Lipid metabolism in horses with hyperadrenocorticism

J. H. van der Kolk From the Department of Large Animal Medicine and Nutrition, Veterinary Faculty, Utrecht University, PO Box 80.152, 3508 TD Utrecht, The Netherlands.

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Th. Wensing From the Department of Large Animal Medicine and Nutrition, Veterinary Faculty, Utrecht University, PO Box 80.152, 3508 TD Utrecht, The Netherlands.

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H. C. Kalsbeek From the Department of Large Animal Medicine and Nutrition, Veterinary Faculty, Utrecht University, PO Box 80.152, 3508 TD Utrecht, The Netherlands.

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H. J. Breukink From the Department of Large Animal Medicine and Nutrition, Veterinary Faculty, Utrecht University, PO Box 80.152, 3508 TD Utrecht, The Netherlands.

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Summary

Lipid metabolism was studied in 21 horses with hyperadrenocorticism. To be included in the study, horses had to have histologic evidence of a pars intermedia adenoma found at necropsy (n = 9), a baseline ACTH concentration greater than 400 pg/ml (n = 6), or a plasma cortisol concentration 2 hours after iv administration of 25 IU of acth greater than 413 nmol/Lin = 16).

Mean ± sd baseline plasma cortisol concentration was 338 ± 261 nmol/L (n = 20), mean ± sd plasma insulin concentration was 97 ± 54 μU/ml (n = 15), mean ± sd plasma β-hydroxybutyrate concentration was 1.8 ± 1.2 mg/dl (n = 21), and mean ± sd plasma nonesterified fatty acids concentration was 6.2 ± 6.4 mg/dl (n = 21). None of the horses had hyperlipemia.

Compared with clinically normal horses, horses with hyperadrenocorticism had increased lipolysis and increased ketogenesis. It was concluded that cortisol cannot be the sole factor contributing to insulin resistance in horses with hyperadrenocorticism.

Summary

Lipid metabolism was studied in 21 horses with hyperadrenocorticism. To be included in the study, horses had to have histologic evidence of a pars intermedia adenoma found at necropsy (n = 9), a baseline ACTH concentration greater than 400 pg/ml (n = 6), or a plasma cortisol concentration 2 hours after iv administration of 25 IU of acth greater than 413 nmol/Lin = 16).

Mean ± sd baseline plasma cortisol concentration was 338 ± 261 nmol/L (n = 20), mean ± sd plasma insulin concentration was 97 ± 54 μU/ml (n = 15), mean ± sd plasma β-hydroxybutyrate concentration was 1.8 ± 1.2 mg/dl (n = 21), and mean ± sd plasma nonesterified fatty acids concentration was 6.2 ± 6.4 mg/dl (n = 21). None of the horses had hyperlipemia.

Compared with clinically normal horses, horses with hyperadrenocorticism had increased lipolysis and increased ketogenesis. It was concluded that cortisol cannot be the sole factor contributing to insulin resistance in horses with hyperadrenocorticism.

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