11β‐Hydroxysteroid dehydrogenase type 1‐driven cortisone reactivation regulates plasminogen activator inhibitor type 1 in adipose tissue of obese women

Ayachi, Safia; Paulmyer‐Lacroix, Odile; Verdier, Monique; Alessi, Marie‐Christine; Dutour, A.; Grino, Michel

doi:10.1111/j.1538-7836.2006.01811.x

Cited by 17 publications

(9 citation statements)

References 64 publications

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“…Whereas the stimulation of PAI-1 gene expression in liver and adipose tissue could be subsequent to the increase in circulating insulin concentrations (35), changes in adipose tissue PAI-1 mRNA levels could be directly controlled by enhanced 11␤-HSD-1 mRNA expression. We have previously shown that 11␤-HSD-1-driven cortisone reactivation regulates PAI-1 in adipose tissue of obese women (36).…”

Section: Discussionmentioning

confidence: 96%

Postnatal Programming of Glucocorticoid Metabolism in Rats Modulates High-Fat Diet–Induced Regulation of Visceral Adipose Tissue Glucocorticoid Exposure and Sensitivity and Adiponectin and Proinflammatory Adipokines Gene Expression in Adulthood

et al. 2008

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OBJECTIVE-Alterations of the perinatal environment, which lead to increased prevalence of the metabolic syndrome in adulthood, program an upregulation of systemic and/or adipose tissue glucocorticoid metabolism (11␤-hydroxysteroid dehydrogenase type 1 [11␤-HSD-1]-induced corticosterone reactivation). We hypothesized that postnatal programming could modulate high-fat diet-induced adipose tissue dysregulation in adulthood. RESEARCH DESIGN AND METHODS-We compared the effects of chronic (since weaning) high-or low-fat diet in postnatally normofed (control) or overfed (programmed) rats. RESULTS-Postnatal programming accentuated high-fat dietinduced overweight, insulin resistance, glucose intolerance, and decrease in circulating and epididymal adipose tissue adiponectin. Neither manipulation altered liver function. Postnatal programming or high-fat diet increased systemic corticosterone production, which was not further modified when both manipulations were associated. Postnatal programming suppressed high-fat diet-induced decrease in mesenteric adipose tissue (MAT) glucocorticoid sensitivity and triggered high-fat dietinduced increase in MAT glucocorticoid exposure, subsequent to enhanced MAT 11␤-HSD-1 gene expression. MAT tumor necrosis factor (TNF)-␣, TNF-receptor 1, interleukin (IL)-6, resistin, and plasminogen activator inhibitor-1 mRNAs were not changed by high-fat feeding in control rats and showed a large increase in programmed animals, with this effect further enhanced by highfat diet for TNF-␣ and IL-6. CONCLUSIONS-Our data show for the first time that postnatal manipulation programs high-fat diet-induced upregulation of MAT glucocorticoid exposure, sensitivity, and inflammatory status and therefore reveal the pivotal role of the environment during the perinatal period on the development of diet-induced adipose tissue dysregulation in adulthood. They also urge the need for clinical trials with specific 11␤-HSD-1 inhibitors. Diabetes 57:669-677, 2008

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Section: Discussionmentioning

confidence: 96%

Postnatal Programming of Glucocorticoid Metabolism in Rats Modulates High-Fat Diet–Induced Regulation of Visceral Adipose Tissue Glucocorticoid Exposure and Sensitivity and Adiponectin and Proinflammatory Adipokines Gene Expression in Adulthood

et al. 2008

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“…Interestingly, this stimulatory effect of glucocorticoids on PAI-1 production by adipose tissue appeared to be inhibited by coincubation with an inhibitor of 11 ␤ -HSD-1 [170] . Indeed, in situ hybridization revealed increased PAI-1 mRNA expression in visceral adipose tissue of obese subjects, which was positively related to the expression of 11 ␤ -HSD-1 mRNA, suggesting that local conversion of cortisone to cortisol may contribute to the observed elevation of PAI-1 levels in obesity [170] . Similarly, a 3-hour intravenous infusion of hydrocortisone enhanced PAI-1 circulating concentrations in both obese and normal women, and the percent increase between 180 and 240 min was significantly higher in obese subjects compared with controls [171] .…”

Section: Pai-1 and The Hpa Axismentioning

confidence: 98%

Adipokines and Cardiovascular Risk in Cushing’s Syndrome

et al. 2011

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Cushing’s syndrome (CS) is associated with increased cardiovascular morbidity and mortality. Recent evidence also suggests that increased cardiovascular risk may persist even after long-term remission of CS. Increased central obesity, a typical feature of CS, is associated with altered production of adipokines, which contributes to the pathogenesis of several metabolic and cardiovascular complications observed in this condition. In vitro and in vivo studies have shown a relationship between cortisol and adipokines in several experimental settings. In patients with either active or ‘cured’ CS, an increase in leptin and resistin levels as well as the release of pro-inflammatory cytokines, such as tumor necrosis factor-α and interleukin-6, may be associated with increased cardiovascular risk. For other adipokines, including adiponectin, results are inconclusive. Studies are needed to further elucidate the interactions between clinical and subclinical increases in cortisol production and altered adipokine release in CS.

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“…Signals were detected by enhanced chemiluminescence using Uptilight horseradish peroxidase blot reagent (Interchim Chemicals, Mannheim, Germany). sPLA 2 -IIA secretion from adipose tissue explants EAT and SAT explants supernatants from five patients with CAD (group 2) were obtained by incubating 50 mg of tissue in 1 ml of DMEM/HAMF12 (Sigma Aldrich, St. Louis, MO) for 24 h at 37 C as described (12). After incubation the samples were centrifuged (10,000 ϫ g 10 min 4 C) and stored at Ϫ20 C. Quantification was processed using hsPLA 2 -IIa enzyme immunoassay kit (Cayman Chemicals, Ann Arbor, MI).…”

Section: Western Blottingmentioning

confidence: 99%

Secretory Type II Phospholipase A2 Is Produced and Secreted by Epicardial Adipose Tissue and Overexpressed in Patients with Coronary Artery Disease

Dutour

Achard

Sell

et al. 2010

The Journal of Clinical Endocrinology &Amp; Metabolism

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11β‐Hydroxysteroid dehydrogenase type 1‐driven cortisone reactivation regulates plasminogen activator inhibitor type 1 in adipose tissue of obese women

Cited by 17 publications

References 64 publications

Postnatal Programming of Glucocorticoid Metabolism in Rats Modulates High-Fat Diet–Induced Regulation of Visceral Adipose Tissue Glucocorticoid Exposure and Sensitivity and Adiponectin and Proinflammatory Adipokines Gene Expression in Adulthood

Postnatal Programming of Glucocorticoid Metabolism in Rats Modulates High-Fat Diet–Induced Regulation of Visceral Adipose Tissue Glucocorticoid Exposure and Sensitivity and Adiponectin and Proinflammatory Adipokines Gene Expression in Adulthood

Adipokines and Cardiovascular Risk in Cushing’s Syndrome

Secretory Type II Phospholipase A2 Is Produced and Secreted by Epicardial Adipose Tissue and Overexpressed in Patients with Coronary Artery Disease

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