Nutritional Support for Metabolic Syndrome and Insulin Resistance in Horses

OUTLINE

  1. Digestive Tract function:
    1. Horse as a grazing animal
    2. Horse as a meal-fed animal
  2. NSC limitations in the equine diet
  3. Effects of high NSC in the foregut and hindgut function
  4. Nutritionally-related diseases
    1. Overweight Horse
    2. Insulin Resistance/Equine Metabolic Syndrome
    3. Laminitis
    4. Cushing’s Syndrome (hyperadrenocorticism)
    5. Hyperkalemic Periodic Paralysis (HYPP)
  5. Suggestions for Managing the Diet of today’s horses

 
A. The Equine Digestive Tract

Understanding the structure and function of the horse’s gastrointestinal (GI) system is critical to making rational decisions about the nutritional program.

The horse is a nonruminant herbivore. The structure of the GI tract is unlike that of the cow or pig. One of the main differences is the functional cecum in the horse that behaves much like the rumen of a cow. An important difference is the horse’s cecum is positioned DISTAL to the small intestine, while the rumen of the cow is PROXIMAL to the small intestine. Thus, many of the benefits of microbial fermentation are lost due to the position of the cecum in the horse.

Foregut
The foregut of the horse is comprised of the mouth, esophagus, stomach and small intestine. The primary function of the foregut is the digestion and absorption of protein, fat, sugars, starch, vitamins and most minerals. Digestion is aided by enzymes secreted by the horse itself and occurs mainly in the early part of the small intestine.. End-products of digestion are absorbed in the latter portion of the small intestine. Proteins are absorbed as amino acids, fats as fatty acids and glycerol, starch and sugar as simple sugars (glucose) and minerals and vitamins as the simple vitamin or mineral or as a small complex.

Hindgut
The hindgut of the horse in comprised of the cecum, large and small colon and the rectum. Two of the primary functions of the hindgut are digestion of dietary fiber and reabsorption of water. Enzymes secreted by the microorganisms (bacteria, protozoa and fungi) break down fiber from cell walls, which is primarily made up of cellulose, hemicellulose and lignin.

The fermentation of fiber results in the production of volatile fatty acids (VFA; usually acetic, propionic and butyric), vitamins B, C and K, and microbial protein. As mentioned above, the cecum positioned after the small intestine minimizes the utilization of some of the fermentation products, mainly the microbial protein. The VFAs are absorbed across the hindgut wall, as are many of the vitamins.

Managing the Horse’s GI Tract in Confinement
The horse evolved as a grazing animal, eating numerous small meals per day. A horse in the wild may graze 18-20 hours a day to maintain body condition. As a result, the horse has the smallest stomach compared to his body size of any domestic animal.

Additionally, the horse in the wild is typically grazing on sparse vegetation, not the lush pastures often seen today. Had a horse in the wild come across a lush area of vegetation, he would consume it, not sure when his next large meal would be found.

The horse’s evolutionary response when on lush pastures for long periods of time will be to
eat continually, often leading to obesity, colic and laminitis.

When keeping horses in stall or drylot confinement, it is preferable to feed as many times per day as feasible. Not more feed per day, just divided into more frequent, smaller meals. Such a practice can increase the horse’s feed efficiency up to 10% and reduce likelihood of colic and laminitis. It will also reduce the blood glucose/insulin response due to lower bolus of sugar and starch per meal.
On pasture, for horses that are overweight, are sugar/starch sensitive like horses with insulin resistance, equine metabolic syndrome, Cushing’s Syndrome or have been laminitic, it is wise to limit of eliminate time on pasture and maintain such horse on a drylot with controlled intake of good quality, primarily grass hay.

Horse with large daily calorie requirements, like lactating mares, growing foals and certain horses in hard work, can do well on pasture, but do not let these horses become overweight.

B. NSC Limitations - Terminology:

1. NSC = non-structural carbohydrates (sugars, starches, other soluble carbohydrates)

  • typically highly digestible in foregut
  • tends to drive up blood glucose and insulin levels – can be detrimental
  • passage to hindgut is undesirable

NSC is equal to the sugar plus starch content of a feedstuff.

Chemical Classification:

  • Starch - a polysaccharide found primarily in the grain or seed and/or root portions of plants.
  • Water Soluble Carbohydrates (WSC) - carbohydrates solubilized and extracted in water. Includes monosaccharides, disaccharides and some polysaccharides (mainly fructan). Fructan is a major storage carbohydrate in grasses. USE FOR “SUGAR” IN FORAGES!! 
    Thus, for a forage, NSC = Starch + WSC.
  • Ethanol Soluble Carbohydrates (ESC) - carbohydrates solubilized and extracted in 80% ethanol. Includes primarily monosaccharides and disaccharides. USE FOR “SUGAR” IN CONCENTRATES!!
    Thus, for a grain or concentrate, NSC = Starch + ESC.

2. SC = structural carbohydrates (cellulose, hemicellulose, lignin)

  • digested by enzymes from micoorganisms in hindgut (fermentation)
  • end products of digestion = volatile fatty acids (acetic, propionic, butyric)
  • little digestion in the foregut
  • feed sources vary tremendously in nature of the fiber and it’s digestibility

Why Do Fat & Fiber Behave Differently than Sugar & Starch in the Diet of the Horse??

1. NSC:
The digestion and absorption of NSC (starch is absorbed from the small intestine as simple sugar - glucose) causes an increase in blood GLUCOSE which, in turn, causes and increase in blood INSULIN. Sugars are metabolized to LACTIC ACID when used for energy in the muscle and other body tissues.

  • INSULIN negatively affects most other hormones in the horse’s body. Thus, aggravates the hormonal environment of the Cushing’s horse and contributes to developmental disease in young horses by inhibiting growth hormone.
  • LACTIC ACID :
    • lowers pH in the stomach (can contribute to ulcers)
    • lowers pH in the hindgut (negatively alters microbial population, favoring pathogenic bacteria)

2. FATS:
Fats (oils) in the horse’s diet are highly digestible (> 95%) and are absorbed as fatty acids and glycerol. When used for energy by the muscles, fats are metabolized to carbon dioxide (CO2) and water (H2O) – no significant metabolic effects.

3. DIGESTIBLE FIBERS:
Fibers are digested at varying rates in the hindgut by microbial enzymes and are metabolized to volatile fatty acids – again, no significant metabolic effects. Fiber is the most natural energy source for the horse.

Fiber digestibility is related to the amounts of cellulose, hemicelluloses and lignin in the feedstuff. The most digestible is hemicelluloses, next is cellulose, while lignin is totally indigestible to the horse.
Excellent sources of digestible fiber are: soft, green forage (hay/pasture), beet pulp, soyhulls)

C. Effects of high NSC in the foregut and hindgut function

Effect of High NSC Content in Small Intestine:
As stated above, absorption of simple sugars from dietary NSC across the small intestinal wall causes an increase in plasma glucose, which causes an increase in plasma insulin The elevated insulin level results in:

  • facilitation of glucose and amino acid absorption into cells
  • increase in glycolysis
  • increased conversion of glucose to fat (fat cannot be converted back to glucose)
  • decrease in gluconeogenesis
  • decrease in lipolysis (can’t get weight off obese horses)
  • inhibition of growth hormone (can contribute to DOD)
  • alters serotonin levels in brain potentially causing hyperactivity

Effect of NSC Content in the Large Intestine:
At high feeding rates, by volume and/or concentration of NSC, excess NSC can bypass small
intestine’s capacity to digest and absorb the NSC and it passes into the cecum/colon, resulting in:

  • rapid fermentation by microbes (structural CHO slowly fermented), producing large amounts of gas
  • favorable environment for the production of Lactobacillus, which produces lactate that is poorly absorbed across the cecum and colon walls causing a reduction in pH.
  • Effects of lower hindgut pH :
    • Grazing horses – normal pH = 6.4 – 6.7
    • Cecal pH of 6.0 ~ sub-clinical acidosis
    • pH < 6.0 associated with:
      • osmotic diarrhea
      • overgrowth of undesirable bacteria
      • lysis of beneficial bacteria
      • Risk of endotoxemia and laminitis

Characterizing the blood insulin response to a high (38%) versus low (18%) NSC feed fed at the same intake level (approximately 4 pounds per day) in horses with insulin resistance or Cushing’s Syndrome: The following chart shows the time course for the plasma insulin levels in a cross-over study:

One can see that even for the “low” NSC feed, the insulin remains elevated for over 240 minutes (4 hours). For the “high” NSC feed, insulin remains elevated for over 360 minutes (6 hours). In a horse fed twice a day, this means insulin may be elevated for 8 – 12 hours each day. During the elevation, many of the negative effects of insulin discussed above are in action.

It is reasonable to hypothesize that many hours of elevated insulin per day for many years could certainly lead to insulin resistance, as the body becomes less sensitive due to over exposure.

What Factors Affect the horse’s Response to NSC in the Diet?

In order of importance:

  • INDIVIDUAL VARIATION(Horse-to-horse) – by far the most important factor to consider; every horse will respond differently to a similar NSC intake
  • Amount of Feedstuff Consumed (Pounds) – both per meal and per day; the more NSC consumed at each meal or for the day will increase the glucose/insulin response
  • Rate at Which Feedstuff is Consumed (i.e. Forage vs. Concentrate) – the faster the horse consumes a feedstuff, the more pronounced the glucose/insulin response will be. For example, a horse will eat a 16% NSC pellet faster than it will consume 16% NSC hay, will then consume more NSC per unit of time, resulting in a higher response
  • NSC Content of Feedstuff (% NSC) – the concentration of NSC in a feed, in combination with amount of feed and rate of intake are related to the response. But. Just the % NSC alone if a relatively small factor – case in point, if a horse eats one kernel of corn at 75% NSC, they will be little to no response. Eating 4 pounds of corn in a few minutes will, intuitively produce a much greater response
  • Processing of Feedstuff – grinding and/or heat-treatment increases glycemic response

What is “Low Starch” (more appropriately, low NSC)?

The studies below were designed and funded by the Equine and Specialty Research Team of Cooperative Research Farms (www.crfarms.org), and were conducted at Michigan State University, East Lansing, Michigan.

Entitled Effects of Concentrate Starch Levels on the Glucose and Insulin Responses in Horses (E08 MSU27) and Effects of Concentrate Starch Levels on the Glucose and Insulin Responses in Insulin Resistant Horses (E10 MSU31), the purpose of the studies was to evaluate the effects of feeding different amounts of NSC (starch plus sugar) in concentrates to normal and insulin resistant horses on glucose and insulin response after feeding. Insulin resistant horses showed the characteristic regional fat deposits The four concentrate treatments were formulated to supply 0.66, 1.38, 2.10 and 2.82 grams of NSC per kilogram of body weight per meal. All horses received all concentrates in random order.

The combined results from the two studies are shown below. The red line depicts the upper end of the reference range for glucose in the horse. The blue lines show the data for insulin resistant horses, the brown lines show the responses of the normal horses.

It is evident that IR horses had higher resting glucose levels than normal horses, even though both groups were within the reference range. Further, the IR horses showed more profound blood glucose responses to increasing NSC intakes, exceeding the upper reference range level at 1.38, 2.1 and 2.82 g/kg BW NSC intake.

As insulin causes the major issues of concern, like laminitis and hyperactivity, we can concentrate on insulin responses.

The combined corresponding results for insulin from the two studies are shown below. The red line depicts the level of insulin in the horse (100 uIU/ml) at which the risk of laminitis in high, according to Dr. Treiber et al (Treiber KH, et al. Insulin resistance in equids; possible role in laminitis. J Nutr 2006;136:2094S–2098S.). The blue lines show the data for insulin resistant horses, the brown lines show the responses of the normal horses.

Looking at the corresponding plasma insulin levels on the following charts:

We can see at an NSC intake of 0.66 g/kg. BW, both normal and IR horses do not greatly exceed the 100 uIU/ml insulin level. But as NSC intake increases, to 1.38 g/kg BW and above, the IR horses are at greater risk of laminitis. Only at the higher NSC intake levels do normal horses reach risky levels of insulin.

A more detailed look at the data shows an interesting difference between IR and normal horses. It is the difference in the insulin response relative to the blood glucose response. Increases in glucose typically drive insulin levels. What we see in these studies is a much more pronounced insulin response in the IR horses compared to the normal horses, even when glucose if within the reference range.

The blue lines show the ratio of insulin to glucose for insulin resistant horses, the brown lines show the ratio of insulin to glucose for the normal horses.

We see that, at all levels of NSC intake, the IR horses have a much greater insulin response to glucose levels than normal horses. The difference in insulin to glucose responses between IR and normal horses become less at higher levels of NSC intake. This suggests higher NSC intakes of 2.1 and 2.82 g/kg BW cause even normal horses to have as great a laminitis risk at IR horse.
What does all this mean?

  • We must recognize there is a tremendous variation from horse-to-horse in its response to NSC intake, even within IR and normal populations
  • Insulin resistant horses are at a greater risk for insulin-related issues like laminitis.
  • “Safe” levels of NSC intake are different for IR horses compared to normal horses
  • Even normal horses can be at risk at higher levels of NSC intake
  • It is prudent to supply as many calories as possible with non-NSC calorie sources like fat and digestible fiber.

Recommendations

  1. For horses who are diagnosed with, or at risk for, Cushing's disease, equine metabolic syndrome and insulin resistance, concentrate NSC (starch plus ESC simple sugars) levels should not exceed 20% when the concentrate is fed at 0.5% of body weight daily; and, NSC intake per horse should not exceed 0.5 g/kg BW per meal or 1.0 g/kg BW daily, in order to minimize blood glucose concentrations postprandial.
     
  2. For normal horses (those who do not have, or are not at risk for, Cushing's disease, equine metabolic  syndrome  and  insulin  resistance),  concentrate  NSC  (starch  plus  ESC  simple sugars) levels should not exceed 33% when the concentrate is fed at 0.5% of body weight daily; and, NSC intake per horse should not exceed 1.0 g/kg BW per meal or 2.0 g/kg BW daily, in order to minimize blood glucose concentrations postprandial.

Appendix Table I. Maximum concentrate NSC recommendations for metabolically challenged and normal horses (metric version).

Item Metabolically challenged horses Normal horses
maximum % NSC in concentrate (when fed at .5% of body weight daily) 20 33
maximum NSC intake per meal, g per kg of body weight 0.5 1.0
maximum NSC intake per day, g per kg of body weight 1.0 2.0
1 starch plus ESC simple sugars 
2 horses who are diagnosed with, or at risk for, Cushing's disease, equine metabolic syndrome and insulin resistance.

Appendix Table II. Maximum concentrate NSC recommendations for metabolically challenged and normal horses (US-English version).

Item Metabolically challenged horses Normal horses
maximum % NSC in concentrate (when fed at .5% of body weight daily) 20 33
maximum NSC intake per meal, lb per 100 lb of body weight 0.05 0.10
maximum NSC intake per day, lb per 100 lb of body weight 0.10 0.20
1 starch plus ESC simple sugars 
2 horses who are diagnosed with, or at risk for, Cushing's disease, equine metabolic syndrome and insulin resistance.

D. Nutritionally-Related Diseases Affected by High NSC Diets

  1. Overweight Horse (obesity)
    Causes:
    1. Too much energy (calories) consumed
    2. Too little exercise
    3. Certain medical conditions (Metabolic Syndrome, Cushing’s…)
    4. Combination of above

    Solutions:

    1. Increase exercise (forced??)
    2. Treat medical conditions
    3. See nutritional recommendations following Cushing’s Syndrome : basically, decrease calories and NSC in diet
       
  2. Equine Metabolic Syndrome (including Insulin Resistance):
    • Reduced sensitivity to insulin over time due to exposure?
    • Associated with long-term feeding of high NSC diets.
    • Linked to obesity, laminitis, colic, exertional rhabdomyolysis, OCD.
    • Often confused with Cushing’s Syndrome because of the presence of insulin resistance

  3. Laminitis
    Causes:
    • Diet rich in soluble carbohydrate (i.e. rich spring grass, corn, etc.)
    • Obesity/overeating
    • Toxemia
    • Trauma
    • Drug related
    • Pituitary Tumor (Cushing’s Syndrome)
       

    Signs:

    • rocked-back” stance
    • heat in hooves
    • throbbing digital pulse
    • long-term – “founder lines” on hooves
       

    Nutritional Management:

    • Short-term (acute phase when deemed acceptable by veterinarian)
      • grass or mixed hay
      • limit or ELIMINATE pasture
      • provide essential amino acids, vitamins and minerals in low calorie, low NSC product
    • Long-term
      • Above and...
      • may add balanced fat source for adding weight.
      • provide essential amino acids, vitamins and minerals in low calorie, low NSC product
         
  4. Cushing’s Syndrome (hyperadrenocorticism )
    • Dysfunction of Anterior Pituitary -not nutritional in origin.
    • Signs – long, curly haircoat, won’t shed in summer, unthrifty, tend to muscle waste
    • Complicated – prone to laminitis, but difficult to keep weight on.
    • Dietary aims: see nutritional recommendations
      • Protein quality (essential amino acid balance) is critical for muscle structure and function as well as overall tissue repair.
      • Supply as many calories as possible with FAT to minimize glucose/insulin response
         
  5. Hyperkalemic Periodic Paralysis (HYPP )
    • Inherited genetic defect that affects muscle potassium function.
    • Symptoms vary widely among horses, from mild muscle tremors to death from cardiac arrest and/or respiratory failure.
    • DNA test is available to identify horses that carry the defective gene(s).
    • Can be NN (normal), NH or HH (positive).
    • Dietary Implications:
      • HYPP positive horses are sensitive to high levels of potassium in their diets, as well as sudden changes in potassium levels.
      • Desire potassium level < 1.0% in TOTAL DIET.
    • Unfortunately, forage is the highest potassium feedstuff (see chart below).
    • Must balance risk of GI dysfunction with keeping blood K levels in check. Usually want forage intake at a minimum of 1% of body weight.
    • Provide balance of nutrients with concentrate formulated with low potassium (<1%) and highly digestible fiber source, such as beet pulp and soy hulls .
    • If horse is NN or NH, but NOT symptomatic – feed 1% of body weight as forage and enough low potassium concentrate to maintain desired condition; added fat may help as NSC may aggravate HYPP.
    • If horse IS symptomatic – eliminate forage and feed enough of a high DIGESTIBLE fiber (>16%) feed to maintain desired condition in as many feedings per day as possible (4-5 times).
Amount of Potassium (K) in Traditional Horse Feeds (NRC, 1989)
FEED %K
   
FORAGES
Alfalfa (pasture) 2.27 
Alfalfa (early bloom hay) 2.56 
Alfalfa (mid-bloom hay) 1.56 
*Beet Pulp (20% CF)  0.22 
Ky. Bluegrass (pasture)  2.27 
Ky. Bluegrass (hay) 1.52 
Bromegrass (pasture) 3.16 
Bromegrass (hay) 1.99 
Red Clover (pasture)  2.49 
Red Clover (hay)  1.81 
Oat Straw 2.33 
Orchard grass (pasture) 2.09 
Orchard grass (hay) 2.69 
Timothy (pasture)  2.06 
Timothy (hay) 2.41
Wheat Straw 1.40
CONCENTRATES 
Barley 0.50
Corn 0.37 
Oats 0.45 
Soybean Meal 2.36 
Wheat Bran 1.37 
Yeast 1.81
*Brewers Grain (dehydrated) (15% CF) 0.09

NOTE: Equine Polysaccharide Storage Myopathy (EPSM) and Recurrent Exertional Rhabdomyolysis (RER) “Tying-up” are addressed in Performance Horse Nutrition Article

What feed can be used to minimize NSC but assure adequate intake of other critical nutrients (amino acids, vitamins, minerals)?

  • LOW INTAKE (1-2 pounds per day)
  • LOW NSC (under 15%)
  • DENSE CONCENTRATION OF CRITICAL  “NON-CALORIE” NUTRIENTS
  • (protein, vitamins, minerals)
  • OFTEN REFERRED TO AS “RATION BALANCERS”
  • If more calories are needed, use balanced fat source and highly digestible fiber sources.

SUMMARY  

  • Many nutrition-related health issues we see in horses today are related to feeding HIGH NSC DIETS.
  • It is important to consider NUMEROUS factors when assessing the proper course of action:
    • INDIVIDUAL VARIATION (Horse-to-horse)
    • Amount of Feedstuff Consumed (Pounds)
    • Rate at Which Feedstuff is Consumed
    • NSC Content of Feedstuff (% NSC)
    • Processing of Feedstuff (grinding and/or heat-treatment)
  • It is important to consider the horse’s TOTAL DIET when determining the proper course of action.
  • Supplying needed calories with FAT and HIGHLY DIGESTIBLE FIBER is the safest way to manage horses with metabolic issues related to high NSC diets.
  • Recommend feeding as often during the day as possible   (4-5x per day?)

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D.J. Burke, Ph.D.