Steven L. Davis

Endocrine Regulation of Growth in Ruminants

Hormone regulation of growth involves multiple hormones acting in concert. It is currently believed that the principal hormones are growth hormone and the somatomedins. These hormones, however, would be of limited effect without the presence of thyroid hormones and, at puberty, gonadal steroid hormones. Normal growth is additionally dependent upon insulin and glucocorticoids. Interactions among these hormones and cellular mechanism of hormone action are still poorly understood. It appears that optimal secretion of growth hormone and the somatomedins is dependent on breed, age, sex and nutrient intake. Generally those variables which are related to enhanced long term growth hormone secretion are also associated with greater rates of growth. Therefore, it should be theoretically possible to artificially enhance growth rate of domestic animals by enhancing growth hormone secretion, injecting synthetically derived growth hormone or by alteration of skeletal muscle cell responsiveness to a given amount of hormone. Although very little is known about the latter area, it would ultimately seem to be the most attractive approach because of proposed inherent genetic limitations in cell responsiveness to hormonal stimulation. In addition, any of the approaches suggested above may be further limited if applied singly rather than in the presence of additional amounts of secondary hormones associated with growth.

Thyrotropin and Prolactin Secretory Patterns during 24-Hours Infusion of Thyrotropin-Releasing Hormone in Calves

Plasma levels of thyrotropin (TSH), prolactin (Prl), growth hormone (GH), thyroxine (T4), and triiodothyronine (T3) were measured in response to continuous 24-h infusion of synthetic thyrotropin-releasing hormone (TRH) in normal and surgically thyroidectomized (THYX) calves in a series of 2 experiments. In the 1st experiment, the low dose of TRH (0.077 microgram/min) had no effect on any hormone levels measured. Plasma TSH concentration increased significantly (p less than 0.05) in response to TRH infusion (0.77 microgram/min) in both experiments, but plasma TSH levels plateaued and then declined in both cases despite continued TRH infusion and irrespective of the presence or absence of a thyroid gland. A similar pattern of secretion, though less markedly decreased over time, was observed for plasma Prl in both experiments. The higher dose (0.77 microgram/min) of TRH had no effect on plasma GH concentration in the 1st infusion, but did result in a significant (p less than 0.05) increase in overall mean concentration of GH in both normal and THYX calves in the 2nd experiment. Removal of the thyroid gland, thus removing the source of increasing T4 and T3 levels seen in normal calves infused with TRH, failed to alter the secretory patterns of TSH and Prl. These data suggest that feedback inhibition by increasing plasma thyroid hormone concentrations was not responsible for the failure of TSH and, to a lesser extent, Prl to maintain chronically elevated plasma levels in response to continuous 24-h TRH infusion. It is suggested that a depletion of pituitary TSH and Prl stores readily secretable in response to a constant dosage level of TRH may be responsible for the secretory patterns observed.

Antenatal diagnosis of cretin lambs by measurement of amniotic fluid thyrotropin.

Summary Elevated TSH levels are highly reliable in predicting neonatal lamb hypo-thyroidism. However, the method is not as sensitive as serum TSH measurement, and mild hypothyroidism can exist with normal amniotic fluid thyrotropin and elevated serum TSH.

Influence of prostaglandins and thyrotropin releasing hormone (TRH) on hormone secretion and growth in wether lambs.

A series of experiments were conducted in ewes and whether (castrate male) lambs to evaluate the influence of prostaglandins on secretion of anabolic hormones and to determine if repeated injections of prostaglandin (PG) F2alpha would chronically influence the secretion of these hormones and perhaps growth rate as well. A single intravenous injection of PGA1 and PGB1 (100 microgram/kg) exerted no significant (P greater than .10) influence on plasma concentrations of prolactin (PRL), growth hormone (GH) or thyrotropin (TSH) in ewes. PGA1, but not PGB1, stimulated an increase in the plasma concentration of insulin. Infusion of PGF2alpha for 5.5 hr into ewes resulted in increased (P less than .05) plasma concentrations of both GH and ARL while TSH and insulin were not significantly influenced. Prostaglandin F2alpha, when injected subcutaneously into wether lambs (10 mg twice weekly) stimulated (P less than .05) plasma GH concentrations after the first injection, but not after 3 weeks of treatment. Changes in plasma PRL or TSH were not observed consistently in the lambs treated chronically with PGF2alpha or TRH. Prostaglandin F2alpha, in the present studies, and PGE1 in previously reported studies (1-3), has been demonstrated to be stimulatory to the secretion of PRL and GH. In contrast, PGA1 and PGB1, which lack an 11-hydroxyl group, failed to influence the secretion of either PRL or GH. It would, therefore, appear that the 11-hydroxyl group is a structural requirement for prostaglandins to influence the secretion of these two hormones in sheep. Treatment with thyrotropin releasing hormone (TRH), alone or in combination with PGF 2alpha, significantly (P less than .05) increased growth rate (average daily gains) while PGF2alpha did not, despite the fact that both compounds exerted similar effects on plasma GH.