On the Site of Action of Luteinizing Hormone

Dt, Armstrong

doi:10.1038/213633a0

Cited by 14 publications

(5 citation statements)

References 5 publications

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“…The observation that cholesterol already present within the cell serves as the major source of steroids is in agreement with similar conclusions by others (Armstrong, 1967;Solod et al, 1966). The fact that cholesterol from the foetal calf serum was not readily converted into steroids indicates that it probably enters the cells slowly.…”

Section: Discussionsupporting

confidence: 92%

Influence of luteinizing hormone and adenosine 3′:5′-cyclic monophosphate on the metabolism of free and esterified cholesterol in mouse Leydig-cell tumours

Moyle

Jungas

Greep

1973

Biochemical Journal

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1. Male C57B1/6J mice bearing Leydig-cell tumours known to synthesize steroids in response to luteinizing hormone (LH) were given intravenous injections of [1,2-(3)H]cholesterol (50-100muCi per animal). Single-cell suspensions were prepared from the tumours 5-9 days after the injection of [(3)H]cholesterol and were incubated at 37 degrees C in foetal calf serum supplemented with 50mm-Tris-HCl, pH7.4. At various times after the start of incubation cells were collected by filtration of portions of the suspension and their sterols analysed. Within 10min after LH (5mug/ml) or 3':5'-cyclic AMP (20mm) was added to the cell suspensions an increased conversion of ester cholesterol into free cholesterol could be demonstrated. 2. To observe this rapid effect of LH it was necessary to incubate the cells for 60min before addition of hormone. 3. The specific radioactivity of testosterone produced was approximately equal to that of the intracellular cholesterol regardless of the presence or absence of LH. 4. The amount of free cholesterol produced in response to LH was far greater than that needed for steroid synthesis. 5. Free cholesterol, but not esterified cholesterol, was released into the incubation medium linearly with time and this release was unaffected by LH. LH may stimulate steroidogenesis in part by increasing the concentration of free cholesterol within the cell.

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Section: Discussionsupporting

confidence: 92%

Influence of luteinizing hormone and adenosine 3′:5′-cyclic monophosphate on the metabolism of free and esterified cholesterol in mouse Leydig-cell tumours

Moyle

Jungas

Greep

1973

Biochemical Journal

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“…In the other two groups (treatment with LH alone or with prolactin + LH) the decrease of the synthesis and the content of esterified cholesterol were accom¬ panied by a significant increase in the androgen production. The response of the testi¬ cular tissue from hypophysectomized rats to LH is similar to that of other steroidproducing gonadal tissues including rabbit testis (Hall, 1963), rabbit ovarian inter¬ stitial gland (Armstrong, 1967), rat corpus luteum and interstitium ) and the bovine corpus luteum (Savard & Casey, 1964;Armstrong & Black, 1968). The fact that testosterone synthesis was increased significantly more by prolactin+ LH than by LH alone, but both treatments caused approximately the same degree of depletion of esterified cholesterol, seems to imply that prolactin in¬ creases the amount of esterified cholesterol available for conversion into steroid hormones which depends mainly on LH.…”

Section: Discussionmentioning

confidence: 79%

The Role of Prolactin in the Regulation of Testis Function: The Synergistic Effects of Prolactin and Luteinizing Hormone on the Incorporation of [1-14c]acetate Into Testosterone and Cholesterol by Testes From Hypophysectomized Rats in Vitro

Hafiez¹,

Bartke²,

Lloyd³

1972

Journal of Endocrinology

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Hypophysectomized adult male rats were treated twice daily for 3\ m=1/ 2\ days with 0\m=.\9% NaCl solution, 200 \g=m\g ovine prolactin, 5 \g=m\g ovine luteinizing hormone (LH), or 200 \g=m\gprolactin +5 \g=m\gLH, starting 18 days after the operation. Minced testes from these animals were incubated in Krebs\p=m-\Ringer bicarbonate buffer containing [1-14C]acetate for 3 h at 37 \s=deg\C.The conversion of acetate into testosterone was calculated. It was not changed by prolactin treatment, was increased by LH (P < 0\m=.\01), and further increased by prolactin + LH (P < 0\m=.\01) to approximately the level observed in intact adult controls. The amount of testosterone in some of the incubates was measured by gas liquid chromatography. It was not changed in prolactin\x=req-\ treated animals and was increased in LH-treated animals (P < 0\m=.\02com-pared with hypophysectomized controls). Treatment with prolactin+LH resulted in an increase in testosterone above that after treatment with LH alone (P < 0\m=.\01) and to a value similar to that in intact adult males. The incorporation of acetate into esterified cholesterol was decreased (P < 0\m=.\05) in groups treated with LH or prolactin + LH in which testosterone synthesis was increased. The incorporation of acetate into free cholesterol was not changed by any of the treatments. These results demonstrate synergistic action of prolactin and LH on the synthesis of testosterone in vitro confirming our earlier suggestions.

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“…3. His work first demonstrated the role of LH in the regulation of progesterone secretion by the corpus luteum in rabbits (Kilpatrick et al 1964) and rats (Armstrong et al 1964;Armstrong 1967), and thus established the similarity of mechanisms of regulation of luteal steroidogenesis among mammalian species. These findings were of fundamental importance in shifting the thinking about corpus luteum regulation from prolactin (previously regarded as 'the luteotrophic hormone') to luteinising hormone.…”

mentioning

confidence: 98%

“…A major theme of Dr Armstrong's pioneering research focused on the use of in vitro techniques for studies of hormone actions on the ovary. His research on the actions of gonadotrophic hormones on glucose and cholesterol metabolism in the ovary provided the first evidence for the now widely accepted role of luteinising hormone (LH) in regulating ovarian steroid biosynthesis by influencing substrate availability to the rate-limiting mitochondrial steroidogenic enzyme(s) (Armstrong and Greep 1962;Armstrong 1963Armstrong , 1967Armstrong et al 1963;Solod et al 1966;Major et al 1967;Jackanicz and Armstrong 1968;Behrman and Armstrong 1969;Behrman et al 1970;Armstrong 1971, 1972;Robinson et al 1975). 3.…”

mentioning

confidence: 99%

Recipient of the 2018 IETS Pioneer Award: David Thomas Armstrong, BSA, MSc, PhD

2018

Reprod. Fertil. Dev.

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On the Site of Action of Luteinizing Hormone

Cited by 14 publications

References 5 publications

Influence of luteinizing hormone and adenosine 3′:5′-cyclic monophosphate on the metabolism of free and esterified cholesterol in mouse Leydig-cell tumours

Influence of luteinizing hormone and adenosine 3′:5′-cyclic monophosphate on the metabolism of free and esterified cholesterol in mouse Leydig-cell tumours

The Role of Prolactin in the Regulation of Testis Function: The Synergistic Effects of Prolactin and Luteinizing Hormone on the Incorporation of [1-14c]acetate Into Testosterone and Cholesterol by Testes From Hypophysectomized Rats in Vitro

Recipient of the 2018 IETS Pioneer Award: David Thomas Armstrong, BSA, MSc, PhD

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