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Effect of progressive cachectic parasitism and growth hormone treatment on hepatic 5'-deiodinase activity in calves
Authors:Kahl Stanislaw  Elsasser T H  Sartin J L  Fayer R
Institution:

a Growth Biology Laboratory, US Department of Agriculture, Agricultural Research Service, Animal and Natural Resources Institute, Building 200, Room 211E, Beltsville, MD 20705, USA

b Department of Physiology and Pharmacology, College of Veterinary Medicine, Auburn University, Auburn, AL 36849, USA

c Animal Waste Pathogen Laboratory, US Department of Agriculture, Agricultural Research Service, Animal and Natural Resources Institute, Beltsville, MD 20705, USA

Abstract:Thyroid status is compromised in a variety of acute and chronic infections. Conversion of thyroxine (T4) into the metabolically active hormone, triiodothyronine (T3), is catalyzed by 5′-deiodinase (5′D) mainly in extrathyroidal tissues. The objective of this study was to examine the effect of protozoan parasitic infection (Sarcocystis cruzi) on hepatic 5′D (type I) activity and plasma concentrations of T3 and T4 in placebo- or bovine GH (bGH)-injected calves. Holstein bull calves (127.5±2.0 kg BW) were assigned to control (C, ad libitum fed), infected (I, 250,000 S. cruzi sporocysts per os, ad libitum fed), and pair-fed (PF, non-infected, fed to intake of I treatment) groups placebo-injected, and three similar groups injected daily with pituitary-derived bGH (USDA-B-1, 0.1 mg/kg, i.m.) designated as CGH, IGH and PFGH. GH injections were initiated on day 20 post-infection (PI), 3–4 days prior to the onset of clinical signs of the acute phase response (APR), and were continued to day 56 PI at which time calves were euthanized for liver collection. Blood samples were collected on day 0, 28, and 55 PI. Alterations in nutritional intake did not affect type I 5′D in liver. Treatment with bGH increased (P<0.05) 5′D activity in C (24.6%) and PF (25.5%) but not in I calves. Compared to PF calves, infection with S. cruzi reduced 5′D activity 25% (P<0.05) and 47.8% (P<0.01) in placebo- and bGH-injected calves, respectively. Neither nutrition nor bGH treatment significantly affected plasma concentrations of T4 and T3 on day 28 and 55 PI. However, plasma thyroid hormones were reduced by infection. On day 28 PI, the average plasma concentrations of T3 and T4 were reduced in infected calves (I and IGH) 36.4% (P<0.01) and 29.4% (P<0.05), respectively, compared to pair-fed calves (PF and PFGH). On day 55 PI, plasma T3 still remained lower (23.7%, P<0.01 versus PF) in infected calves while plasma T4 returned to control values. The data suggest that parasitic infection in growing calves inhibits both thyroidal secretion and extrathyroidal T4 to T3 conversion during the APR. After recovery from the APR, thyroidal secretion returns to normal but basal and bGH-stimulated generation of T3 in liver remains impaired.
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