scholarly journals Obesity-associated lipidomic remodeling of the adrenal gland indicates an important role of the FADS2-arachidonic acid axis in adrenocortical hormone production

2020 ◽  
Author(s):  
Anke Witt ◽  
Peter Mirtschink ◽  
Alessandra Palladini ◽  
Ivona Mateska ◽  
Heba Abdelmegeed ◽  
...  
Keyword(s):  
Mass Spectrometry ◽  
Arachidonic Acid ◽  
Adrenal Gland ◽  
Cell Cultures ◽  
Adrenal Glands ◽  
Gland Cell ◽  
Obese Mice ◽  
Hormone Production ◽  
Adrenocortical Hormone

AbstractObjectiveAdrenocortical hormone levels increase in obesity, potentially contributing to development of obesity-associated pathologies. Here we explored whether lipidomic remodeling of the adrenal gland could mediate altered adrenocortical steroidogenesis during obesity.MethodsLipidomic analysis was performed in adrenal glands using shotgun mass spectrometry (MS), and steroid profiling of sera by liquid chromatography tandem mass spectrometry (LC-MS/MS) from lean and obese mice. Gene expression analysis was performed in adrenal glands and adrenocortical cell populations. The role of Fatty Acid Desaturase 2 (FADS2) and arachidonic acid on steroid hormone production was studied in primary adrenal gland cell cultures.ResultsAdrenal glands of obese mice displayed a distinct lipidomic profile, encompassing longer and more unsaturated storage lipids and phospholipids compared to adrenal glands of lean mice. Arachidonoyl acyl chains were abundant in the adrenal gland phospholipidome and increased upon obesity. This was accompanied by increased Fads2 expression, the rate-limiting enzyme of arachidonic acid synthesis, and enhanced plasma adrenocortical hormone levels. Inhibition of FADS2 in primary adrenal gland cell cultures abolished steroidogenesis, which was restored by arachidonic acid supplementation.ConclusionsOur data suggest that the FADS2 – arachidonic acid axis regulates adrenocortical hormone synthesis, while alterations in the content of arachidonoyl chains in the adrenal gland phopsholipidome could account for disturbed adrenocortical hormone production.HighlightsThe adrenal gland lipidome is remodeled in obesity.Arachidonoyl groups are abundant in the adrenal gland phospholipidome and increase in obesity.FADS2 is highly expressed in the adrenal gland and its expression is further increased in obesity.FADS2 inhibition blunts adrenocortical steroidogenesis in primary adrenal gland cell cultures, while arachidonic acid supplementation restores it.

scholarly journals Morphological features of primary cultures of adrenal cells of neonatal animals of different species

2019 ◽  
Keyword(s):  
Adrenal Gland ◽  
Cell Cultures ◽  
Adrenal Glands ◽  
Primary Cultures ◽  
Cell Monolayer ◽  
Calf Serum ◽  
Morphological Features ◽  
Primary Cell ◽  
Endocrine Gland ◽  
Primary Cell Cultures

The adrenal gland is an endocrine gland, which in the process of organogenesis is formed from ecto- and mesoderm derivatives. The mechanisms that make cell types of different origins unite, migration routes, and cell interactions are still not fully understood. One of the tools for studying these mechanisms is the primary cell culture obtained from the adrenal gland. The aim of our work was to compare the morphological features of primary cell cultures of model animals belonging to different orders – pigs, rabbits and mice in vitro under various cultivation conditions (growth surface pattern, presence of growth factors), as well as developing methodological approaches for obtaining and maintaining primary cultures of adrenal cell of neonatal animals. Cultivation was performed under standard conditions of temperature and humidity, carbon dioxide concentration, on culture surfaces with normal and reduced adhesiveness in a nutrient medium DMEM enriched with 10% fetal calf serum (FTS) or growth supplements B-27 and FGF. It was established that cell cultures of adrenal neonatal rabbits and piglets that were cultured under conditions of normal adhesion and using FCS had a heterogeneous composition, and were presented as a monolayer consisting of cells of several morphological types, and multicellular spheroids (MS). When cultivated on the surface with reduced adhesive properties in cultures of adrenal glands of piglets and rabbits, a cell monolayer was not formed, but flotation MCs were formed. After transferring MCs of both species to the adhesive culture surface on day 14, cell eviction, their migration from the MCs and formation of a monolayer are observed. Similar stages in the development of primary cell cultures derived from rabbits and piglets suggest the existence of a universal cellular composition in the neonatal adrenal glands of these species and allow applying the same approaches to the primary cultures derived from them. Unlike other studied species, monolayer and MS formation does not occur in cell cultures of mouse neonatal adrenal glands. Cultures consist of single attached and floating cells and small cell aggregates.

Role of the adrenal in hastening blood coagulation after exposure to stress

1959 ◽  
Vol 197 (1) ◽  
pp. 205-206 ◽  
Author(s):  
Meyer Friedman ◽  
Herman N. Uhley
Keyword(s):  
Adrenal Gland ◽  
Blood Coagulation ◽  
Adrenal Glands ◽  
Cholesterol Content

The possible role of the adrenal gland in the hastening of blood coagulation in rats exposed to a particular form of stress was investigated. It was observed that there was a marked fall in adrenal cholesterol content during the period of stress. However, the hastening in blood coagulation after exposure to the stress was not altered by removal of the adrenal glands. It, therefore, was concluded that the coagulation phenomenon observed was independent o adrenal activity.

scholarly journals Ultrasound evaluation of fetal adrenal gland volume. The role of fetal adrenal glands in the pathogenesis of preterm labor

2014 ◽  
Vol 85 (1) ◽  
Author(s):  
Arkadiusz Krzyżanowski ◽  
Katarzyna Karwasik-Kajszczarek ◽  
Izabela Dymanowska-Dyjak ◽  
Adrianna Kondracka ◽  
Anna Kwaśniewska
Keyword(s):  
Adrenal Gland ◽  
Preterm Labor ◽  
Adrenal Glands ◽  
Gland Volume ◽  
Ultrasound Evaluation ◽  
Adrenal Gland Volume

scholarly journals Role of prostaglandins in hypoxia-stimulated erythropoietin production

1985 ◽  
Vol 249 (1) ◽  
pp. C3-C8 ◽  
Author(s):  
A. Kurtz ◽  
W. Jelkmann ◽  
J. Pfeilschifter ◽  
C. Bauer
Keyword(s):  
Arachidonic Acid ◽  
Adenylate Cyclase ◽  
Cell Cultures ◽  
Mesangial Cells ◽  
Cyclase Activity ◽  
Adenylate Cyclase Activity ◽  
Cyclooxygenase Inhibitor ◽  
Erythropoietin Production ◽  
Stimulation Of

The role of prostaglandins in the mediation of hypoxia-stimulated erythropoietin (Ep) production by cultured rat renal mesangial cells was examined. It was found that an increase in prostaglandin E2 (PGE2) production accompanied the rise in Ep due to hypoxia (2% O2). The hypoxia-stimulated increase in Ep production was abolished in the presence of the cyclooxygenase inhibitor indomethacin (10(-5) M). When PGE2 (10(-6) M was added simultaneously with indomethacin, however, no diminution in hypoxia-stimulated Ep production was observed. Addition of arachidonic acid (AA, 10(-5) M), PGE2 (10(-6) M), or PGI2 (10(-4) M) enhanced Ep production under normoxic conditions (20% O2), while PGF2 alpha (10(-6) M) had no effect on Ep production. AA, PGE2, and PGI2 were found to stimulate adenosine 3',5'-cyclic monophosphate formation by the cultured mesangial cells. Enhancement of adenylate cyclase activity by forskolin (10(-5) M) also increased Ep production in the cell cultures. Our results suggest that hypoxia-stimulated Ep production by cultured mesangial cells is mediated by prostaglandins with subsequent stimulation of adenylate cyclase activity.

EFFECT OF PROSTAGLANDIN E2 AND A2 ON STEROID SYNTHESIS BY THE RAT ADRENAL GLAND

1975 ◽  
Vol 65 (1) ◽  
pp. 55-63 ◽  
Author(s):  
A. SPÄT ◽  
SARA JÓZAN
Keyword(s):  
Adrenal Gland ◽  
Prostaglandin E2 ◽  
Adrenal Glands ◽  
Prostaglandin E ◽  
Sodium Restriction ◽  
Aldosterone Secretion ◽  
Steroid Synthesis ◽  
Aldosterone Production ◽  
Hypophysectomized Rats

SUMMARY Prostaglandin E2 increased aldosterone output by superfused capsular adrenal glands obtained from sodium-repleted, hypophysectomized rats but corticosterone did not show a statistically significant increase. Prostaglandin A2 increased corticosterone but not aldosterone production by incubated capsular glands obtained from sodium-repleted, hypophysectomized rats. Both aldosterone and corticosterone production rates were increased by PGA2 after previous sodium restriction. Corticosterone production rate of the decapsulated adrenal gland was not significantly modified by prostaglandin A2 in a concentration effective on the capsular adrenal gland. A possible role of prostaglandins in the regulation of aldosterone secretion is discussed.

PATHWAYS OF DEHYDROEPIANDROSTERONE SULPHATE BIOSYNTHESIS IN THE HUMAN FOETAL ADRENAL GLAND

1970 ◽  
Vol 47 (3) ◽  
pp. 295-307 ◽  
Author(s):  
B. A. COOKE ◽  
R. A. COWAN ◽  
PATRICIA D. TAYLOR
Keyword(s):  
Mass Spectrometry ◽  
Liquid Chromatography ◽  
Adrenal Gland ◽  
Isotope Dilution ◽  
Adrenal Glands ◽  
Gas Liquid Chromatography ◽  
Dehydroepiandrosterone Sulphate ◽  
Main Pathway

SUMMARY The pathways of dehydroepiandrosterone sulphate (DHAS) biosynthesis in adrenal glands from the human previable foetus have been investigated by incubating pregnenolone, 17 α-hydroxypregnenolone and pregnenolone sulphate with homogenates of this tissue for different periods of time. The steroids formed were identified and measured by reverse isotope dilution or by gas—liquid chromatography and mass spectrometry of their derivatives. The results obtained are consistent with a main pathway from pregnenolone to DHAS via non-sulphated intermediates, i.e. 17 α-hydroxypregnenolone and DHA. The rate of pregnenolone sulphate metabolism to DHAS via 17 α-hydroxypregnenolone sulphate was found to be very slow compared with the rapid metabolism of pregnenolone to DHAS. These results are discussed in relation to the availability and nature of DHAS precursors in vivo.

Effects of mineralocorticoids and glucocorticoids on compensatory adrenal growth in rats

1985 ◽  
Vol 248 (4) ◽  
pp. E450-E456 ◽  
Author(s):  
R. Phillips ◽  
C. Crock ◽  
J. Funder
Keyword(s):  
Adrenal Gland ◽  
Compensatory Growth ◽  
Adrenal Glands ◽  
Pituitary Hormones ◽  
Female Rats ◽  
Male Rats ◽  
Unilateral Adrenalectomy ◽  
Male And Female ◽  
Male And Female Rats

The rapid compensatory growth seen in the remaining adrenal gland of the rat after unilateral adrenalectomy appears to require a functioning neural arc between the adrenal glands and the hypothalamus, but the role of adrenal or pituitary hormones is unclear. We have examined the effect of several steroids on the compensatory adrenal growth (CAG). Female and male rats (average wt 140 g) were unilaterally adrenalectomized and treated with aldosterone (2.1 micrograms/day), corticosterone (B, 28 micrograms/day), dexamethasone (28 micrograms/day), 9 alpha-fluorocortisol (9 alpha FC, 28 micrograms/day), or deoxycorticosterone (DOC, 28 micrograms/day) by continuous infusion for 3 days and then killed. The growth in the remaining adrenal was compared both with sham-operated rats treated with steroid infusions and with noninfused controls. In rats of this size females have larger adrenals than males; untreated male rats have significantly heavier left than right adrenals. In male rats the extent of CAG after no treatment or treatment with aldosterone B, 9 alpha FC, or DOC depended on the size of the adrenal gland removed. In both male and female rats CAG was not significantly affected by aldosterone, in contrast with a recent report, nor by B, 9 alpha FC, or DOC; no significant CAG was seen after dexamethasone. Taken together, these results and previous reports suggest that neurally mediated activation of pituitary and/or local adrenal growth factors may be responsible for CAG.

MODIFICATION OF RESPONSE TO ADRENOCORTICO-TROPHIC HORMONE BY THE SIMULTANEOUS ADMINISTRATION OF GONADOTROPHIC HORMONES OR OESTROGEN

1957 ◽  
Vol 15 (3) ◽  
pp. 255-265 ◽  
Author(s):  
BARBARA E. CLAYTON ◽  
JOYCE E. HAMMANT
Keyword(s):  
Guinea Pigs ◽  
Adrenal Glands ◽  
Chorionic Gonadotrophin ◽  
Simultaneous Administration ◽  
Adrenocorticotrophic Hormone ◽  
Direct Inhibition ◽  
Intact Female ◽  
Hormone Production ◽  
Adrenocortical Hormone ◽  
Trophic Hormone

SUMMARY 1. The urinary excretion of 17-ketosteroids (KS) and 17-ketogenic steroids (KG) has been used as a measure of response to administered adrenocorticotrophic hormone (ACTH). 2. In intact female guinea-pigs the excretion of KG was less when pregnant mares' serum gonadotrophin (PMS) and chorionic gonadotrophin (CG) were administered simultaneously with ACTH, as compared with ACTH alone. The ovaries were essential for this effect. The KS response was not affected by gonadotrophin administration. These observations were reproduced in intact female and ovariectomized guinea-pigs by the administration of oestradiol, but not of progesterone, with ACTH. It is suggested that there is probably a direct inhibition of adrenocortical hormone production by the adrenal glands as a result of treatment with oestrogen, or secretion of oestrogen by ovaries stimulated by administered gonadotrophins. 3. No modification of response to ACTH was obtained by the simultaneous administration of PMS + CG or oestradiol to male guinea-pigs.

scholarly journals Effects of lipoxygenase metabolites of arachidonic acid on the growth of human mononuclear marrow cells and marrow stromal cell cultures

1998 ◽  
Vol 7 (1) ◽  
pp. 31-33 ◽  
Author(s):  
V. Desplat ◽  
F. Dupuis ◽  
F. Trimoreau ◽  
C. Dulery ◽  
V. Praloran ◽  
...  
Keyword(s):  
Arachidonic Acid ◽  
Cell Cultures ◽  
Stromal Cell ◽  
Mononuclear Cells ◽  
Thymidine Incorporation ◽  
Cell Types ◽  
Cell Number ◽  
Lipoxygenase Inhibitor ◽  
Marrow Stromal Cell

The effects of various lipoxygenase metabolites of arachidonic acid (AA) were investigated on the growth of freshly isolated human bone marrow mononuclear cells and marrow stromal cell cultures. LTB4, LXA4, LXB4, 12-HETE and 15-HETE (1 μM) decreased [3H]-thymidine incorporation on marrow stromal cell cultures without affecting cell number. Only 12-HETE showed a dose-response effect on [3H]-thymidine incorporation. While LTB4(1 μM) decreased thymidine incorporation on marrow mononuclear cells, LTC4, LXA4, LXB4, 12-HETE and 15-HETE had no effect. The lipoxygenase inhibitor NDGA had no effect on both cell types suggesting no role of endogenous lipoxygenase metabolites on cell growth. These results suggest no important role of lipoxygenase metabolites of AA on the proliferation of human marrow mononuclear cells and marrow stromal cell cultures.

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