic plasticity associates maternal nutrition with susceptibility of progeny to obesity or insulin resistance, where maternal dietary excess promotes obesity in progeny by altering the hypothalamic neuropeptide production causing increased appetite in offspring. (Parlee and MacDougald, 2014), the ‘cure’ to the obesity epidemic and insulin resistance starts in the womb.
References:
Asplin, K.E., Sillence, M.N., Pollitt, C.C., McGowan, C.M., 2007. Induction of Laminitis by prolonged hyperinsulineaemia in clinically normal horses. The Veterinary Journal 174 (2007) 530-535.
Becvarova, I., Pleasant, R.S., 2012. Managing obesity in pasture-based horses. Compendium (Yardley, PA), April 2012, Vol.34(4), pp.E1-4
Dowler, L. E., Siciliano, P.D., Pratt - Phillips, S.E., Poore, M., 2012. Determination of Pasture Dry Matter Intake Rates in Different Seasons and Their Application in Grazing Management. Journal of Equine Veterinary Science, Feb, 2012, Vol.32(2), p.85(8)
Frank, N., 2006. Insulin Resistance in Horses. From: Proceedings of the Annual convention of the AAEP. Vol. 52 / 2006.
Frank, N., 2011. Equine Metabolic Syndrome. Veterinary Clinics of North America: Equine Practice 27, 73-92.
Frank, N., Tadros, E. M., 2014. Insulin dysregulation. Equine Veterinary Journal, 2014, Vol.46(1), pp.103-112
Glunk, E.C. ; Siciliano, P.D., 2011. Effect of Restricted Grazing on Dry Matter Intake Rate. Journal of Equine Veterinary Science, 2011, Vol.31(5), pp.296-297
Glunk, E.C., Pratt-Phillips, S.E., Siciliano, P.D., 2013. Effect of restricted pasture access on pasture dry matter intake rate, dietary energy intake, and fecal pH in horses. Journal of Equine Veterinary Science, 2013, Vol.33, pp.421-426
Geor, R.J., 2008. Metabolic Predispositions to Laminitis in Horses and Ponies: Obesity, Insulin Resistance and Metabolic Syndromes. Journal of Equine Veterinary Science, 2008, Vol.28(12), pp.753-759
Illingworth, J., 2011. Pancreatic islets, release of insulin and its effects. MB ChB Year 1: Nutrition and Energy. http://www.bmb.leeds.ac.uk/teaching/icu3/lecture/21/index.htm
Johnson, P.J., Messer, N., Kellon, E., 2004. Treatment of Equine Metabolic Syndrome. Compendium on continuing education for the practicing veterinarian, 2004, Vol.26(2), pp.126-130
Kapper, D., 2004. Applied Nutrition. In: Reed S, Bayly WM, Sellon C (Eds) Equine Internal Medicine, second edition. Saunders, St. Louis, Missouri, pp 1543-1605
Longland, A.C., Byrd, B.M., 2006. Pasture Nonstructural Carbohydrates and Equine Laminits. Journal of nutrition, 2006, Vol.136(7S), pp.2099S-2102S
Mcgowan, C.M., Dugdale, A.H., Pinchbeck, G.L., Argo, C.Mcg., 2013. Dietary restriction in combination with a nutraceutical supplement for the management of equine metabolic syndrome in horses. The Veterinary Journal, May 2013, Vol.196(2), pp.153-159
Nutrient Requirements of Horses. Sixth revised edition, 2009. National Research Council of the National Academies Press, Washington, DC, USA.
Orsini, J., Galantino-Homer, H., Pollitt, C., 2009. Laminitis in Horses: Through the Lens of Systems Theory. Journal of Equine Veterinary Science, vol 29, No 2 (2009).
Parlee, S.D., Macdougald, O.A., 2014. Maternal nutrition and risk of obesity in offspring: The Trojan horse of developmental plasticity. BBA - Molecular Basis of Disease, March 2014, Vol.1842(3), pp.495-506
Respondek, F., Myers, K.,Smith, T. L., Wagner, A., Geor, R.J., 2011. Dietary supplementation with short-chain fructo-oligosaccharides improves insulinsensitivity in obese horses. Journal of animal science, January 2011, Vol.89(1), pp.77-83
Saltiel, A.R., Kahn, C.R., 2001. Insulin signalling and the regulation of glucose and lipid metabolism. Nature, 2001, Vol.414(6865), p.799
Sillence, M.N., 2012. ‘Supersize me’: On equine obesity. The Veterinary Journal, November 2012, Vol.194(2), pp.137-138
Stephenson, H.M., Green, M.J., Freeman, S.L., 2011. Prevalence of obesity in a population of horses in the UK. Veterinary Record, 5 February 2011, Vol.168(5), p.131
Stewart‐hunt, L., Pratt‐phillips, S., Mccutcheon, L. J., Geor, R. J., 2010. Dietary energy source and physical conditioning affect insulin sensitivity and skeletal muscle glucose metabolism in horses. Equine Veterinary Journal, 2010, Vol.42, pp.355-360
Tadros, E.M., Frank, N., 2013. Endocrine disorders and laminitis. Equine Veterinary Education, 2013, Vol.25(3), pp.152-162
Thatcher, C.D., Pleasant, R.S., Geor, R.J., Elviner, F. , 2012. Prevalence of Overconditioning in Mature Horses in Southwest Virginia during the Summer. Journal of Veterinarian Internal Medicine (2012) 26;1413-1418
Vick, M.M., Adams, A.A., Murphy, B. A., Sessions, D.R., Horohov, D.W., Cook, R.F., Shelton, B.J., Fitzgerald, B.P., 2007. Relationships among inflammatory cytokines, obesity, and insulin sensitivity in the horse. Journal of animal science, May 2007, Vol.85(5), pp.1144-55
Wyse, C.A., McNie, K.A., Tannahil, V.J. et al., 2008. Prevalence of obesity in riding horses in Scotland. Vet Rec 2008;162:590-591.
Introduction
Obesity and the onset of Insulin Resistance (IR) in the horse have emerged as a growing problem among the domestic horse population in much of the western world. A recent study on the prevalence of obesity among horses in Southwest Virginia (Thatcher et al., 2012) found that 51% of the horses studied had a BCS between 7-9 on the Henneke scale. This corroborates earlier findings in Scotland by Wyse et al. (2008) where 45% of 319 horses studied were considered fat or very fat. These findings differ greatly from studies where body condition scoring was conducted by owner survey instead of using standardized assessments as was done in both studies mentioned above. This shows that horse owners overall greatly underestimate their horses’ BCS (Thatcher et al., 2012). “It seems that in the UK, the fat horse or pony is now so commonplace that it has come to represent the norm in the eyes of many owners” (Sillence, 2012).
Improved pasture with high NSC concentration, combined with little to no exercise is known to contribute to obesity and studies have shown that pasture dry matter intake may be up to 5.2 % of BW/day when pasture is available 24/7. For a 500 kg horse that would total up to 26 kg of dry matter and 10 kg of WSC of which 73% fructan at the highest measured concentration of 38.4% WSC (Longland and Byrd, 2006), although it has to be taken into account that it is difficult to measure pasture intake accurately as Glunk et al. (2013) reported years later and these numbers are at the top end of the scale as an example. Studies on pasture restriction have shown that dry matter intake rate is increased for at least the first few hours on grass when pasture access is restricted (Glunk and Siciliano, 2011; Dowler et al., 2012; Glunk et al. 2013). Dry matter intake from pasture could be as high as 55% of daily requirements in the first 4 hours on grass (Dowler et al., 2012). This makes it more difficult for horse owners to limit caloric intake and prevent horses from becoming obese.
The enormous diversity of complete horse feeds and supplements available don’t make it any easier to objectively select the best option. Sales pitch, not knowledge about equine nutrition, often seems to be a determining factor in the decision to feed concentrates, especially with labeling like ‘Performance Enhancer’ and other misleading euphemisms. Underestimating the work load may also be a factor when horses are fed more calories than they need.
Disciplines like halter classes actually award horses that are borderline obese, giving horse owners a wrong perspective of what a healthy body condition looks like.
What is Insulin Resistance (IR)
Insulin is a peptide hormone secreted by β-cells of the pancreas in response to raised blood glucose. The main function is to stimulate glucose uptake in most cells (except red cells and brain cells; Illingworth, 2010.), maintain glucose homeostasis and promote efficient glucose utilization while inhibiting hepatic gluconeogenesis (Saltiel and Kahn, 2001; Geor, 2008). Reference resting insulin range in horses is 10-30μU/mL (mU/L), but >20μU/mL could already indicate IR (Tadros and Frank, 2013)
Insulin resistance can be described as a reduced response to insulin concentrations in the blood mainly by the cells of skeletal muscle and adipose tissue. This results in reduced glucose uptake and metabolism, thereby creating an increased concentration of insulin (hyperinsulinemia) in the blood resulting in vascular and cardiovascular problems which increases the risk of laminitis (Kapper, 2004; Asplin et al., 2007; Vick et al., 2007), abnormal reproductive function (Vick et al., 2007) and (in young growing horses) altered bone metabolism (Kapper, 2004). Most insulin resistant horses maintain euglycaemia (normal blood sugar level) and hyperglycaemia would indicate that regulation and maintenance of blood glucose is dysregulated due to other failing systems (Frank, 2011)
The reduced response to insulin may have different causes, such as: a lower density or malfunction of insulin receptors; defects in signaling pathways (how cells receive, process, and respond to information from their environment); dysfunction of GLUT-4 (Frank, 2006). GLUT4 is an insulin regulating glucose transporter protein and a key factor in IR in horses (Frank, 2006). GLUT4 services skeletal muscle, adipose tissue and the heart (Illingworth, 2010).
How Does Obesity Cause Insulin Resistance (IR)?
Although there is no universally accepted definition of obesity in horses, Geor (2008) considers horses with a BCS of 8 - 9 on the Henneke scale obese and states that a BCS of 7 might also be considered obese. Geor (2008) also notes that the Henneke scale does not detect differences in regional adiposity (as seen in Equine Metabolic Syndrome).
Obese horses may show normal insulin sensitivity when tested. Tadros and Frank (2013) question whether this is a result of higher tolerance for obesity, or whether in these particular horses IR simply requires more time to develop. As body mass index increases, adipose tissues release more inflammatory cytokines in the form of tumour necrosis factor (TNF) which inhibits insulin receptor signalling and thus lowers insulin sensitivity (Saltiel and Kahn, 2001; Vick et al., 2007; Tadros and Frank, 2013). Although other inflammatory factors play a role when a horse is obese, like interleukin-1 (IL1) and interleukin-6 (IL6), TNF is the most influential and on its own able to induce IR (Vick et al., 2007). Obesity also influences the production of several hormones by adipocytes, where lower concentrations of adiponectin result in lower insulin sensitivity and impaired vasodilation Tadros and Frank, (2013).
How Does Insulin Resistance (IR) Cause Laminitis?In healthy horses, when insulin is released, slow vasodilation occurs through synthesis of nitric oxide, while at the same time stimulation of endothelin-1 causes vasoconstriction. Since insulin activates both, there is a balance. Tadros and Frank (2013) theorized that since the vasodilatory effect of insulin and the insulin-dependent stimulation of glucose uptake are both mediated by Phosphatidylinositol-3 kinase (PI3K, a signaling pathway to direct GLUT4 to the cell membrane in order to facilitate glucose transport into the cell), then, theoretically, when this PI3K pathway becomes disrupted due to IR, so would the vasodilatory effect of insulin. The stimulation of vasoconstriction would still be in tact as that pathway remains functional and would be further stimulated by hyperinsulinemia, as insulin clearance is impaired. Ischemia would be the result. Ischemia is described as one of the cascading effects causing laminitis in the Systems Theory of Orsini et al. (2009), although they theorize that “inflammation would likely be the first domino to fall that sets the cascade of failure in motion”. Inflammatory cytokines released by adipose tissue in abundance in obese horses are keeping these horses in a “mild, but chronic inflammatory state” (Vick et al., 2007). The Tadros and Frank (2013) theory above does not explain the pounding digital pulse and increased heat in the hoof wall during laminitis, but just prolonged hyperinsulinemia alone (at toxic levels) is enough to induce laminitis in healthy lean horses, independent of changes in blood glucose or insulin sensitivity and causes a prolonged vascular response, as concluded by Asplin et al. (2007). Tadros and Frank (2013) thus concluded that hyperinsulinemia induced vasodilation in the Asplin study would overcome vasoconstriction promoted by IR, but in the Asplin study the horses were not insulin resistant and neither were they infused with glucose. Asplin et al. (2007) conclusion further states that glucose uptake to hoof lamellae is not insulin dependent, while the vasculature is. However, Frank (2006) reports that GLUT4 proteins are found in keratinocytes which would suggest that hoof tissue is at least partly insulin dependent. The glucose transporter in lamellar epidermal basal cells is GLUT1, as established by Asplin et al., (2007), which, by the way, is also found in endothelium (interior lining of blood vessels) according to Illingworth, (2010). This would make blood vessels at least partly insulin independent and contrary to statements of Asplin et al. (2007) and Geor (2008) who states that insulin also regulates vascular endothelial function. Asplin et al. (2007) described increased pulse soon after insulin bolus was administered, which then returned to normal until the onset of laminitis and this can not really be explained by hyperinsulinemia alone. There does not seem to be consensus how exactly insulin resistance (which results in hyperinsulinemia) causes laminitis, but there is consensus that insulin resistance is a high risk factor for laminitis.
Managing Weight and Weight Loss
Weight loss and exercise are key components in managing obese horses with IR or at risk for developing IR (Becvarova and Pleasant, 2012; Johnson et al., 2004). Considering that horses that are used to unrestricted pasture or ad lib access to hay may have been accustomed to a much higher than recommended % of daily DM intake, McGowan et al. (2013) warn that restricting the diet to less than 1.5% of BW dry matter intake will have behavioural implications. They therefore suggest a less severe DM intake restriction by selecting hay with lower % NSC or soaking the hay to limit NSC to 10 – 12%. A balancer supplement might be needed to counter nutrient losses during soaking. Becvarova and Pleasant, (2012) use the following formula to predict optimal body weight:
Starting body weight (kg) – ((Starting BCS – Desired BCS) x 22.5 kg)
- Weight Loss At Pasture
- Becvarova and Pleasant (2012), calculated that horses with unrestricted (fescue) pasture access may consume between 1.2 and 1.6 times the calories for maintenance requirements and calculated that at the very minimum, light exercise would be required to prevent weight gain. This number may be more during different time of year or under certain environmental conditions, depending on sward height, growing stage, climate and type of forage, when NSC is relatively high (Longland and Byrd, 2006). The NRC (2007) example of light work is: 1-3 hrs per week, 40% walk, 50% trot, 10% canter. Weight loss for pastured horses (after complete physical examination) can be achieved by use of a grazing muzzle, but since pasture restriction increases pasture dry matter intake rate (Glunk and Siciliano, 2011; Dowler et al., 2012; Glunk et al. 2013), the horse would have to wear the grazing muzzle at all times while at pasture. It is estimated that a grazing muzzle reduces the intake from pasture by 25-33% (Becvarova and Pleasant, 2012). A grazing muzzle also limits pasture intake to that of the leafy top part of the grass, avoiding horses to graze down much of the stem where NSC collects (in cool season grasses) as stated by Longland and Byrd (2006). According to the experience of the authors of ‘Managing Obesity in Pasture-Based Horses’ Iveta Becvarova (DVM, MS, DACVN) and R. Scott Pleasant, (DVM, MS, DACVS), “hyperinsulinemia in obese horses almost always resolves with weight loss” (Becvarova and Pleasant, 2012).
- Weight Loss When Stabled / Dry Lot
- McGowan et al. (2013) studied the effects of dietary restriction of soaked hay at 1.25% of BW in DM and NSC of 11% after soaking, in combination with a ration balancer (to make up for vitamin and mineral loss during soaking of the hay). This resulted in 1% loss of body mass (BM) per week and an improvement in insulin sensitivity after 6 weeks as was shown in the combined insulin-glucose tolerance test (CGIT). However, authors stated that tests should focus on insulin responses rather than glucose responses.
Pharmcological Intervention
- Levothyroxine Sodium given to obese horses induces weight loss and increases insulin sensitivity. It has been shown to prevent obese horses from developing insulin resistance as stated by Tadros and Frank, (2013). The author of this paper knows of one scenario where Levothyroxine was prescribed for an obese horse instead of a weight loss method and that was for a horse that was boarded and where management was unable to facilitate a weight loss regimen. Horses were on round bales with 1 ¾” slow feeder nets. This worked well for all horses except for this 6 year old Fjord mare in light work.
- Metformin Hydrochloride has been used in humans for a long time, but research for use in horses has been inconclusive and the reason seems to be that oral bio-availability is lower in horses than in humans (Tadros and Frank, 2013).
Dietary Supplementation
A study to evaluate the effects of short-chain fructo-oligosaccharides that had been proven to increase insulin sensitivity in obese dogs, rodents and calves in prior studies, resulted in moderate improvement of insulin sensitivity in obese (Arabian) horses with an average BW of 523 kg at a dose of 45 g / day. Further studies are required to make findings more comprehensible. (Respondek et al., 2011)
Management of Insulin Resistance
Exercise leads to increased glucose uptake and use by skeletal muscle via insulin-independent mechanisms that persist for up to 24 hrs. (Johnson et al., 2004). Management of IR requires exercise, weight loss if overweight, a low NSC diet which means limited or no pasture access when NSC is high. Hay should be analyzed and soaked if necessary to lower NSC (McCowan et al., 2013; Tadros and Frank, 2013)
Conclusion
Prevention is always better than the cure. The numbers don’t lie, obesity has become a serious problem in the equine industry and equine professionals will have to be more vigilant when encountering over-conditioned or obese horses as research has made clear that there is imminent danger of horses developing IR when overweight, besides the strain that the extra weight already puts on a horse’s system. Horse owners hear many different perspectives and adherence to any type of counselling, whether it is management, behavioural or nutritional has always been proven difficult as many professionals have reported. Simply stating: “Your horse has to lose weight” without stressing why this is important and without looking at the management perspectives that a horse owner has to deal with will not result in an owner actively trying. No matter how easy the fix may seem, many horse owners are limited by the time they can spend with their horse as well as by the availability and cooperation of the boarding facility’s management and staff to implement any necessary changes.
Furthermore, as it seems that phenotypic plasticity associates maternal nutrition with susceptibility of progeny to obesity or insulin resistance, where maternal dietary excess promotes obesity in progeny by altering the hypothalamic neuropeptide production causing increased appetite in offspring. (Parlee and MacDougald, 2014), the ‘cure’ to the obesity epidemic and insulin resistance starts in the womb.
References:
Asplin, K.E., Sillence, M.N., Pollitt, C.C., McGowan, C.M., 2007. Induction of Laminitis by prolonged hyperinsulineaemia in clinically normal horses. The Veterinary Journal 174 (2007) 530-535.
Becvarova, I., Pleasant, R.S., 2012. Managing obesity in pasture-based horses. Compendium (Yardley, PA), April 2012, Vol.34(4), pp.E1-4
Dowler, L. E., Siciliano, P.D., Pratt - Phillips, S.E., Poore, M., 2012. Determination of Pasture Dry Matter Intake Rates in Different Seasons and Their Application in Grazing Management. Journal of Equine Veterinary Science, Feb, 2012, Vol.32(2), p.85(8)
Frank, N., 2006. Insulin Resistance in Horses. From: Proceedings of the Annual convention of the AAEP. Vol. 52 / 2006.
Frank, N., 2011. Equine Metabolic Syndrome. Veterinary Clinics of North America: Equine Practice 27, 73-92.
Frank, N., Tadros, E. M., 2014. Insulin dysregulation. Equine Veterinary Journal, 2014, Vol.46(1), pp.103-112
Glunk, E.C. ; Siciliano, P.D., 2011. Effect of Restricted Grazing on Dry Matter Intake Rate. Journal of Equine Veterinary Science, 2011, Vol.31(5), pp.296-297
Glunk, E.C., Pratt-Phillips, S.E., Siciliano, P.D., 2013. Effect of restricted pasture access on pasture dry matter intake rate, dietary energy intake, and fecal pH in horses. Journal of Equine Veterinary Science, 2013, Vol.33, pp.421-426
Geor, R.J., 2008. Metabolic Predispositions to Laminitis in Horses and Ponies: Obesity, Insulin Resistance and Metabolic Syndromes. Journal of Equine Veterinary Science, 2008, Vol.28(12), pp.753-759
Illingworth, J., 2011. Pancreatic islets, release of insulin and its effects. MB ChB Year 1: Nutrition and Energy. http://www.bmb.leeds.ac.uk/teaching/icu3/lecture/21/index.htm
Johnson, P.J., Messer, N., Kellon, E., 2004. Treatment of Equine Metabolic Syndrome. Compendium on continuing education for the practicing veterinarian, 2004, Vol.26(2), pp.126-130
Kapper, D., 2004. Applied Nutrition. In: Reed S, Bayly WM, Sellon C (Eds) Equine Internal Medicine, second edition. Saunders, St. Louis, Missouri, pp 1543-1605
Longland, A.C., Byrd, B.M., 2006. Pasture Nonstructural Carbohydrates and Equine Laminits. Journal of nutrition, 2006, Vol.136(7S), pp.2099S-2102S
Mcgowan, C.M., Dugdale, A.H., Pinchbeck, G.L., Argo, C.Mcg., 2013. Dietary restriction in combination with a nutraceutical supplement for the management of equine metabolic syndrome in horses. The Veterinary Journal, May 2013, Vol.196(2), pp.153-159
Nutrient Requirements of Horses. Sixth revised edition, 2009. National Research Council of the National Academies Press, Washington, DC, USA.
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