Oleoyl-estrone affects lipid metabolism in adrenalectomized rats treated with corticosterone through modulation of SREBP1c expression

Serrano, Marta; Grasa, María del Mar; Janer, Gemma; Fernández-López, José Antonio

doi:10.1016/j.jsbmb.2009.06.003

Cited by 6 publications

(8 citation statements)

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“…(Grasa et al, 2001) The anti-adiposity effects of oleoyl-estrone were abrogated with corticosteroid treatment, suggesting inhibition of glucocorticoid signaling may be a key mechanism through which oleoyl-estrone reduces fat mass. (Serrano et al, 2009) In contrast, however, elevated estrone exposure has been posited to contribute directly to increases in body weight and adiposity. (Remesar et al, 1999) In acute food deprivation in rats, serum estrone levels rose whereas estrone fatty esters declined, findings potentially consistent with their respective putative effects on energy conservation and utilization.…”

Section: Estrogens Beyond 17β-estradiol: Estrone and 17α-estradiolmentioning

confidence: 99%

Estrogens and Body Weight Regulation in Men

Rubinow

2017

Advances in Experimental Medicine and Biology

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Our understanding of the metabolic roles of sex steroids in men has evolved substantially over recent decades. Whereas testosterone once was believed to contribute to metabolic risk in men, the importance of adequate androgen exposure for the maintenance of metabolic health has been demonstrated unequivocally. A growing body of evidence now also supports a critical role for estrogens in metabolic regulation in men. Recent data from clinical intervention studies indicate that estradiol may be a stronger determinant of adiposity than testosterone in men, and even short-term estradiol deprivation contributes to fat mass accrual. The following chapter will outline findings to date regarding the mechanisms whereby estrogens contribute to the regulation of body weight and adiposity in men. It will present emergent clinical data as well as preclinical findings that reveal mechanistic insights into estrogen-mediated regulation of body composition. Findings in both males and females will be reviewed, to draw comparisons and to highlight knowledge gaps regarding estrogen action specifically in males. Finally, the clinical relevance of estrogen exposure in men will be discussed, particularly in the context of a rising global prevalence of obesity and expanding clinical use of sex steroid-based therapies in men.

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Section: Estrogens Beyond 17β-estradiol: Estrone and 17α-estradiolmentioning

confidence: 99%

Estrogens and Body Weight Regulation in Men

Rubinow

2017

Advances in Experimental Medicine and Biology

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“…Thus, we considered the possibility that the induction of PPARg after food restriction ( Figure 3) is a consequence of glucocorticosteroid activation by elevated activity of 11βHSD1 in adipose tissue. Serrano et al [33] showed that corticosterone administration to adrenalectomized rats induces gene expression of lipogenic enzymes, including FAS and ACL, in periovaric WAT. It has also been shown that dexamethasone induces ME activity in differentiated 3T3-L1 cells [34].…”

Section: Discussionmentioning

confidence: 99%

Chronic food restriction up-regulates 11-β-hydroxysteroid dehydrogenase

et al. 2011

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Corticosterone — product of 11-β-hydroxysteroid dehydrogenase type I (11βHSD1) stimulates adipocytes differentiation and activates lipogenic enzymes gene expression in white adipose tissue (WAT) of rats. The aim of the study was to examine the effect of chronic food restriction, often practised by obese individuals trying to lose body mass, on: a) 11βHSD1 gene expression, b) expression of genes associated with adipocyte differentiation (PPARg, SREBP-1, adiponectin), and c) expression of genes associated with lipogenesis in WAT of rats. Two-month old rats were divided into a control and a food restricted group obtaining 50% of food consumed by controls for 30 days. mRNA levels of studied genes in perirenal WAT were analysed by real-time PCR. 11βHSD1 and lipogenic enzymes activities were measured by radiometric conversion assay and by spectrophotometric assay respectively. Food restriction caused significant increase of 11βHSD1, PPARg, SREBP1, adiponectin and lipogenic enzymes mRNA levels in perirenal WAT. 11βHSD1 and some lipogenic enzymes activities were also increased by food restriction. The coordinated up-regulation of 11βHSD1, and genes associated with adipocyte differentiation and lipogenesis by food restriction suggests that such nutritional condition shifts WAT metabolism, that would permit this tissue to synthesize and accumulate triacylglycerols immediately after refeeding.

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“…It has been postulated that OE decreases WAT energy content by deregulating the equilibrium between lipogenesis (and triacylglycerol synthesis) and lipolysis [12,13]. In spite of marked differences between WAT sites, the cells of rats treated with OE were shrunk by the loss of fat; their decreased cAMP levels agreed with a generalized depression of lipogenesis.…”

Section: Discussionmentioning

confidence: 99%

“…This process is in part mediated, at least in liver, by SREBP1c [13], under conditions in which glycolysis is not completely blocked irrespective of a large availability of fatty acids [14]. Notwithstanding, basically the OE mechanism of action remains largely unknown.…”

Section: Introductionmentioning

confidence: 99%

Comparative effects of oleoyl-estrone and a specific β3-adrenergic agonist (CL316, 243) on the expression of genes involved in energy metabolism of rat white adipose tissue

2010

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BackgroundThe combination of oleoyl-estrone (OE) and a selective β3-adrenergic agonist (B3A; CL316,243) treatment in rats results in a profound and rapid wasting of body reserves (lipid).MethodsIn the present study we investigated the effect of OE (oral gavage) and/or B3A (subcutaneous constant infusion) administration for 10 days to overweight male rats, compared with controls, on three distinct white adipose tissue (WAT) sites: subcutaneous inguinal, retroperitoneal and epididymal. Tissue weight, DNA (and, from these values cellularity), cAMP content and the expression of several key energy handling metabolism and control genes were analyzed and computed in relation to the whole site mass.ResultsBoth OE and B3A significantly decreased WAT mass, with no loss of DNA (cell numbers). OE decreased and B3A increased cAMP. Gene expression patterns were markedly different for OE and B3A. OE tended to decrease expression of most genes studied, with no changes (versus controls) of lipolytic but decrease of lipogenic enzyme genes. The effects of B3A were widely different, with a generalized increase in the expression of most genes, including the adrenergic receptors, and, especially the uncoupling protein UCP1.DiscussionOE and B3A, elicit widely different responses in WAT gene expression, end producing similar effects, such as shrinking of WAT, loss of fat, maintenance of cell numbers. OE acted essentially on the balance of lipolysis-lipogenesis and the blocking of the uptake of substrates; its decrease of synthesis favouring lipolysis. B3A induced a shotgun increase in the expression of most regulatory systems in the adipocyte, an effect that in the end favoured again the loss of lipid; this barely selective increase probably produces inefficiency, which coupled with the increase in UCP1 expression may help WAT to waste energy through thermogenesis.ConclusionsThere were considerable differences in the responses of the three WAT sites. OE in general lowered gene expression and stealthily induced a substrate imbalance. B3A increasing the expression of most genes enhanced energy waste through inefficiency rather than through specific pathway activation. There was not a synergistic effect between OE and B3A in WAT, but their combined action increased WAT energy waste.

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Oleoyl-estrone affects lipid metabolism in adrenalectomized rats treated with corticosterone through modulation of SREBP1c expression

Cited by 6 publications

References 50 publications

Estrogens and Body Weight Regulation in Men

Estrogens and Body Weight Regulation in Men

Chronic food restriction up-regulates 11-β-hydroxysteroid dehydrogenase

Comparative effects of oleoyl-estrone and a specific β3-adrenergic agonist (CL316, 243) on the expression of genes involved in energy metabolism of rat white adipose tissue

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