Differential regulation of insulin-like growth factor I by growth hormone and thyroid hormone in the heart of juvenile hypophysectomized rats

1992 ◽  
Vol 24 (6) ◽  
pp. 631-639 ◽  
Author(s):  
Joel M. Kupfer ◽  
Stanley A. Rubin
2000 ◽  
Vol 96 (2) ◽  
pp. 140-149 ◽  
Author(s):  
Melanie P. Foster ◽  
Eric R. Jensen ◽  
Encarnacion Montecino-Rodriguez ◽  
Hyosuk Leathers ◽  
Nelson Horseman ◽  
...  

1989 ◽  
Vol 257 (2) ◽  
pp. F252-F261 ◽  
Author(s):  
R. Lajara ◽  
P. Rotwein ◽  
J. D. Bortz ◽  
V. A. Hansen ◽  
J. L. Sadow ◽  
...  

We examined the regulation of insulin-like growth factor I (IGF-I) in kidney during the renal hypertrophy produced by two different experimental models: growth hormone treatment of hypophysectomized rats and compensatory hypertrophy subsequent to unilateral nephrectomy. Immunostaining for IGF-I in collecting ducts was enhanced in kidneys from growth hormone-repleted hypophysectomized rats, and the levels of IGF-I mRNAs were increased. In compensatory hypertrophy, no enhancement of the intensity of immunostaining was observed in kidneys of nephrectomized rats until 5 days postnephrectomy, at which time immunostainable IGF-I was increased markedly in medullary collecting ducts of hypertrophied kidneys compared with kidneys from sham-operated animals. No difference in steady-state levels of any IGF-I mRNA species was detected in whole kidneys or in collecting ducts from nephrectomized or sham-operated rats at any time postnephrectomy. Our findings demonstrate an increase in both IGF-I mRNA and in immunostainable IGF-I in collecting duct in the setting of growth hormone-induced renal hypertrophy but suggest that other, possibly translational, mechanisms underlie the induction of IGF-I synthesis during compensatory hypertrophy.


1996 ◽  
Vol 134 (5) ◽  
pp. 563-567 ◽  
Author(s):  
Mehboob A Hussain ◽  
Ole Schmitz ◽  
Jens OL Jorgensen ◽  
Jens S Christiansen ◽  
Jorgen Weeke ◽  
...  

Hussain MA, Schmitz O, Jorgensen JOL, Christiansen JS, Weeke J, Schmid C, Froesch ER. Insulin-like growth factor I alters peripheral thyroid hormone metabolism in humans. Eur J Endocrinol 1996;134:563–7. ISSN 0804–4643 Insulin-like growth factor I (IGF-I) is considered to mediate some of the growth-promoting and metabolic effects of growth hormone (GH). Growth hormone treatment of healthy and GH-deficient subjects is accompanied by increased conversion of thyroxine (T4) to triiodothyronine (T3) in peripheral tissues. Whether these effects are mediated by IGF-I is unknown. To assess the respective roles of these hormones on thyroid hormone metabolism we have treated two groups of subjects. The first group consisted of eight healthy subjects who were treated with IGF-I 10 μg·kg−1·h−1 sc for 5 days). The second group consisted of eight subjects with combined GH and thyrotropin (TSH) deficiency due to acquired pituitary disease. They were treated with IGF-I (10 μg·kg−1·h−1 sc for 7 days), GH (2 IU m−2 sc q.i.d.) or both hormones together. The IGF-I treatment in healthy subjects led to an increase in free T3 (FT3) and a reduction in TSH levels, whereas FT4 and total T4 (TT4) levels remained unchanged. In the second group—in which all subjects were substituted with oral lthyroxine—treatment with IGF-I led to an elevation of FT3 in the face of unchanged T4 levels. Growth hormone alone and GH plus IGF-I resulted in a more pronounced elevation in T3 level. The results suggest that IGF-I partially mediates the well-known effects of GH on peripheral conversion of T4 to T3. However, GH has more pronounced effects on thyroid hormones that apparently are not mediated by IGF-I. ER Froesch, Division of Endocrinology and Metabolism, Department of Internal Medicine, University Hospital of Zürich, Rámistr, 100, 8091 Zürich, Switzerland


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