The Role of Lipoproteins in Steroidogenesis and Cholesterol Metabolism in Steroidogenic Glands*

Gwynne, John T.; Strauss, Jerome F.

doi:10.1210/edrv-3-3-299

Cited by 550 publications

(211 citation statements)

References 159 publications

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“…Hypothyroidism and corpus luteum function in vitro evidence suggests that the main source of cholesterol for steroidogenesis is derived form the circulation in most species, including the rat (Azhar et al 1981, Gwynne & Strauss 1982.…”

Section: Discussionmentioning

confidence: 99%

Hypothyroidism prolongs corpus luteum function in the pregnant rat

Hapon¹,

Motta²,

Ezquer³

et al. 2007

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It has been shown that hypothyroidism in the rat produces a prolongation of pregnancy associated with a delay in the fall of circulating progesterone (P 4 ) at term. The aim of the present work is to determine whether the delayed P 4 decline in hypothyroid mother rats is due to a retarded induction of P 4 degradation to 20aOH P 4 or to a stimulation of its synthesis, and to investigate the possible mechanisms that may underlie the altered luteal function. We determined by RIA the circulating profile of the hormones (TSH, PRL, LH, P 4 , PGF2a, and PGE2) involved in luteal regulation at the end of pregnancy and, by semiquantitative RT-PCR, the expression of factors involved in P 4 synthesis (CytP450scc, StAR, 3bHSD, PRLR) and metabolism (20aHSD, PGF2aR, iNOS and COX2). Our results show that the delay in P 4 decline and parturition is the resultant of retarded luteal regression, caused by a combination of decreases in luteolytic factors, mainly luteal PGF2a, iNOS mRNA expression and also circulating LH, and increased synthesis or action of luteotrophic factors, such as luteal and circulating PGE2 and circulating PRL. All these changes may be direct causes of the decreased 20aHSD mRNA and protein (measured by western blot analysis) expression, which in the presence of unchanged expression of the factors involved in P 4 synthesis results in elevated luteal and circulating P 4 that prolonged pregnancy and also may favor longer survival of the corpus luteum.

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Section: Discussionmentioning

confidence: 99%

Hypothyroidism prolongs corpus luteum function in the pregnant rat

Hapon¹,

Motta²,

Ezquer³

et al. 2007

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“…Thus, the uptake of LDL was greatest in the liver, as expected from the normal metabolic routing of most circulating LDL via the hepatic high affinity receptors. The similarly large uptake by the adrenals was less expected because, in the rat, most of the cholesterol for steroid production comes from high density lipoprotein (HDL) (Gwynne & Strauss, 1982). LDL uptake was much less in the heart and even less in the aorta, presumably reflecting their comparative deficiency in high affinity receptors (Vasile et al, 1983).…”

Section: Discussionmentioning

confidence: 99%

Effect of inhibition of nitric oxide synthesis on the uptake of LDL and fibrinogen by arterial walls and other organs of the rat

Cardona-Sanclemente

Born

1995

British J Pharmacology

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1 The effects of administering 3 mg ml-I N0-nitro-L-arginine methyl ester (L-NAME), an inhibitor of nitric oxide (NO), on the uptake of low density lipoprotein (LDL), fibrinogen and blood pressure were determined in conscious, unrestrained, cannulated normotensive and spontaneously hypertensive (SHR) Wistar rats.2 The uptake of LDL and fibrinogen, labelled respectively with 1251 or '31I via the adduct tyramine cellobiose TC-fibrinogen), were compared in aortic walls, heart, skeletal muscle, lung, liver, kidney and adrenal during the final 24 h of 6 days' administration of L-NAME in the drinking water. 3 In control normotensive rats, the systolic blood pressure did not change significantly over 6 days, while administration of L-NAME in normotensive rats increased the blood pressure progressively and significantly to about 170mmHg over the same period. 4 In normotensive rats L-NAME increased significantly the uptake of both LDL and fibrinogen by aortic walls and heart, but not by muscle, lung, liver, kidney and adrenal. 5 The blood pressure in SHR was about 170 mmHg before administration of L-NAME and did not increase significantly after 6 days of treatment. In these rats the uptake of LDL or of fibrinogen was increased only in the heart but not in aortic walls nor in any of the other organs. 6 In normotensive rats the increase in blood pressure caused by inhibition of NO generation was associated with increases in the uptake of the atherogenic plasma proteins LDL and fibrinogen by the wall of the aorta and by the heart but not by the skeletal muscle, lung, liver, kidney and adrenal. The slightly higher blood pressure of SHR treated with L-NAME was not associated with increased uptake of LDL or fibrinogen by aorta nor by any organ except heart. Thus, while in normotensive rats the increase in blood pressure caused by inhibition of NO generation was associated with increase in the uptake of atherogenic plasma proteins LDL and fibrinogen by the wall of the aorta and by the heart, in SHR which showed uptakes similar to the normotensive animals, the non-significant increase in blood pressure induced by inhibition of NO generation was not associated with increased uptake of LDL or fibrinogen in any organ except the heart. 7 These results are consistent with effects, demonstrated earlier, of infusing the pressor agents noradrenaline, adrenaline and angiotensin II, which produce increases in uptake of LDL and fibrinogen by aortic wall, whereas this is not so in spontaneously hypertensive rats.

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“…P4 is a steroid hormone that is synthesised from cholesterol (Azhar et al 1981;Gwynne and Strauss 1982). Because the CL produces large amounts of P4, the CL needs a large amount of cholesterol (Ferreri and Menon 1992).…”

Section: Introductionmentioning

confidence: 99%

“…Because the CL produces large amounts of P4, the CL needs a large amount of cholesterol (Ferreri and Menon 1992). Because cholesterol is not water soluble, it circulates in the blood as a lipoprotein composed of multiple protein and lipid subunits (Gwynne and Strauss 1982).…”

Section: Introductionmentioning

confidence: 99%

Expressions of lipoprotein receptors and cholesterol efflux regulatory proteins during luteolysis in bovine corpus luteum

Horihata

Yoshioka

Sano

et al. 2017

Reprod. Fertil. Dev.

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The corpus luteum (CL) synthesises and secretes progesterone (P4), which is essential for the establishment and maintenance of pregnancy in mammals. P4 is synthesised from cholesterol. Cholesterol is internalised by low-density lipoprotein receptor (LDLR) and/or scavenger receptor B1 (SR-BI), and is effluxed by Scavenger receptor B1 during luteolysisProgesterone, which is essential for pregnancy in mammals, is synthesised from cholesterol in the corpus luteum (CL). We investigated the involvement of cholesterol uptake receptors and efflux transporters in bovine CL regression (luteolysis), and found that the expression of scavenger receptor B1, a cholesterol uptake receptor, decreased during luteolysis. The decline in cholesterol uptake may reduce progesterone production in the CL during luteolysis.

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The Role of Lipoproteins in Steroidogenesis and Cholesterol Metabolism in Steroidogenic Glands*

Cited by 550 publications

References 159 publications

Hypothyroidism prolongs corpus luteum function in the pregnant rat

Hypothyroidism prolongs corpus luteum function in the pregnant rat

Effect of inhibition of nitric oxide synthesis on the uptake of LDL and fibrinogen by arterial walls and other organs of the rat

Expressions of lipoprotein receptors and cholesterol efflux regulatory proteins during luteolysis in bovine corpus luteum

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