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Felipe Rodriguez and Trinidad Jolin

Abstract.

The present study was carried out to examine the role of endogenous dopamine and somatostatin in the mechanisms involved in the restricted feeding-induced inhibition of TSH secretion in rats. GH secretion was examined in parallel. Restricted feeding by 50% or 75% was associated with a decrease in the pituitary and circulating levels of TSH and GH in both untreated and TRH-treated groups (p<0.001), the changes being proportional to the feeding level. Intravenous injections of the dopamine antagonists, domperidone or haloperidol, failed to affect the magnitude of the differences in plasma TSH and GH levels among control and food-restricted groups, indicating that dopaminergic mechanisms had little effect on the regulation of TSH and GH secretion during restricted feeding in rats. Cerebroventricular injection of somatostatin anti-serum resulted in a marked increase in plasma TSH and GH levels in all the experimental groups (p<0.001). The increase in plasma GH and TSH induced by somatostatin anti-serum was greater in rats fed a 25% diet than in either controls or rats fed 50% of the diet; the values for the latter two groups were also different (p<0.001). The decreased TSH and GH values in somatostatin anti-serum-treated food restricted rats as compared with those in control animals on somatostatin anti-serum or normal rabbit serum can probably be attributed to the decreased available pituitary TSH and GH pools. The data indicate that long-term restricted feeding affects anterior pituitary function in rats, presumably reflecting alterations in the secretion of an inhibiting hormone, somatostatin.

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Manuela Rodriguez, Felipe Rodriguez, Trinidad Jolin and Pilar Santisteban

Rodriguez M, Rodriguez F, Jolin T, Santisteban P. Comparative effects of food restriction, fasting, diabetes and thyroidectomy on growth hormone and thyrotropin gene expression in the rat pituitary. Eur J Endocrinol 1995;133:110–6. ISSN 0804–4643

To examine the molecular basis for the decreased pituitary growth hormone (GH) and thyrotropin (TSH) content during restricted feeding, fasting and diabetes, we measured steady-state levels of mRNA for TSH-α TSH-β and GH in the pituitary from normal rats either fed ad libitum (C), limited to 75%, 50% and 25% (FR75, FR50, FR25, respectively) of ad libitum intake, or deprived of food for 2 and 4 days (F2 and F4, respectively), and also in streptozotocin-diabetic (D) and D insulin-treated animals. The results from these experimental groups were compared with those in thyroidectomized (Tx) rats. Pituitary mRNA was quantified by Northern blot hybridization with cDNA probes specific for rat TSH-α, TSH-β and GH. Although changes in the pituitary GH mRNA during restricted feeding, fasting and diabetes were similar qualitatively to those induced by hypothyroidism, GH mRNA levels in Tx rats (> 10% of C values) were less than in the other experimental groups (p < 0.001). Pituitaries from FR50, FR25 and D rats also contained less GH mRNA than F2 and F4 animals (p < 0.05). Thyroidectomy resulted in a marked increase in both TSH-β and TSH-α mRNAs, the changes in TSH-β mRNA being greater than those in TSH-α mRNA. In contrast, FR50, FR2 5, F2, F4 and D rats exhibited a decrease in pituitary TSH-β mRNA (60%, 50%, 35%, 36% and 33%, respectively, of C values; p < 0.01–0.05) and in TSH-α mRNA levels (81%, 64%, 46%, 43% and 36%, respectively, of normal values; p < 0.02–0.05), TSH-β mRNA showing the greater changes. However, pituitaries from F2, F4 and D rats contained less TSH-β and TSH-α mRNA levels than FR50 and FR25 animals (p < 0.05). Insulin therapy partially restored the changes in mRNA for GH, TSH-β and TSH-α observed in D rats. In addition, the pituitary nuclear triiodothyronine in Tx, FR50, FR25, F2, F4 and D rats was reduced to 19%, 73%, 52%, 76%, 51% and 41%, respectively of C values (p < 0.05–0.001). These data suggest that GH, TSH-α and TSH-β gene expression are modulated by metabolic and/or endocrine changes accompanying restricted feeding, fasting and diabetes.

P Santisteban, Instituto de Investigaciones Biomédicas, CSIC, Arturo Duperier 4, 28029 Madrid, Spain

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Felipe Rodriguez, Mario Mellado, Eladio Montoya and Trinidad Jolin

Abstract.

The aim of the present study was to identify the mechanisms involved in the reduction of TSH secretion during prolonged food restriction. The basal TSH secretion rate, the TSH secreted in response to TRH, both in vivo and in vitro, and the TSH, nuclear T3, and plasma membrane TRH binding sites in the pituitary were determined in rats receiving 75% (FR75), 50% (FR50) and 25% (FR25) of the food consumed by the ad libitum fed rats (controls). The basal TSH secretion rate (μg·h−1g·(100 g)−1) in FR75, FR50 and FR25 groups were decreased by 19, 42 and 74% of control values, respectively, whereas the TSH secreted in response to TRH in vivo and in vitro was reduced by 21 and 13% in FR50, and 55 and 44% in FR25, respectively, of the corresponding control values. Food restriction increased the TRH binding sites from 229 in controls to 322, 479 and 521 (fmol/mg protein), in FR75, FR50 and FR25 groups, respectively, whereas the opposite was seen in nuclear T3(controls 862, FR75 841, FR50 342 FR25 233 fmol/mg DNA). Moreover, a decrease in the pituitary TSH concentration was observed in FR50 and FR25 rats. The data suggest that an alteration in the amount of TRH reaching the pituitary gland is probably the main responsible for the low plasma TSH values during food restriction. However, an inhibitory effect at the pituitary level cannot be ruled out.