Fructose is a simple sugar present in honey and fruits, but can also exist as a polymer (fructans) in pasture grasses.  Mammals are unable to metabolize fructans, but certain gram-positive bacteria contain fructanases and can convert fructans to fructose in the gut.  Recent studies suggest that fructose generated from bacteria or directly obtained from the diet can induce both increased intestinal permeability and features of metabolic syndrome, especially the development of insulin resistance. The development of insulin resistance is driven in part by the metabolism of fructose by fructo- kinase C in the liver, which results in oxidative stress in the hepatocyte. Similarly, the metabolism of fructose in the small bowel by intestinal fructokinase may lead to increased intestinal permeability and endotoxemia. Although speculative, these observations raise the possibility that the mechanism by which fructans induce laminitis could involve intestinal and hepatic fructokinase. Further studies are indicated to determine the role of fructanases, fructose, and fructokinase in equine metabolic syndrome and laminitis.

Modern feeding and housing practices of horses are typically directed at achieving a high level of athletic performance.  There are some unfortunate consequences including an increased incidence of disease. Some of these diseases can be directly linked to dietary practices, while in others diet contributes as an important co-factor.  Breeding practices to select for specific traits have also inadvertently resulted in the preferential selection of horses with genetic mutations within several breeds.  In several of these genetic disorders specific dietary management is required for affected horses to achieve an acceptable level of performance.  Diseases in which diet has a significant influence are discussed including equine metabolic syndrome, laminitis, diseases attributed to deficiency of vitamin E and/or selenium, exertional myopathies, nutritional secondary hyperparathyroidism, hyperkalaemic periodic paralysis, and the developmental orthopaedic disease complex.

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Although the treatment and management of laminitis in the horse requires a holistic and often multidisciplinary approach from the veterinarian, farrier, and nutritionist, this review focuses on pharmacologic interventions that might have prophylactic benefit, specifically in the horse with laminitis as a result of pituitary pars intermedia dysfunction and equine metabolic syndrome.

Article Outline

• Pharmacologic treatment of PPID
• • Dopamine Agonists
  • Cyproheptadine
  • Inhibitors of Cortisol Synthesis
  • Drug Selection in PPID
• Pharmacologic treatment of EMS
• • l-Thyroxine
  • Lessons from Human Metabolic Syndrome?
  • Metformin
  • Thiazolodinediones
• Summary

Equine pituitary pars intermedia dysfunction (PPID), also known as equine Cushing's syndrome, is a widely recognized disease of aged horses. Over the past two decades, the aged horse population has expanded significantly and in addition, client awareness of PPID has increased. As a result, there has been an increase in both diagnostic testing and treatment of the disease. This review focuses on the pathophysiology and clinical syndrome, as well as advances in diagnostic testing and treatment of PPID, with an emphasis on those findings that are new since the excellent comprehensive review by Schott in 2002.

• Anatomy and physiology of the equine pituitary pars intermedia
• Anatomy
• Physiology
   
   
• 
   
• Epidemiology
• Pathophysiology
• Clinical signs of PPID
• Hirsutism
• Muscle Atrophy
• Laminitis
• PU/PD
• Hyperhidrosis
• Abnormal Fat Distribution and Insulin Resistance
• Opportunistic Infections and Immunosuppression
• Behavioral Abnormalities
• Reproductive Infertility
• Neurologic Disease
• Clinical Pathology
• Diagnostic tests for PPID
• Dexamethasone Suppression Test
• Endogenous Plasma ACTH or α-MSH Concentration
• TRH Stimulation Test
• Combined Dexamethasone Suppression/TRH Stimulation Test
• Domperidone Response Test
• Serum Insulin Concentration
• Cortisol Circadian Rhythm Loss
• Urinary Cortisol/Creatinine Ratio
• ACTH Stimulation Test
• Advanced Imaging Modalities
• Necropsy
• Treatment
• Summary
• References

The concept of an equine metabolic syndrome (EMS) was first proposed in 2002. This concept has developed over time, and EMS was recently described in a consensus statement released by the American College of Veterinary Internal Medicine. In human medicine, metabolic syndrome (MetS) refers to a set of risk factors that predict the risk of cardiovascular disease, including obesity, glucose intolerance and insulin resistance (IR), dyslipidemia, microalbuminuria, and hypertension. EMS shares some of the features of MetS, including increased adiposity, hyperinsulinemia, IR, but differs in that laminitis is the primary disease of interest.

• Components of the syndrome
   
• 
   
• Breed predisposition
• Clinical presentation
• Laminitis
   
• 
  
  
• Complications of Hospitalization
• Obesity and Regional Adiposity
   
• 
• 
• Preputial or Mammary Gland Swelling
  
  
• 
  
  
• Pathophysiology
• Predisposition
• Hyperinsulinemia
• Hepatic Insulin Resistance
• Peripheral Insulin Resistance
• Obesity
• Lipotoxicity
• Inflammation
• Adipokines
• Diagnosis
• Screening Tests
• Dynamic Tests
• Management
• Weight Reduction
• Pasture Access
• Medical treatment
• Levothyroxine Sodium
• Metformin Hydrochloride
• Other Antidiabetic Drugs
• Summary

Few studies have examined the effect of dietary restriction in horses with equine metabolic syndrome (EMS). This study aimed to determine improvements in insulin sensitivity following dietary restriction for 6 weeks, and to determine if the improvement would be greater in horses receiving short-chain fructo-oligosaccharides (sc-FOS). Dietary management involved feeding grass hay, restricted to 1.25% of body mass (BM) as daily dry matter intake and soaked in cold water prior to feeding, with the addition of a vitamin and mineral nutraceutical supplement with or without the addition of sc-FOS (10 g/100 kg).

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