Trends in Endocrinology & Metabolism
Review
Special issue: Endocrine HypertensionAdipose cell–adrenal interactions: current knowledge and future perspectives
Special issue: Endocrine Hypertension
Introduction
Far from being considered simply a depot for fuel storage, adipose tissue is now recognized as a highly active endocrine organ that can produce and secrete many hormones and proteins, the so-called adipokines, which exert a wide range of biological actions 1, 2. Adipokines are involved in the physiological regulation of adipocyte development and fat storage, glucose homeostasis, lipid metabolism, eating behavior, inflammation and vascular tone; thus, they have a role in obesity-associated disorders, including type 2 diabetes and hypertension.
A link between adipose tissue and the adrenal gland – in particular, glucocorticoids – has already been demonstrated. Both neuroendocrine dysregulation of the hypothalamic–pituitary–adrenal (HPA) axis and alteration of cortisol metabolism might have a role in the pathophysiology of abdominal obesity, development of the metabolic syndrome and cardiovascular disease [3]. Less is known about the interaction between adipose tissue and aldosterone. In this article, we discuss the reciprocal effects of aldosterone on adipose tissue and on adipokine-mediated effects on aldosterone production.
Section snippets
Adipose tissue and the renin–angiotensin–aldosterone system: roles in adipogenesis
Increased levels of circulating angiotensinogen (AGT), renin and aldosterone, and angiotensin-converting enzyme (ACE) activity have been reported in obese patients 4, 5, 6. Increased gene expression in the renin–angiotensin–aldosterone system (RAAS) has been observed in adipose tissue from animal models of obesity and obese human subjects 7, 8, 9. In addition, the role of the local renin–angiotensin system (RAS) in adipocytes has been extensively investigated. Transgenic mice overexpressing
Adipose tissue and the local RAS: role in insulin sensitivity
Angiotensin II (Ang II) and insulin share common intracellular signaling pathways. Stimulation of the Ang II type 1 receptor (AT1R) by Ang II exerts a direct inhibitory effect on insulin-mediated glucose uptake by membrane translocation of the main glucose transporter (GLUT4) [16]. The Ang II type 2 receptor (AT2R) also has a crucial role: whereas angiotensin receptor blocker (ARB) increases insulin-induced glucose uptake in both white and brown adipose tissue, uptake is impaired in the white
Adipose tissue and the adrenal gland: role of aldosterone
The association between high serum aldosterone levels and increased fat mass has been reported in several studies in recent years 23, 24, 25, 26, 27. The association is more evident in women than in men, and weight loss is accompanied by a fall in serum aldosterone levels 27, 28, 29. The mechanisms involved are unclear, although the concomitant reduction of renin levels could contribute per se. Another possible mechanism involves the decrease in levels of aldosterone-stimulating factors
Adipose tissue and the adrenal gland: role of mineralocorticoid-releasing factors
The molecular mechanisms underlying the relationship between obesity and hyperaldosteronism have not been established. Hypotheses that have been proposed include genetic predisposition [36], the involvement of adipose tissue RAS [37] and overactivity of the renal sympathetic nervous system, perhaps leptin induced and responsible for renin release 38, 39. Other proposed molecular mechanisms involve the stimulation of aldosterone secretion by an oxidized derivative of linoleic acid [40] or by
Future perspectives
Adipose-specific mineralocorticoid-stimulating factors need to be identified and characterized. Although the identity of such compounds is unknown, various groups have shown that fat-derived substances induce steroidogenesis in adrenocortical cells and cell lines. Experimental studies of adipose tissue from patients with PA would be extremely helpful for establishing the role of aldosterone excess in adipose tissue homeostasis and adipokine production. After the physiopathological mechanisms of
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Cited by (18)
Steroid biosynthesis in adipose tissue
2015, SteroidsCitation Excerpt :Other future study questions include, for example, the effect of postmenopausal estrogen therapy on adipose concentrations of estrogens and their fatty acyl esterified forms. Adipose tissue can contribute to the circulating level of steroids by either (1) local conversion of steroids or (2) synthesis and secretion of a wide range of adipokines into circulation, which can regulate steroidogenesis in the adrenals and gonads [1,150,151]. Obesity is associated with hyperaldosteronism [152].
Role of RAAS and adipokines in cardiovascular protection: Effect of different doses of angiotensin II receptor blocker on adipokines level in hypertensive patients
2014, Journal of the American Society of HypertensionCitation Excerpt :This relationship appears to be polar opposites with aldosterone as well as Angiotensin II levels being increased, whereas adiponectin levels are decreased, particularly in obese humans.12,13 Early studies of adipogenesis indicated that adipose tissues express the mineralocorticoid receptor, which can be activated by aldosterone during adipose differentiation.14,15 Recent reports have suggested that aldosterone negatively regulates the adiponectin produced by adipose tissue, thereby contributing to the reduction of adiponectin sensitivity in the heart.16
Effects of food restriction on steroidogenesis in dispersed adrenocortical cells from Yarrow's Spiny Lizard (Sceloporus jarrovii)
2012, General and Comparative EndocrinologyCitation Excerpt :In these same lizards, Cox et al. [17] reported evidence that the fraction of consumed energy allocated to growth was slightly greater in males than in females, while the fraction allocated to storage was greater in females than in males. Given the roles of B [42,46] and ALDO [44,56] in lipid metabolism and energy balance and partitioning, these findings in lizard adrenocortical cells may reflect sex-specific responses to this particular nutritional stressor to maximize energy allocation for growth. To our knowledge, the present study and our previous work are the first to suggest “phasing” of steroid responses to ACTH by dispersed adrenocortical cells derived from any species.
The role of the mineralocorticoid receptor in adipocyte biology and fat metabolism
2012, Molecular and Cellular EndocrinologyCitation Excerpt :This was the first direct evidence that adipose angiotensin II is released into circulation in humans and consequently may contribute to the association observed between obesity and hypertension. In light of recent experimental data, the existence of a reciprocal cross-talk existing between the adipose organ and the adrenal gland has been suggested (Ronconi et al., 2008). Several studies have reported that some adipocyte-derived factors were able to directly stimulate aldosterone secretion by the adrenal glands (Goodfriend et al., 2004).
The crosstalks between adipokines and catecholamines
2011, Molecular and Cellular EndocrinologyCitation Excerpt :In addition to endocrine communication via blood circulation, the crosstalks can also occur at paracrine level as adipose tissue exists in many organs including pancreas and adrenal gland (Ehrhart-Bornstein et al., 2003; Pinnick et al., 2008). The crosstalks between adipose tissue and the adrenal gland have been supported by the observations that aldosterone produced by adrenal cortex induces adipogenesis while adipocytes release some unidentified factors to stimulate aldosterone production (Ronconi et al., 2008). In addition, it has been shown that leptin stimulates catecholamine secretion from porcine chromaffin cells (Takekoshi et al., 1999).
Mineralocorticoid receptors in the metabolic syndrome
2009, Trends in Endocrinology and Metabolism