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Trends in endocrinology and metabolism, 2020-03, Vol.31 (3), p.205-217
2020
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Autor(en) / Beteiligte
Titel
Mineralocorticoid Receptors in Metabolic Syndrome: From Physiology to Disease
Ist Teil von
  • Trends in endocrinology and metabolism, 2020-03, Vol.31 (3), p.205-217
Ort / Verlag
United States: Elsevier Ltd
Erscheinungsjahr
2020
Quelle
Access via ScienceDirect (Elsevier)
Beschreibungen/Notizen
  • Over the past decade, several studies have shown that activity of extra-renal mineralocorticoid receptors (MR) regulates vascular tone, adipogenesis, adipose tissue function, and cardiomyocyte contraction. In mice, abnormal activation of MR in the vasculature and in adipose tissue favors the occurrence of several components of the metabolic syndrome (MetS), such as hypertension, obesity, and glucose intolerance. Accordingly, high levels of aldosterone are associated with obesity and MetS in humans, suggesting that altered activation of aldosterone-MR system in extra-renal tissues leads to profound metabolic dysfunctions. In this context, in addition to the classical indications for heart failure and hypertension, MR antagonists (MRAs) nowadays represent a promising approach to tackle cardiovascular and metabolic disorders occurring in the MetS. Over the past 10 years, a number of studies performed with transgenic mice have shown that vascular-specific and adipocyte-specific MRs affect vascular function and adipose tissue (AT) development, respectively.Preclinical and human studies revealed a ‘metabolic role’ for the aldosterone-MR system, demonstrating that its excessive activation is associated with the development of endothelial dysfunction, atherosclerosis, AT, and glucose metabolism dysfunctions.In obese mice, MRAs counteract vascular and AT dysfunctions and reverse impaired glucose tolerance.In humans, MRA treatment is able to activate BAT function, however, their efficacy in improving metabolic function of obese subjects still awaits demonstration.
Sprache
Englisch
Identifikatoren
ISSN: 1043-2760
eISSN: 1879-3061
DOI: 10.1016/j.tem.2019.11.006
Titel-ID: cdi_proquest_miscellaneous_2327931892

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