2013
DOI: 10.1016/j.jnutbio.2013.07.002
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The renin–angiotensin system in adipose tissue and its metabolic consequences during obesity

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Cited by 136 publications
(95 citation statements)
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References 219 publications
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“…Adipose tissue exerts the largest source of extra hepatic circulating angiotensin, and adipose tissue-derived angiotensin has been suggested to be a factor contributing to the association between obesity and hypertension [24], with plasma levels of both angiotensinogen and angiotensin II showing positive correlations with BMI [42]. In our study, however, plasma angiotensin II levels are not altered with disease state.…”
contrasting
confidence: 62%
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“…Adipose tissue exerts the largest source of extra hepatic circulating angiotensin, and adipose tissue-derived angiotensin has been suggested to be a factor contributing to the association between obesity and hypertension [24], with plasma levels of both angiotensinogen and angiotensin II showing positive correlations with BMI [42]. In our study, however, plasma angiotensin II levels are not altered with disease state.…”
contrasting
confidence: 62%
“…Adipose tissue exerts the largest source of extra hepatic circulating angiotensin [24], and here we found angiotensin pathways to be altered along with significant upregulation of AGT alongside, AGTR2 gene expression. We therefore investigated whether circulating levels of angiotensin II were altered.…”
Section: Circulating Angiotensin II Levelssupporting
confidence: 51%
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“…Local renin-angiotensin systems are widely distributed, and one is also present in adipocytes (for review see [56]). Additionally, substrates from isolated adipocytes may directly stimulate the secretion of aldosterone [57,58].…”
Section: Dysglycemia Dyslipidemia and Hypertensionmentioning
confidence: 99%
“…Согласно данной гипотезе, увеличение синтеза ангиотензиногена и ангиотензина II в адипоцитах способствует повышению концентрации этих белков в циркуляторном русле, что приводит к развитию гипертонии у человека. Более того, ангиотензин II, помимо влияния на сердечно-сосудистую систему и почки, вызывает инсулинорезистентность, нарушение толерантности к глюкозе, подавляет диффе-ренцировку адипоцитов, способствуя их гипертрофии, стимулирует липогенез и секрецию провоспалительных адипокинов адипоцитами (Frigolet et al, 2013), в резуль-тате чего развивается метаболический синдром. При этом активность РАС в жировой ткани не зависит от ак-тивности системной РАС: экспрессия ренина в жировой ткани не коррелирует с концентрацией этого фермента в крови (Marcus et al, 2013).…”
Section: моделирование патологий вавиловский журнал генетики и селекцunclassified