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United States Department of Agriculture

Agricultural Research Service

Title: Effect of Progressive Cachectic Parasitism and Growth Hormone Treatment on Hepatic 5'-Deiodinase Activity in Calves

Authors
item Kahl, Stanislaw
item Elsasser, Theodore
item Sartin, J. - AUBURN UNIVERSITY
item Fayer, Ronald

Submitted to: Domestic Animal Endocrinology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: January 9, 2002
Publication Date: October 1, 2002
Citation: Kahl, S., Elsasser, T.H., Sartin, J.L., Fayer, R. 2002. Effect of progressive cachectic parasitism and growth hormone treatment on hepatic 5'-deiodinase activity in calves. Domestic Animal Endocrinology. 22:211-221.

Interpretive Summary: Thyroid status of growing animals is an important determinant of metabolic rate and affects the amount of nutrients used for maintenance and growth. Whereas prohormone thyroxine (T4) is synthesized only in the thyroid gland, triiodothyronine (T3), the most metabolically active thyroid hormone, is produced by enzymatic 5'-deiodination of the T4 in extrathyroidal tissues. Therefore, the extrathyroidal activity of iodothyronine 5'-deiodinase (5'D is an important control point for regulating the metabolic status of animal tissues in various physiological and pathological situations. In the present study we investigated how growth hormone (GH) regulation of thyroid status in growing calves is affected by mild systemic parasitism modeled with Sarcocystis cruzi. We demonstrated that infection with the protozoan parasite S. cruzi in calves suppressed thyroidal secretion during the acute phase response (APR) to infection. After the recovery period from APR, the ethyroid gland returned to normal activity but extrathyroidal T4 to T3 conversion remained depressed for several weeks resulting in a decreased pool of circulating T3. Decreased thyroidal secretion or extrathyroidal T3 production could not be alleviated by GH treatment. These results suggest that decreased thyroid activity during APR of S. cruzi infection could be a part of somatotropic axis-directed down regulation of growth and can be regarded as a short-term adaptive mechanism to save energy for metabolic purposes of higher priority than growth. However, prolonged decrease in peripheral T3 generation becomes pathological on its own, and may be involved in a long-term impairment of growth performance in calves.

Technical Abstract: Conversion of thyroxine (T4) into the metabolically active hormone, tri- iodothyronine (T3), is catalyzed by 5'-deiodinase (5'D) mainly in liver. This study examined the effect of parasitic infection (Sarcocystis cruzi) on hepatic type I 5'D activity and plasma concentrations of T3 and T4 in placebo- or bovine GH (bGH)-injected Holstein bull calves (127.5 kg BW). Animals were assigned to control (C, ad libitum fed), infected (I, 250,000 sporocysts per os, ad libitum fed), and pair-fed (PF, non-infected, fed to intake of I) groups, and 3 similar groups injected daily with pituitary- derived bGH (0.1 mg/kg, i.m.) designated as CGH, IGH and PFGH. bGH injections started on d 20 postinfection (PI), 4 d prior to the onset of clinical signs of the acute phase response (APR), and continued to d 56 PI when calves were euthanized for liver collection. Blood was collected on d 0, 28, and 55 PI. Decrease in nutritional intake did not affect hepatic 5'D. bGH treatment 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 reduced (P<0.05) 5'D activity 25% and 47.8%, in placebo- and bGH-injected calves, respectively. Neither nutrition nor bGH affected plasma levels of T4 and T3 on d 28 and 55 PI. On d 28 PI, plasma T3 and T4 were reduced (P<0.05) in I calves (I+IGH), respectively, 36.4% and 29.4%, compared to PF calves (PF+PFGH). On d 55 PI, plasma T3 remained lower (23.7%, P<0.01 vs. PF) in I calves while plasma T4 returned to control values. The data suggest that parasitic infection in calves inhibits both thyroidal secretion and extrathyroidal T4 to T3 conversion during the APR. After the APR, thyroidal secretion returns to normal but basal and bGH-stimulated generation of T3 in liver remains impaired.

Last Modified: 12/19/2014
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