Abstract
Obesity has been a considered as phenomenon around the globe, leading to a variety of disorders such as metabolic diseases, asthma, and cardiovascular disease. Obesity and overweight are often related to increased levels of aldosterone in the blood, which implies a direct relationship between obesity, high blood pressure and mineralocorticoid levels. Adipocyte is believed to have a part in the fight against homeostasis, and recent studies have now shown that human fat is a highly active endocrine tissue. The research thus examined whether obesity is a rik factor for hypertension. The steroid genesis in human adrenocortical cells, NCI-H295R and bovine adrenocortical cells, was increased by isolation of human adi-cyte secretion products, focusing on the secretion of mineral corticoids. The outcoems indidcated that hypertension associated to obesity has direct relation between the metabolism of fat tissue and the production of adrenal mineralocorticoids.
Highlights
Obesity, visceral obesity, is significantly linked to high blood hypertension
Fat cell-derived secretagogs induced adrenocortical steroidosis with the main impact on aldosterone release in human cells NCI-H295R. (Fig. 1). This is recently confirmed in primary culture in bovine adrenocortic cells when fat-cell medial (FCCM) is compared with the maximum forskolin stimulation 210-5M (FSK). 24 h. n.d.: nondetectable cells were cultured
Fatcell-conditioned medium stimulant activity (FCCM) demonstrated an independent impact of an adipose angiotensin II Valsartan is used in the presence of an Angiotensin type 1 receptor antagonist
Summary
Visceral obesity, is significantly linked to high blood hypertension. Hyperaldosteronism is frequently linked to obesity (Drenick & Johnson, 2013), and plasma aldosterone levels are compared with fatty tissue volume (Blair et al, 2007). A causal connection between high blood aldosterone levels and hypertension in obese individuals was suggested (Contreras et al, 2004). The increase of aldosterone in obesity is frequently independent to the activity of the plasma renin.
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