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At least 649 records · Page 36Linked to original sources
PubMed1980

Progesterone effects on adrenal cortex of intact and ovariectomized rat.

Studies on the effects of progesterone on rat adrenal cortex were performed on two age groups of intact or ovariectomized female rats. Ovariectomy was performed on animals weighing 150-170 g and autopsies were carried out 6 weeks and 8.5 months after surgery (4- and 11-month-old animals). 12 days before autopsy part of the animals were treated with progesterone at a daily dose of 5 mg per rat, the others received a single injection of depot-estradiol or jointly with progesterone and estradiol. Intact female rats of a corresponding age were treated with progesterone or vehicle only. In younger intact female rats progesterone lowers the relative adrenal weight and corticosterone output by whole adrenal homogenates. In older rats despite the lowering in absolute and relative adrenal weights there were no changes in corticosterone output. In ovariectomized rats of both age groups progesterone had no marked effects on studied parameters while estradiol resulted in an increase in adrenal weights and corticosterone output. Part of the changes evoked by estradiol were prevented by concomitant progesterone administration. The above described changes were accompanied by morphologic alterations. Performed studies show that progesterone effects on the rat adrenal cortex are modified by the ovaries and depend on the age of animals.

Adrenal Cortex↗
PubMed1979

Immunohistochemical localization of adrenodoxin and adrenodoxin reductase in bovine adrenal cortex.

The zonal distribution of adrenodoxin and adrenodoxin reductase (EC 1.6.7.1) in the bovine adrenal cortex as well as their intracellular localization has been studied by the direct method of peroxidase-labelled antibody (Fab' or F(ab')2 fraction) technique. The results indicated that both proteins localized mainly in zonae fasciculata and reticularis whereas very few were present in the zona glomerulosa. Only parenchymal cells in the adrenal cortex were proved to contain both proteins. The intracellular localization of both adrenodoxin and the reductase was demonstrated to be exclusively on the inner membrane of mitochondria of these parenchymal cells by immunoelectron microscopy. The validity of the immunocytochemical method employed in this study to determine the fine localization of both proteins in the mitochondria as well as the significance of the zonal distribution in relation to the function of each individual zone is discussed.

Adrenal Cortex↗
PubMed2006

Adiponectin receptor expression in the human adrenal cortex and aldosterone-producing adenomas.

Adiponectin is an adipocyte-derived circulating peptide that plays an important role in adipose tissue metabolism, insulin sensitivity and cardiovascular disease. The adrenal gland, by secreting glucorticoid and mineralocorticoid hormones, intervenes in cardiovascular and glucose metabolism regulation and is surrounded by adipose tissue. Hence, we investigated the hypothesis that adiponectin receptor types 1 and 2 (adipo-R1 and adipo-R2) are expressed in the human adrenal gland and in adrenocortical zona glomerulosa cell-derived aldosterone-producing adenoma (APA) tissue. We used real-time reverse transcription-polymerase chain reaction to demonstrate the mRNA of adipo-R1 and adipo-R2 in 10 histologically normal human adrenal cortexes that were obtained from patients with renal cancer undergoing nephrectomy with ipsilateral adrenalectomy and in 10 APAs. Melting curve analysis and sequencing were used to confirm the specificity of the amplicons obtained. Results consistently showed the expression of specific mRNAs of adiponectin receptors in all histologically normal human adrenal cortexes and APAs. This novel finding suggests that adiponectin could play a regulatory role in adrenocortical function and growth in humans.

Adrenal Cortex↗
PubMed1989

Morphometric analyses of adrenal gland growth in fetal and neonatal sheep. I. The adrenal cortex.

This, the first linear morphometric analysis of the epigenesis of the fetal mammalian adrenal cortex, has shown that in the fetal sheep during the latter two thirds of gestation and in the newborn lamb, there are two periods of rapid growth separated by a period of much reduced growth. The fetal ages studies were 53 days (0.36 gestation), a period when the fetal adrenal cortex is actively steroidogenic; 100 days (0.68 gestation), a period of adrenocortical quiescence; 130 days (0.88 gestation), the period of increasing responsiveness to ACTH and cortisol production; 144 days (0.98 gestation), the period of maximal adrenocortical steroidogenesis; and 2 days postpartum, when cortisol production is normally maintained. The first adrenocortical growth period extends to mid-gestation, then growth slows to 0.85 gestation when the second growth period begins. The changes between the first growth period (0.36 gestation) and the period of quiescence (0.68 gestation) are characterised by the attainment of normal adrenocortical zonation and the separation of the medulla. The rate of adrenocortical cell division slows and the zona fasciculata cells become smaller in size. The volume density of the adrenocortical blood sinusoids decreases significantly. The onset of the second growth phase is associated with the previously reported increased levels of fetal plasma ACTH at 0.85 gestation and is expressed initially as a hypertrophic response. Cellular hypertrophy increases from 0.88 gestation to 0.98 gestation and then declines over the birth period. The rate of adrenocortical cell division increases from 0.88 gestation and maintains a maximal rate from 0.98 gestation to 2 days postpartum. These interactions of cellular hypertrophy and hyperplasia, which result in adrenocortical growth, may be explained as a response to fetal ACTH, which has the ability to stimulate the production of peptide growth and differentiation factors, e.g. IGF-II, and cortisol, which then control adrenocortical development in an autocrine and paracrine fashion.

3-Hydroxysteroid Dehydrogenases↗
PubMed2002

Development and function of the human fetal adrenal cortex.

The development and function of the primate adrenal cortex are characterized by rapid growth, high steroidogenic activity, and a particular morphological appearance. The fetal adrenal glands grow rapidly and exponentially and at term are similar in weight to adult adrenals. From birth to 1 year their mass is reduced as they undergo a process of differentiation. Growth then remains slow until age 7 years. Thereafter, growth accelerates and the adrenals reach adult weight by the end of puberty. In the first trimester of gestation, fetal adrenal growth is thought to be independent of adrenocorticotropic hormone (ACTH), but after 15 weeks, ACTH is absolutely required for normal morphological and functional development. Other factors of fetal and/or placental origin, acting independently of or in conjunction with ACTH, are also required. Basic fibroblast growth factor, epidermal growth factor/transforming growth factor beta, and insulin-like growth factor (IGF)-I and -II, all acting in an autocrine and/or paracrine fashion, have been postulated to stimulate fetal adrenal cell proliferation. Corticotropin-releasing hormone may also play an important role in primate fetal adrenal function, primarily at the end of gestation. Finally, the estrogens are also important in the development of the pituitary-adrenal axis in primates.

Adrenal Cortex↗