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Evaluation of glucose metabolism in three horses with lower motor neuron degeneration

Johannes H. van der KolkDepartment of Equine Sciences, Faculty of Veterinary Medicine, Utrecht University, Yalelaan12 3508 TD Utrecht, The Netherlands.

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Kim E. P. M. RijnenDepartment of Equine Sciences, Faculty of Veterinary Medicine, Utrecht University, Yalelaan12 3508 TD Utrecht, The Netherlands.

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Françoise ReyDepartment of Equine Sciences, Faculty of Veterinary Medicine, Utrecht University, Yalelaan12 3508 TD Utrecht, The Netherlands.

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Ellen de Graaf-RoelfsemaDepartment of Equine Sciences, Faculty of Veterinary Medicine, Utrecht University, Yalelaan12 3508 TD Utrecht, The Netherlands.

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Guy C. M. GrinwisDepartment of Pathobiology, Faculty of Veterinary Medicine, Utrecht University, Yalelaan12 3508 TD Utrecht, The Netherlands.

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Inge D. WijnbergDepartments of Equine Sciences, Faculty of Veterinary Medicine, Utrecht University, Yalelaan12 3508 TD Utrecht, The Netherlands.

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Abstract

Objectives—To determine whether increased glucose metabolism is the potential cause of the decreased plasma glucose curve determined after oral glucose tolerance testing in horses with lower motor neuron degeneration.

Animals—3 horses with signs suggestive of lower motor neuron degeneration, 1 horse with malignant melanoma with multiple metastases, and an obese but otherwise healthy horse.

Procedures—Glucose metabolism was assessed by use of the hyperglycemic clamp and euglycemic hyperinsulinemic clamp techniques.

Results—Mean rate of glucose metabolism of horses with lower motor neuron degeneration was significantly greater (mean, 3.7 times greater than control horses; range, 2.1 to 4.8 times greater) than that reported in 5 healthy control horses (41 ± 13 µmol/kg/min vs 11 ± 4.5 µmol/kg/min, respectively). In addition, one of the affected horses, an 8-year-old warmblood gelding, had a 5.6- times increased sensitivity to exogenously administered insulin, compared with that reported in 5 healthy control horses. Pancreatic insulin secretion was not insufficient in horses with lower motor neuron degeneration. Findings in the 2 diseased control horses were unremarkable.

Conclusions and Clinical Relevance—Increased glucose metabolism in horses with lower motor neuron degeneration may be the cause of the decreased plasma glucose curve detected after oral glucose tolerance testing. This finding could aid in developing supportive treatments with respect to adequate glucose and vitamin E supplementation. (Am J Vet Res 2005;66:271–276)

Abstract

Objectives—To determine whether increased glucose metabolism is the potential cause of the decreased plasma glucose curve determined after oral glucose tolerance testing in horses with lower motor neuron degeneration.

Animals—3 horses with signs suggestive of lower motor neuron degeneration, 1 horse with malignant melanoma with multiple metastases, and an obese but otherwise healthy horse.

Procedures—Glucose metabolism was assessed by use of the hyperglycemic clamp and euglycemic hyperinsulinemic clamp techniques.

Results—Mean rate of glucose metabolism of horses with lower motor neuron degeneration was significantly greater (mean, 3.7 times greater than control horses; range, 2.1 to 4.8 times greater) than that reported in 5 healthy control horses (41 ± 13 µmol/kg/min vs 11 ± 4.5 µmol/kg/min, respectively). In addition, one of the affected horses, an 8-year-old warmblood gelding, had a 5.6- times increased sensitivity to exogenously administered insulin, compared with that reported in 5 healthy control horses. Pancreatic insulin secretion was not insufficient in horses with lower motor neuron degeneration. Findings in the 2 diseased control horses were unremarkable.

Conclusions and Clinical Relevance—Increased glucose metabolism in horses with lower motor neuron degeneration may be the cause of the decreased plasma glucose curve detected after oral glucose tolerance testing. This finding could aid in developing supportive treatments with respect to adequate glucose and vitamin E supplementation. (Am J Vet Res 2005;66:271–276)