Cortisol: the villain in Metabolic Syndrome?

Paredes, Sílvia; Ribeiro, Laura

doi:10.1590/1806-9282.60.01.017

Cited by 46 publications

(41 citation statements)

References 54 publications

(159 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Interestingly, perilipin, the product of this gene, has been implicated in the regulation of basal lipolysis (Londos et al 1995(Londos et al , 1999Souza et al 1998), and lower perilipin levels have been associated with leaner body constitution (Martinez-Botas et al 2000). It is tempting to speculate that increased perilipin levels as a result of constant receptor stimulation, under stress conditions or exogenous administration of synthetic glucocorticoids, could play a role in the process of visceral fat accumulation associated with these conditions (Paredes and Ribeiro 2014). (Fig.…”

Section: Discussionmentioning

confidence: 99%

Dynamics of chromatin accessibility and long-range interactions in response to glucocorticoid pulsing

et al. 2015

View full text Add to dashboard Cite

Although physiological steroid levels are often pulsatile (ultradian), the genomic effects of this pulsatility are poorly understood. By utilizing glucocorticoid receptor (GR) signaling as a model system, we uncovered striking spatiotemporal relationships between receptor loading, lifetimes of the DNase I hypersensitivity sites (DHSs), long-range interactions, and gene regulation. We found that hormone-induced DHSs were enriched within ±50 kb of GR-responsive genes and displayed a broad spectrum of lifetimes upon hormone withdrawal. These lifetimes dictate the strength of the DHS interactions with gene targets and contribute to gene regulation from a distance. Our results demonstrate that pulsatile and constant hormone stimulations induce unique, treatment-specific patterns of gene and regulatory element activation. These modes of activation have implications for corticosteroid function in vivo and for steroid therapies in various clinical settings.

show abstract

Section: Discussionmentioning

confidence: 99%

Dynamics of chromatin accessibility and long-range interactions in response to glucocorticoid pulsing

et al. 2015

View full text Add to dashboard Cite

show abstract

“…In females, follicular or luteal phase of the menstrual cycle, as well as pre- or post-menopausal status are also known to influence the HPA axis activity [33, 56, 57]. Importance of such additional determining factors that may influence peripheral cortisol release, independently of visceral obesity, are emphasized by previous clinical findings [9, 31]. These previous studies report that higher cortisol levels appear to induce metabolic syndrome in people suffering of severe visceral obesity, whereas similarly obese individuals with low cortisol output do not show characteristics of metabolic syndrome [9, 31].…”

Section: Discussionmentioning

confidence: 99%

“…Importance of such additional determining factors that may influence peripheral cortisol release, independently of visceral obesity, are emphasized by previous clinical findings [9, 31]. These previous studies report that higher cortisol levels appear to induce metabolic syndrome in people suffering of severe visceral obesity, whereas similarly obese individuals with low cortisol output do not show characteristics of metabolic syndrome [9, 31]. Thus, high cortisol output appears to aggravate complications of obesity.…”

Section: Discussionmentioning

confidence: 99%

“…The potential involvement of glucocorticoids in obesity is supported by numerous factors (for review see [2, 3]). Among other actions, they induce gluconeogenesis leading to hyperglycemia and hyperinsulinemia promoting fat deposition in case of enhanced caloric intake, they promote the differentiation and proliferation of human adipocytes [8], and they also play a role in the development of metabolic syndrome associated with visceral obesity [9]. Such findings raise the possibility that visceral fat accumulation and enhanced activity of the HPA axis may be linked to each other, but characteristics of this relationship remain unknown [10].…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

In Obesity, HPA Axis Activity Does Not Increase with BMI, but Declines with Aging: A Meta-Analysis of Clinical Studies

et al. 2016

View full text Add to dashboard Cite

BackgroundObesity is one of the major public health challenges worldwide. It involves numerous endocrine disorders as etiological factors or as complications. Previous studies strongly suggested the involvement of the hypothalamic-pituitary-adrenal (HPA) axis activity in obesity, however, to date, no consistent trend in obesity-associated alterations of the HPA axis has been identified. Aging has been demonstrated to aggravate obesity and to induce abnormalities of the HPA axis. Thus, the question arises whether obesity is correlated with peripheral indicators of HPA function in adult populations.ObjectivesWe aimed to meta-analyze literature data on peripheral cortisol levels as indicators of HPA activity in obesity during aging, in order to identify possible explanations for previous contradictory findings and to suggest new approaches for future clinical studies.Data Sources3,596 records were identified through searching of PubMed, Embase and Cochrane Library Database. Altogether 26 articles were suitable for analyses.Study Eligibility CriteriaEmpirical research papers were eligible provided that they reported data of healthy adult individuals, included body mass index (BMI) and measured at least one relevant peripheral cortisol parameter (i.e., either morning blood cortisol or 24-h urinary free cortisol).Statistical MethodsWe used random effect models in each of the meta-analyses calculating with the DerSimonian and Laird weighting methods. I-squared indicator and Q test were performed to assess heterogeneity. Meta-regression was applied to explore the effect of BMI and age on morning blood and urinary free cortisol levels. To assess publication bias Egger’s test was used.ResultsObesity did not show any correlation with the studied peripheral cortisol values. On the other hand, peripheral cortisol levels declined with aging within the obese, but not in the non-obese groups.ConclusionsOur analysis demonstrated that obesity or healthy aging does not lead to enhanced HPA axis activity, peripheral cortisol levels rather decline with aging.

show abstract

“…13,14 Estes fármacos possuem diversos efeitos laterais, entre os quais uma conhecida ação diabetogénica, 12,15 que ocorre através de diferentes mecanismos: 1) aumentam a gliconeogénese hepática; 2) diminuem a captação perifé-rica de glicose; 3) diminuem a sensibilidade à insulina e antagonizam o seu efeito; 4) inibem a secreção de insulina pelas células-β; e, 5) favorecem o aumento de ácidos gordos livres com a consequente lipotoxicidade a afetar negativamente a função da célula-β. 11,12,16 Como resultado final, os glicocorticóides agravam o controlo metabólico de indivíduos diabéticos, sendo também responsáveis pela ocorrência de hiperglicemia em doentes não diabéticos.…”

Section: Fisiopatologia E Especificidades Da Hiperglicemia Induzidas unclassified

Abordagem e Tratamento da Hiperglicemia Induzida por Glicocorticóides

Paredes

Alves

2016

Acta Med Port

Self Cite

View full text Add to dashboard Cite

RESUMOIntrodução: Os glicocorticóides associam-se a vários efeitos adversos, entre os quais se destaca uma importante ação diabetogé-nica. A hiperglicemia induzida pelos glicocorticóides trata-se de uma condição com elevada prevalência e que condiciona importante morbimortalidade. Material e Métodos: Realizou-se uma revisão da literatura relativa à abordagem e tratamento da hiperglicemia induzida pelos glicocorticóides Resultados: Embora não totalmente esclarecidos, sabe-se que vários mecanismos concorrem de forma sinérgica, propiciando o aparecimento da hiperglicemia em doentes não diabéticos e o agravamento do controlo glicémico em diabéticos. A hiperglicemia induzida por glicocorticóides apresenta padrões característicos, mais marcada no momento pós-prandial e muito dependente do horário da toma do glicocorticóide. Apesar da existência de normas de orientação gerais para o tratamento da hiperglicemia em doentes em ambulatório e em doentes hospitalizados não críticos, o mesmo não acontece no que diz respeito ao tratamento da hiperglicemia induzida por glicocorticóides. E, de facto, frequentemente é difícil e exigente a abordagem deste tipo de hiperglicemia, sendo necessária uma atuação específica. Esta abordagem depende não só do glicocorticóide em causa, como também da sua dose, frequência e horário de administração. De igual forma, a escolha do esquema de tratamento também depende do tipo de terapêutica previamente usado. Discussão e Conclusão: Os autores fizeram uma revisão do tema, congregando e definindo linhas orientadoras para o tratamento da hiperglicemia induzida por glicocorticóides, em doentes diabéticos e não diabéticos, em regime de ambulatório ou internamento, que serão úteis em diferentes contextos e transversalmente às diversas especialidades. Palavras-chave: Glucocorticóides/efeitos adversos; Hiperglicemia/diagnóstico; Hiperglicemia/induzida quimicamente; Hiperglicemia/ tratamento. ABSTRACT Introduction:Glucocorticoids have been associated to several side effects, specially a diabetogenic action, the most common and representative effect. Glucocorticoid-induced hyperglycemia is a common medical condition, with general associated morbidity and mortality. Material and Methods: It was performed a literature review about the management and treatment of glucocorticoid-induced hyperglycemia.Results: Through numerous not quite fully understood mechanics, glucocorticoids promote hyperglycemia in non-diabetic patients and worsen diabetes control in diabetic individuals. Glucocorticoid-induced hyperglycemia presents key patterns, enhanced in the postprandial period and scheduled-dependent. Despite the existence of guidelines for hyperglycemia treatment in non-critic hospitalized and non-hospitalized patients, there are no guidelines respecting glucocorticoid-induced hyperglycemia. Nevertheless, it is known that glucocorticoid-induced hyperglycemia is complex and demanding, requiring a specific approach. Indeed, glucocorticoid-induced hyperglycemia treatment depends on the glucocorticoid used, its dose, ...

show abstract

Cortisol: the villain in Metabolic Syndrome?

Cited by 46 publications

References 54 publications

Dynamics of chromatin accessibility and long-range interactions in response to glucocorticoid pulsing

Dynamics of chromatin accessibility and long-range interactions in response to glucocorticoid pulsing

In Obesity, HPA Axis Activity Does Not Increase with BMI, but Declines with Aging: A Meta-Analysis of Clinical Studies

Abordagem e Tratamento da Hiperglicemia Induzida por Glicocorticóides

Contact Info

Product

Resources

About