Abstract
Previous studies have demonstrated that serum TSH and GH decrease during fasting. Taking advantage of the fact that somatostatin antiserum administration is an effective, specific method of blocking endogenous somatostatin activity, we performed the present investigation to explore whether known fasting-induced increases in somatostatin might underlie the mechanism(s) of this decrement. After a 48 hour fast, two groups of male rats were anesthetized and an indwelling right atrial catheter inserted. The control rats (n = 11) were injected with normal sheep serum and the experimental rats (n = 9) were injected with a specific antiserum to cyclic somatostatin; one and one-half hours later, blood was collected in a basal state after which 200 ng TRH was injected. The basal mean (+/- SE) T3 and T4 concentrations were 23 +/- 3 ng/dl and 1.9 +/- 0.1 ug/dl, respectively, in the fasted control group and 30 +/- 2 ng/dl and 2.3 +/- 0.2 ug/dl in the fasted somatostatin antiserum injected rats. While serum T4 and T3 levels were statistically unchanged between these two groups, basal TSH increased from 537 +/- 81 ng/ml in the control rats to 2913 +/- 742 ng/ml in the somatostatin antiserum-treated rats (P less than 0.05). Basal growth hormone levels were also higher in the somatostatin antiserum-injected rats (196 +/- 19 ng/ml vs 72 +/- 7 ng/ml (P less than 0.0025). TSH peak values following TRH injection were not different in the two study groups. In summary, the present study indicates that: (1) somatostatin antiserum increases both basal GH and TSH values in fasting rats; and (2) somatostatin and TRH may act through different pathways to modulate TSH secretion. By implication, therefore, it is suggested that enhanced somatostatin-like activity may represent one mechanism mediating the fasting-induced decrement observed in serum TSH and GH.
Published Version
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