Mechanism of action of α-melanocyte-stimulating hormone in rat preputial glands: the role of androgen metabolism

1982 ◽  
Vol 94 (2) ◽  
pp. 289-294 ◽  
Author(s):  
J. B. Hay ◽  
D. Meddis ◽  
A. J. Thody ◽  
S. Shuster
Keyword(s):  
Reductase Activity ◽  
Hydroxysteroid Dehydrogenase ◽  
Preputial Gland ◽  
Melanocyte Stimulating Hormone ◽  
Hypophysectomized Rats ◽  
Total Lack ◽  
Preputial Glands ◽  
And Control ◽  
Stimulating Hormone

The metabolism of testosterone and 5α-dihydrotestosterone has been studied in vitro in preputial glands of posterior hypophysectomized, totally hypophysectomized and control sham-operated rats. The level of C19 steroid 5α-reductase activity/unit of preputial gland DNA did not fall after removal of the neurointermediate lobe and rose after total hypophysectomy. It was concluded from this that the androgen unresponsiveness of the preputial glands of hypophysectomized rats was not due to a near-total lack of 5α-reductase and hence that the combined synergistic action of testosterone and α-melanocyte-stimulating hormone (α-MSH) on preputial gland activity was unlikely to be due to an α-MSH-mediated restoration of 5α-reductase levels in hypophysectomized rats. Levels of 3α-and 3β-hydroxysteroid dehydrogenase but not of 17β-hydroxysteroid dehydrogenase appeared to be altered by hypophysectomy.

EFFECT OF α-MELANOCYTE-STIMULATING HORMONE AND OVARIAN STEROIDS ON PREPUTIAL GLAND FUNCTION IN THE FEMALE RAT

1981 ◽  
Vol 90 (1) ◽  
pp. 53-58 ◽  
Author(s):  
S. M. DONOHOE ◽  
A. J. THODY ◽  
S. SHUSTER
Keyword(s):  
Pituitary Hormones ◽  
Female Rats ◽  
Male Rats ◽  
Female Rat ◽  
Preputial Gland ◽  
Melanocyte Stimulating Hormone ◽  
Experienced Male ◽  
Hypophysectomized Rats ◽  
Gland Function ◽  
Preputial Glands

Sexually experienced male rats were used to test the attractiveness of preputial gland odours of female rats. The male rats showed a clear preference for the preputial gland odours of hypophysectomized females given oestradiol benzoate (OB) for 3 or 8 days to those of control rats. Progesterone treatment had no effect on the attractiveness of the preputial gland odours of OB-treated hypophysectomized female rats. Administration of α-MSH for either 3 or 8 days, on the other hand, increased the attractiveness to male rats of preputial gland odours of OB-treated hypophysectomized females and the presence of progesterone produced no further change. When administered alone α-MSH had no effect on the attractiveness of the preputial gland odours. Other pituitary hormones, such as ACTH and prolactin, had no effect on the attractiveness of preputial gland odours of OB-treated hypophysectomized rats when administered for 3[unk]days. An increase in preputial gland size was only seen when OB, progesterone and α-MSH were administered together. It would appear that no relationship exists between the size of the preputial glands and their ability to attract male rats. It is concluded that, while α-MSH and progesterone may be important in controlling growth of the preputial glands, an interaction between α-MSH and oestrogen is more important for regulating the production of sex attractants by the preputial glands.

CONTROL OF SEBACEOUS GLAND FUNCTION IN THE RAT BY α-MELANOCYTE-STIMULATING HORMONE

1975 ◽  
Vol 64 (3) ◽  
pp. 503-510 ◽  
Author(s):  
A. J. THODY ◽  
S. SHUSTER
Keyword(s):  
Sebaceous Gland ◽  
Male Rats ◽  
Preputial Gland ◽  
Simultaneous Treatment ◽  
Melanocyte Stimulating Hormone ◽  
Gland Weight ◽  
Hypophysectomized Rats ◽  
Gland Function ◽  
Sebum Secretion ◽  
Stimulating Hormone

SUMMARY The effect of α-MSH on sebum secretion and preputial gland weight was examined in intact, castrated and hypophysectomized male rats and in hypophysectomized rats receiving treatment with either testosterone propionate (TP) or progesterone. After treatment with α-MSHMSH for 2 weeks, increases in sebum secretion occurred in intact, castrated and hypophysectomized rats, but larger responses were found in the hypophysectomized rats that had received treatment with either TP or progesterone, suggesting that α-MSH acts synergistically with TP and progesterone to stimulate sebum secretion. α-Melanocyte-stimulating hormone also increased preputial gland weight in intact rats, but there was no response after castration and only a small response after hypophysectomy. However, when the hypophysectomized rats received simultaneous treatment with either TP or progesterone, α-MSH increased preputial gland weight. It is suggested that α-MSH acts directly on the sebaceous glands to stimulate lipogenesis and, together with steroid hormones, may have an important role in controlling sebaceous gland function in the rat and other hairy mammals. With the evolution of hair, certain of the MSH peptides may have lost their significance as pigmentary hormones and have developed a sebotrophic function. For this reason, it might be more appropriate to refer to these peptides as the 'sebotrophins'.

Characterization of α-melanocyte-stimulating hormone (α-MSH)-like peptides in discrete regions of the rat brain. In vitro release of α-MSH from perifused hypothalamus and amygdala

1990 ◽  
Vol 513 (2) ◽  
pp. 299-307 ◽  
Author(s):  
Denis Tranchand Bunel ◽  
Catherine Delbende ◽  
Catherine Blasquez ◽  
Sylvie Je´gou ◽  
Hubert Vaudry
Keyword(s):  
Rat Brain ◽  
In Vitro Release ◽  
Melanocyte Stimulating Hormone ◽  
Vitro Release ◽  
Stimulating Hormone

Intracellular regulation of 17β-hydroxysteroid dehydrogenase type 2 catalytic activity in A431 cells

1997 ◽  
Vol 153 (3) ◽  
pp. 453-464 ◽  
Author(s):  
C H Blomquist ◽  
B S Leung ◽  
C Beaudoin ◽  
D Poirier ◽  
Y Tremblay
Keyword(s):  
Reductase Activity ◽  
Maximum Velocity ◽  
Hydroxysteroid Dehydrogenase ◽  
A431 Cells ◽  
Intact Cells ◽  
Cell Monolayers ◽  
Intracellular Regulation

Abstract There is growing evidence that various isoforms of 17β-hydroxysteroid dehydrogenase (17-HSD) are regulated at the level of catalysis in intact cells. A number of investigators have proposed that the NAD(P)/NAD(P)H ratio may control the direction of reaction. In a previous study, we obtained evidence that A431 cells, derived from an epidermoid carcinoma of the vulva, are enriched in 17-HSD type 2, a membrane-bound isoform reactive with C18 and C19 17β-hydroxysteroids and 17-ketosteroids. The present investigation was undertaken to confirm the presence of 17-HSD type 2 in A431 cells and to assess intracellular regulation of 17-HSD at the level of catalysis by comparing the activity of homogenates and microsomes with that of cell monolayers. Northern blot analysis confirmed the presence of 17-HSD type 2 mRNA. Exposure of cells to epidermal growth factor resulted in an increase in type 2 mRNA and, for microsomes, increases in maximum velocity (Vmax) with no change in Michaelis constant (Km) for testosterone and androstenedione, resulting in equivalent increases in the Vmax/Km ratio consistent with the presence of a single enzyme. Initial velocity data and inhibition patterns were consistent with a highly ordered reaction sequence in vitro in which testosterone and androstenedione bind only to either an enzyme–NAD or an enzyme–NADH complex respectively. Microsomal dehydrogenase activity with testosterone was 2- to 3-fold higher than reductase activity with androstenedione. In contrast, although cell monolayers rapidly converted testosterone to androstenedione, reductase activity with androstenedione or dehydroepiandrosterone (DHEA) was barely detectable. Lactate but not glucose, pyruvate or isocitrate stimulated the conversion of androstenedione to testosterone by monolayers, suggesting that cytoplasmic NADH may be the cofactor for 17-HSD type 2 reductase activity with androstenedione. However, exposure to lactate did not result in a significant change in the NAD/NADH ratio of cell monolayers. It appears that within A431 cells 17-HSD type 2 is regulated at the level of catalysis to function almost exclusively as a dehydrogenase. These findings give further support to the concept that 17-HSD type 2 functions in vivo principally as a dehydrogenase and that its role as a reductase in testosterone formation by either the Δ4 or Δ5 pathway is limited. Journal of Endocrinology (1997) 153, 453–464

scholarly journals Modulation of 11β-Hydroxysteroid Dehydrogenase Isozymes by Growth Hormone and Insulin-Like Growth Factor: In Vivo and In Vitro Studies1

1999 ◽  
Vol 84 (11) ◽  
pp. 4172-4177 ◽  
Author(s):  
J. S. Moore ◽  
J. P. Monson ◽  
G. Kaltsas ◽  
P. Putignano ◽  
P. J. Wood ◽  
...  
Keyword(s):  
Growth Factor ◽  
Reductase Activity ◽  
Primary Cultures ◽  
Inverse Correlation ◽  
Hydroxysteroid Dehydrogenase ◽  
Insulin Like Growth Factor ◽  
Igf I ◽  
Glucose Output

The interconversion of hormonally active cortisol (F) and inactive cortisone (E) is catalyzed by two isozymes of 11β-hydroxysteroid dehydrogenase (11βHSD), an oxo-reductase converting E to F (11βHSD1) and a dehydrogenase (11βHSD2) converting F to E. 11βHSD1 is important in mediating glucocorticoid-regulated glucose homeostasis and regional adipocyte differentiation. Earlier studies conducted with GH-deficient subjects treated with replacement GH suggested that GH may modulate 11βHSD1 activity. In 7 acromegalic subjects withdrawing from medical therapy (Sandostatin-LAR; 20–40 mg/month for at least 12 months), GH rose from 7.1 ± 1.5 to 17.5 ± 4.3 mU/L (mean ± se), and insulin-like growth factor I (IGF-I) rose from 43.0 ± 8.8 to 82.1 ± 13.7 nmol/L (both P < 0.05) 4 months after treatment. There was a significant alteration in the normal set-point of F to E interconversion toward E. The fall in the urinary tetrahydrocortisols/tetrahydocortisone ratio (THF+allo-THF/THE; 0.82 ± 0.06 to 0.60 ± 0.06; P < 0.02) but unaltered urinary free F/urinary free E ratio (a marker for 11βHSD2 activity) suggested that this was due to inhibition of 11βHSD1 activity. An inverse correlation between GH and the THF+allo-THF/THE ratio was observed (r = −0.422; P < 0.05). Conversely, in 12 acromegalic patients treated by transsphenoidal surgery (GH falling from 124 ± 49.2 to 29.3 ± 15.4 mU/L; P < 0.01), the THF+allo-THF/THE ratio rose from 0.53 ± 0.06 to 0.63 ± 0.07 (P < 0.05). Patients from either group who failed to demonstrate a change in GH levels showed no change in the THF+allo-THF/THE ratio. In vitro studies conducted on cells stably transfected with either the human 11βHSD1 or 11βHSD2 complementary DNA and primary cultures of human omental adipose stromal cells expressing only the 11βHSD1 isozyme indicated a dose-dependent inhibition of 11βHSD1 oxo-reductase activity with IGF-I, but not GH. Neither IGF-I nor GH had any effect on 11βHSD2 activity. GH, through an IGF-I-mediated effect, inhibits 11βHSD1 activity. This reduction in E to F conversion will increase the MCR of F, and care should be taken to monitor the adequacy of function of the hypothalamo-pituitary-adrenal axis in acromegalic subjects and in GH-deficient, hypopituitary patients commencing replacement GH therapy. Conversely, enhanced E to F conversion occurs with a reduction in GH levels; in liver and adipose tissue this would result in increased hepatic glucose output and visceral adiposity, suggesting that part of the phenotype currently attributable to adult GH deficiency may be an indirect consequence of its effect on tissue F metabolism via 11βHSD1 expression.

GABA-ergic control of α-Melanocyte-Stimulating Hormone (α-MSH) release by frog neurointermediate lobe in vitro

1986 ◽  
Vol 17 (5) ◽  
pp. 717-723 ◽  
Author(s):  
S. Adjeround ◽  
M.C. Tonon ◽  
M. Lamacz ◽  
E. Leneveu ◽  
M.E. Stoeckel ◽  
...  
Keyword(s):  
Melanocyte Stimulating Hormone ◽  
Neurointermediate Lobe ◽  
Stimulating Hormone
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