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S. SHUSTER

SUMMARY

Plasma cortisol concentrations increased after injections of nicotine. This increase was variable and was no greater than that seen after substitution of normal saline for nicotine. Plasma cortisol concentrations did not increase after nicotine in patients with hypopituitarism and after inhibition of corticotrophin release with triamcinolone. It is concluded that the increased plasma cortisol concentration after injection of nicotine was due to non-specific pituitary stimulation associated with the experimental procedure and not due to any direct effect of the nicotine. Nicotine resulted in a similar increase in plasma cortisol in four patients with diabetes insipidus. Neither rapid infusion of hypertonic mannitol nor ingestion of ethanol had a consistent effect on the plasma cortisol concentration. It is therefore concluded that the antidiuretic hormone is not the 'corticotrophin release factor' in man.

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K. Smith and S. Shuster

ABSTRACT

Using an exchange assay to measure occupied and unoccupied binding sites, the glucocorticoid receptor in rat skin cytosol has been measured after adrenalectomy and parenteral steroid administration. Adrenalectomy increased the number of receptor sites with maximal effect after 5 days, after which numbers decreased to those of intact animals. Injection of adrenalectomized animals with the unlabelled agonist corticosterone resulted in a rapid dose-related decrease in the number of cytosolic receptor sites at 30 min whereas the antagonist progesterone had no effect. It is concluded that changes in glucocorticoid concentration lead to rapid inverse changes in cytosolic receptor.

J. Endocr. (1984) 102, 161–165

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A. J. THODY and S. SHUSTER

The anterior pituitary has an important role in the control of sebaceous gland activity. This effect is mediated in part by thyrotrophic hormone (TSH) and adrenocorticotrophic hormone (ACTH) through their actions on the thyroid and adrenal glands respectively (Thody & Shuster, 1970a, 1971, 1972a). Ablation and replacement experiments suggest that the gonads also have a major influence (Thody & Shuster, 1970a, b), but although there is evidence that gonadotrophins will stimulate sebaceous glands in the human male (Strauss & Pochi, 1963) no data are available from experimental animals. We therefore decided to examine the effect of gonadotrophins on sebum secretion in the rat.

Male Wistar rats were hypophysectomized when 8–9 weeks old and 4 weeks later received either 0·9 units human menopausal gonadotrophin (Humegon)/day or no treatment. Humegon was dissolved in 0·9% NaCl solution and subcutaneous injections were given daily for a period of 2 weeks. At

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A. J. THODY and S. SHUSTER

SUMMARY

Thyroidectomy of intact and castrated rats produced significant reductions in their rates of sebum secretion. Replacement therapy with thyroxine (T4) increased the rate of sebum secretion of the castrated-thyroidectomized rats. Treatment with testosterone propionate also stimulated sebum secretion in castrated-thyroidectomized rats. When given together these two hormones had an additive effect on the rate of sebum secretion.

Thyrotrophic hormone (TSH) stimulated sebum secretion in castrated-hypophysectomized, but not in thyroidectomized rats.

It is concluded that TSH affects sebum secretion through its action on the thyroid, presumably by stimulation of T4 secretion.

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A. J. THODY and S. SHUSTER

It is generally believed that the activity of the sebaceous glands depends to a large extent on the gonads. The pituitary also appears to be involved in the physiology of these glands (Ebling, Ebling & Skinner, 1969; Nikkari & Valavaara, 1969; Thody & Shuster, 1970). The relationship between the pituitary and the sebaceous glands may be exerted via growth hormone and prolactin for Ebling et al. (1969) have shown that these pituitary hormones facilitate the effect of testosterone on sebum secretion. This present study was carried out to see whether the pituitary influence on sebum secretion is also mediated through the thyroid and adrenal glands.

The rate of sebum secretion was measured (Archibald & Shuster, 1969) in 12- to 15-week-old rats which had received one of the following treatments: castration, castration and adrenalectomy, castration and thyroidectomy, castration and hypophysectomy, or no treatment (intact controls). Castration was carried out when the

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A. J. THODY and S. SHUSTER

Department of Dermatology, University of Newcastle upon Tyne, Newcastle upon Tyne, NE1 4LP

(Received 15 October 1976)

In 1972 we suggested that α-melanocyte-stimulating hormone (α-MSH) had a physiological role as a sebotrophic hormone in the rat (Thody & Shuster, 1972) and it now appears that α-MSH is the previously suspected but unidentified sebotrophic hormone (Thody & Shuster, 1973; Shuster & Thody, 1974).

Since previous studies have mainly been concerned with exogenous MSH we examined the effect on sebum secretion of changes in endogenous MSH secretion induced by drugs.

Adult Wistar rats were housed in a light and temperature-controlled room and maintained on tap water and Oxoid breeding diet. The following treatments were carried out for 2 weeks after which time sebum secretion was measured by the method of Archibald & Shuster (1970). (i) Trifluoperazine (Smith, Kline & French) (0·5 mg/day) was administered intraperitoneally in 0·9% saline to male rats twice

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A. J. THODY and S. SHUSTER

Removal of the pituitary gland from the rat produces a decrease in the rate of sebum secretion (Nikkari & Valavaara, 1969; Ebling, Ebling & Skinner, 1969; Thody & Shuster, 1970 a). However, it is not established which pituitary hormones are involved in the control of sebaceous gland activity. In this study we have examined the effect of a new pituitary hormone, β-lipotrophin (β-LPH) (Birk, & Li, 1964; Li, 1968), on the rate of sebum secretion in the rat.

Female Wistar rats were ovariectomized when 5–6 weeks old and hypophysectomized at 7–8 weeks of age. Two weeks later the rats were divided into two groups and received either no hormone treatment (controls) or 0·1 mg β-LPH/day. The injections were given subcutaneously and continued for 2 weeks. At the end of this time the rate of sebum secretion was measured by the method of Archibald & Shuster (1970).

In this method the

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A. J. THODY and S. SHUSTER

SUMMARY

Testosterone propionate (TP) was administered to female rats at 3 and 6 days of age. When adult the sebum secretion rate of these rats was significantly increased, although the response to TP was normal.

Neonatal androgen treatment had no effect on the preputial gland weight of adult female rats. On the other hand ovarian weight was reduced.

After ovariectomy of normal adult rats there was an increase in sebum secretion to a level comparable to that found in adult rats given TP as neonates. By contrast there was no change in sebum secretion after ovariectomy of adult rats given TP as neonates and the rate of sebum secretion in these rats was comparable to that in ovariectomized normal adults.

It is suggested that after neonatal androgen treatment the normal inhibition of the sebaceous glands by the ovaries was abolished and consequently the rate of secretion was increased. Thus the endocrine state in early life may have a lasting effect on sebaceous gland activity in the adult.

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A. J. THODY and S. SHUSTER

SUMMARY

Adult male rats which had been castrated prepuberally secreted less sebum than intact rats. When hypophysectomy followed castration there was a further decrease in sebum secretion. Treatment of the castrated and hypophysectomized castrated rats with testosterone propionate produced a large and comparable increase in the sebum secretion of both groups. Testosterone propionate also caused a marked increase in the preputial gland weight of the castrated rats, although a much smaller response occurred after hypophysectomy. The effect of hypophysectomy on the response of the sebaceous and preputial glands to testosterone is discussed.

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C. B. HATFIELD and S. SHUSTER

SUMMARY

1. Plasma cortisol concentrations, and the urinary output of free and conjugated Porter-Silber reacting steroids, 17-ketosteroids (17-KS), 'total 17-OH CS', urinary cortisone and cortisol, free and conjugated tetrahydrocortisone and cortisol were measured before and after a 1 l. water load.

2. The plasma cortisol concentration fell within 30 min of water ingestion, and tended to increase as diuresis declined.

3. There was a simultaneous increase in the urinary output of 17-KS, total 17-OH CS, and free Porter-Silber reacting steroids. In contrast, urinary excretion of glucuronide-conjugated corticosteroids did not increase during diuresis.

4. The implications of these findings are discussed and it is concluded that (a) the enhanced corticosteroid output during water diuresis is renal in origin, suggesting that tubular factors play a part in the excretion of these hormones; and (b) the role of the adrenal in the excretion of a water load is permissive.