The effects of glucocorticoids on adipose tissue lipid metabolism

Peckett, Ashley J.; Wright, David C.; Riddell, Michael C.

doi:10.1016/j.metabol.2011.06.012

Cited by 436 publications

(358 citation statements)

References 72 publications

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“…The HPI axis modulates a hormonal cascade resulting in the activation of the interrenal gland and glucocorticoid (GC) production: corticosterone (CORT) in amphibians, reptiles, and birds and cortisol in most mammals and fish (Romero 2004). GCs elicit the mobilization of energetic metabolic substrates (e.g., lipids; Peckett et al 2011), which affect essential functions of the organism such as reproduction, behavior, and growth (Denver et al 2002;Schoech et al 2009;Kindermann et al 2013), thus conditioning the transition between life-history stages (Crespi et al 2013). Prolonged secretion of CORT has been associated with mobilization of energetic substrates and increased metabolic demands in multiple tissues (Peckett et al 2011;Lattin and Romero 2015) while resulting in reduced long-term survival (Bonier et al 2009).…”

Section: Introductionmentioning

confidence: 99%

“…GCs have cascading effects on multiple physiological pathways. Elevated GCs cause an increased metabolic rate involving overproduction of reactive oxygen species (ROS; Peckett et al 2011) that often results in cellular damage (Circu and Aw 2010). Such cellular damage, however, can be buffered by increasing the activity of antioxidant enzymes (Costantini et al 2011;Gomez-Mestre et al 2013).…”

Section: Introductionmentioning

confidence: 99%

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Physiological Stress Responses in Amphibian Larvae to Multiple Stressors Reveal Marked Anthropogenic Effects even below Lethal Levels

Burraco

Gómez-Mestre

2016

Physiological and Biochemical Zoology

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Natural and anthropogenic disturbances cause profound alterations in organisms, inducing physiological adjustments to avoid, reduce, or remedy the impact of disturbances. In vertebrates, the stress response is regulated via neuroendocrine pathways, including the hypothalamic-pituitary-interrenal axis that regulates the secretion of glucocorticoids. Glucocorticoids have cascading effects on multiple physiological pathways, affecting the metabolic rate, reactive oxygen species production, or immune system. Determining the extent to which natural and anthropogenic environmental factors induce stress responses in vertebrates is of great importance in ecology and conservation biology. Here we study the physiological stress response in spadefoot toad tadpoles (Pelobates cultripes) against three levels of a series of natural and anthropogenic stressors common to many aquatic systems: salinity (0, 6, and 9 ppt), herbicide (0, 1, and 2 mg/L acid equivalent of glyphosate), water acidity (pH 4.5, 7.0, and 9.5), predators (absent, native, and invasive), and temperature (217, 257, and 297C). The physiological stress response was assessed examining corticosterone levels, standard metabolic rate, activity of antioxidant enzymes, oxidative cellular damage in lipids, and immunological status. We found that common stressors substantially altered the physiological state of tadpoles. In particular, salinity and herbicides cause dramatic physiological changes in tadpoles. Moreover, tadpoles reduced corticosterone levels in the presence of natural predators but did not do so against invasive predators, indicating a lack of innate recognition. Corticosterone and the antioxidant enzyme glutathione reductase were the most sensitive parameters to stress in this study. Anthropogenic perturbations of aquatic systems pose serious threats to larval amphibians even at nonlethal concentrations, judging from the marked physiological stress responses generated, and reveal the importance of incorporating physiological information onto conservation, ecological, and evolutionary studies.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Physiological Stress Responses in Amphibian Larvae to Multiple Stressors Reveal Marked Anthropogenic Effects even below Lethal Levels

Burraco

Gómez-Mestre

2016

Physiological and Biochemical Zoology

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“…Specifically, in adipose tissues GCs have been shown to increase adiposity in human and rodents by promoting fat differentiation (7,8) and inhibiting energy expenditure by decreasing brown adipose tissue (BAT) thermogenesis (9,10) and by suppressing the browning of subcutaneous fat (11). Furthermore, depending on the length of treatment and the intracellular concentrations, GCs have been shown to increase lipogenesis and lipolysis (12). Extensive geneexpression analyses combined with the computational information provided by genome-wide ChIP sequencing have identified a number of positive gene targets of GR signaling in a variety of tissues and cell types (13), including liver (14), adipocytes (15), and myotubes (16).…”

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confidence: 99%

Forkhead box A3 mediates glucocorticoid receptor function in adipose tissue

Mueller

2016

Proc. Natl. Acad. Sci. U.S.A.

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Glucocorticoids (GCs) are widely prescribed anti-inflammatory agents, but their chronic use leads to undesirable side effects such as excessive expansion of adipose tissue. We have recently shown that the forkhead box protein A3 (Foxa3) is a calorie-hoarding factor that regulates the selective enlargement of epididymal fat depots and suppresses energy expenditure in a nutritional- and age-dependent manner. It has been demonstrated that Foxa3 levels are elevated in adipose depots in response to high-fat diet regimens and during the aging process; however no studies to date have elucidated the mechanisms that control Foxa3’s expression in fat. Given the established effects of GCs in increasing visceral adiposity and in reducing thermogenesis, we assessed the existence of a possible link between GCs and Foxa3. Computational prediction analysis combined with molecular studies revealed that Foxa3 is regulated by the glucocorticoid receptor (GR) in preadipocytes, adipocytes, and adipose tissues and is required to facilitate the binding of the GR to its target gene promoters in fat depots. Analysis of the long-term effects of dexamethasone treatment in mice revealed that Foxa3 ablation protects mice specifically against fat accretion but not against other pathological side effects elicited by this synthetic GC in tissues such as liver, muscle, and spleen. In conclusion our studies provide the first demonstration, to our knowledge, that Foxa3 is a direct target of GC action in adipose tissues and point to a role of Foxa3 as a mediator of the side effects induced in fat tissues by chronic treatment with synthetic steroids.

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“…For this reason, only after knowing the non-pathologic genomic response of Hsd1 and Aqp7 to glucocorticoids/cortisone, it would be possible to determine whether their modified expressions comprise a cause or a consequence of the disease. 7,22,23 Therefore, this study was performed on differentiated adipocytes derived from a non-obese source after confirming the possible role of cortisone in regulating the expression of these genes through the two GREs predicted in each of their promoters. Even when some authors have reported changes in the expression of either Hsd1 24 or some aquaporins [25][26][27][28] in response to glucocorticoid stimuli, no reports have been found that link both of the genes of this research to the MS.…”

Section: Discussionmentioning

confidence: 78%

“…5 Paradoxically, under physiological conditions, the action of GC promotes lipolysis, thus the release of glycerol and fatty acids from AT. 6,7 While excess GC does cause obesity and diabetes, circulating GC levels are normal in obese subjects. 8 This led to the knowledge that the physiological action of GC on AT depends, in part, on their circulating levels and also, and importantly, on their tissue activation prior to impacting on their receptor, which occurs through 11b-Hydroxysteroid dehydrogenase 1 (Hsd1), the latter converting inactive cortisone into active cortisol.…”

Section: Introductionmentioning

confidence: 99%

HSD1 and AQP7 short-term gene regulation by cortisone in 3T3-L1 adipocytes

et al. 2016

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Adipose Tissue (AT) is a complex organ with a crucial regulatory role in energy metabolism and in the development of obesity and the Metabolic Syndrome (MS). Modified responses and the metabolism of hormones have been observed in visceral adiposity during obesity, specifically as related with cortisone. The objective of this study was to assess, in the 3T3-L1 adipocyte cell line, the short-term effect of cortisone on the expression of 11b-Hydroxysteroid dehydrogenase 1 (Hsd1), which is responsible for activation of cortisone into cortisol, and for Aquaporin 7 (Aqp7), involved in glycerol transport through the cell membrane. Total RNA (tRNA) and complementary DNA (cDNA) were obtained from cell samples treated with cortisone (0.1, 1, and 10 mM) during different times (0, 5, 10, 15, and 20 min, and 48 h) to quantify the expression of the aforementioned genes by real time PCR employing MnSOD and Ppia as housekeeping genes. There was a time-dependent response of Aqp7, a dose-dependent response of Hsd1, and an increase observed in the expression of both genes during min 1 of treatment (5-and 6-fold, respectively), followed by a decrease during the following 5-10 min (P < 0.05). With the 1-mM cortisone treatment, both genes showed cubic tendencies in their expression; the Hsd1 tendency is described by the equation y D 0.18£ 3 ¡1.65£ 2 C3.59xC1.31, while the Aqp7 tendency is described by y D 0.33£ 3 -2.67£ 2 C4.93xC1.84. There are immediate and quantitatively important actions of cortisone on the expression of Aqp7 and Hsd1 in 3T3-L1 adipocytes.

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The effects of glucocorticoids on adipose tissue lipid metabolism

Cited by 436 publications

References 72 publications

Physiological Stress Responses in Amphibian Larvae to Multiple Stressors Reveal Marked Anthropogenic Effects even below Lethal Levels

Physiological Stress Responses in Amphibian Larvae to Multiple Stressors Reveal Marked Anthropogenic Effects even below Lethal Levels

Forkhead box A3 mediates glucocorticoid receptor function in adipose tissue

HSD1 and AQP7 short-term gene regulation by cortisone in 3T3-L1 adipocytes

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