scholarly journals Adipocytes, aldosterone and obesity-related hypertension

2016 ◽  
Vol 57 (1) ◽  
pp. F7-F21 ◽  
Author(s):  
Aurelie Nguyen Dinh Cat ◽  
Malou Friederich-Persson ◽  
Anna White ◽  
Rhian M Touyz
Keyword(s):  
Adipose Tissue ◽  
Adrenal Glands ◽  
Experimental Studies ◽  
Cardiovascular Complications ◽  
Plasma Aldosterone ◽  
Therapeutic Interventions ◽  
Obese Patients ◽  
Aldosterone Secretion ◽  
Local Synthesis ◽  
Obesity Epidemic

Understanding the mechanisms linking obesity with hypertension is important in the current obesity epidemic as it may improve therapeutic interventions. Plasma aldosterone levels are positively correlated with body mass index and weight loss in obese patients is reported to be accompanied by decreased aldosterone levels. This suggests a relationship between adipose tissue and the production/secretion of aldosterone. Aldosterone is synthesized principally by the adrenal glands, but its production may be regulated by many factors, including factors secreted by adipocytes. In addition, studies have reported local synthesis of aldosterone in extra-adrenal tissues, including adipose tissue. Experimental studies have highlighted a role for adipocyte-secreted aldosterone in the pathogenesis of obesity-related cardiovascular complications via the mineralocorticoid receptor. This review focuses on how aldosterone secretion may be influenced by adipose tissue and the importance of these mechanisms in the context of obesity-related hypertension.

The “adipose tissue expandability” hypothesis: a potential mechanism for insulin resistance in obese youth

2018 ◽  
Vol 33 (2) ◽  
Author(s):  
Sonia Caprio ◽  
Bridget Pierpont ◽  
Romy Kursawe
Keyword(s):  
Relative Proportion ◽  
Significant Risk ◽  
Cardiovascular Complications ◽  
Therapeutic Interventions ◽  
Obesity Epidemic ◽  
Fat Depots ◽  
Obese Youth ◽  
Total Body ◽  
Relationship Of ◽  
Adipose Tissue Expandability

AbstractObesity has become a major global health challenge of the 21st century, as it is associated with the onset of type 2 diabetes (T2D) and cardiovascular complications, even at a very early age in life. The root causes of pediatric obesity remain incompletely understood. The obesity epidemic together with the relationship of obesity to the growing population burden of chronic disease presents unprecedented research opportunities and challenges. Decades of obesity-related research funded by governments around the world have yielded many important discoveries about both etiological pathways and preventive or therapeutic interventions. Yet, there is a sense that the problem is outpacing these research efforts. Obesity poses a significant risk for the development of cardiovascular disease (CVD) , diabetes and certain cancers thereby shortening life expectancy. Nevertheless, many obese individuals do not develop any of these comorbidities. One hypothesis explaining this dilemma is that total body fat is not the culprit of adverse health in obesity rather the relative proportion of lipids in various fat depots is what determines the metabolic risk. In this review, we describe the role of altered fat partitioning in youth onset obesity and its relation to fatty liver and T2D during adolescence.

scholarly journals Inflammation in Atherosclerosis: From Theory to Practice

2020 ◽  
Vol 6 (10) ◽  
pp. 186-205
Author(s):  
A. Chaulin ◽  
Ju. Grigoryeva
Keyword(s):  
Risk Factors ◽  
Adipose Tissue ◽  
T Lymphocytes ◽  
Inflammatory Cytokines ◽  
Interferon Gamma ◽  
Visceral Adipose Tissue ◽  
Experimental Studies ◽  
Therapeutic Interventions ◽  
Inflammatory Status ◽  
Visceral Adipose

Inflammation causes the formation, progression, and rupture of atherosclerotic plaques, which are an integral part of cardiovascular diseases. Numerous components are involved in the pathogenesis of atherosclerotic inflammation. Experimental studies have shown that the inflammatory subpopulation of monocytes / macrophages mainly accumulates in the atherosclerotic plaque and produces Pro-inflammatory cytokines that enhance atherogenesis. T-lymphocytes can contribute to the inflammatory processes that contribute to thrombosis by stimulating the production of collagen-destroying proteinases and a powerful procoagulant substance, tissue factor. Many research data link obesity, inflammation, and risk factors for atherosclerosis, which is a growing clinical concern given the increasing prevalence of obesity worldwide. Modulators of inflammation originating from visceral adipose tissue cause the liver to produce acute phase reagents involved in thrombosis. Additionally, levels of C-reactive protein increase with increasing levels of visceral adipose tissue. The adipose tissue of obese mice contains an increased number of macrophages and T-lymphocytes, increased activation of T-lymphocytes, and increased expression of interferon-gamma. It was found that interferon-gamma deficiency in mice reduces the production of inflammatory cytokines and the accumulation of inflammatory cells in adipose tissue. Another series of experiments on mice in vitro and in vivo confirmed that adiponectin, an adipocytokine whose plasma levels drop with obesity, acts as an endogenous anti-inflammatory modulator of both innate and acquired immunity in atherogenesis. Thus, the accumulation of experimental data confirms the key role of inflammation as a link between risk factors for atherosclerosis and the biology underlying the complications of this disease. A large Jupiter clinical trial confirms the clinical utility of assessing inflammatory status in therapeutic interventions to limit cardiovascular events. Thus, knowledge of the pathogenetic mechanisms underlying atherosclerotic inflammation is not only of theoretical value, but can also be used in practice when assessing the risk and prescribing therapy.

The Invisible Evil Twin of an Adrenal Adenoma

2019 ◽  
Vol 4 (1) ◽  
pp. 58
Author(s):  
Aimi Fadilah Mohamad ◽  
Fatimah Zaherah Mohamed Shah ◽  
Nur Aisyah Zainordin ◽  
Ur 'Aini Eddy Warman ◽  
Nazimah Ab Mumin ◽  
...  
Keyword(s):  
Adrenal Glands ◽  
Adrenal Adenoma ◽  
Definitive Diagnosis ◽  
Dynamic Tests ◽  
Venous Sampling ◽  
Aldosterone Secretion ◽  
Aldosterone Level ◽  
Suppression Test ◽  
The Right ◽  
Secondary Causes

Primary aldosteronism (PA) causes a persistently elevated blood pressure (BP) due to excessive release of the hormone aldosterone from the adrenal glands. Classically, it is called Conn’s syndrome and is described as the triad of hypertension and hypokalemia with the presence of unilateral adrenal adenoma. It can be cured with surgical resection of the aldosterone-secreting adenoma leading to resolution of hypertension, hypokalemia and increased cardiovascular risk associated with hyperaldosteronism. We present a case of a man with previous ischemic heart disease (IHD) who presented with resistant hypertension. Investigations for secondary causes of hypertension revealed an elevated aldosterone level and saline suppression test confirmed the diagnosis of PA. Radiological examination revealed a left adrenal adenoma and a normal right adrenal gland. However, adrenal venous sampling showed lateralization of aldosterone secretion towards the right. He subsequently underwent a laparoscopic right adrenalectomy which improved his BP control promptly. This case highlights the importance of recognizing the need to investigate for secondary causes of hypertension. It also underscores the importance of dynamic tests, which may not be easily accessible to most clinicians but should pursue, to allow a definitive diagnosis and effective treatment.

scholarly journals Gestational Diabetes Mellitus and Infant Adiposity at Birth: A Systematic Review and Meta-Analysis of Therapeutic Interventions

2021 ◽  
Vol 10 (4) ◽  
pp. 835
Author(s):  
Manoja P. Herath ◽  
Jeffrey M. Beckett ◽  
Andrew P. Hills ◽  
Nuala M. Byrne ◽  
Kiran D. K. Ahuja
Keyword(s):  
Diabetes Mellitus ◽  
Adipose Tissue ◽  
Gestational Diabetes ◽  
Gestational Diabetes Mellitus ◽  
Fat Mass ◽  
Metabolic Disorders ◽  
Later Life ◽  
Therapeutic Interventions ◽  
Increased Risk ◽  
The Impact

Exposure to untreated gestational diabetes mellitus (GDM) in utero increases the risk of obesity and type 2 diabetes in adulthood, and increased adiposity in GDM-exposed infants is suggested as a plausible mediator of this increased risk of later-life metabolic disorders. Evidence is equivocal regarding the impact of good glycaemic control in GDM mothers on infant adiposity at birth. We systematically reviewed studies reporting fat mass (FM), percent fat mass (%FM) and skinfold thicknesses (SFT) at birth in infants of mothers with GDM controlled with therapeutic interventions (IGDMtr). While treating GDM lowered FM in newborns compared to no treatment, there was no difference in FM and SFT according to the type of treatment (insulin, metformin, glyburide). IGDMtr had higher overall adiposity (mean difference, 95% confidence interval) measured with FM (68.46 g, 29.91 to 107.01) and %FM (1.98%, 0.54 to 3.42) but similar subcutaneous adiposity measured with SFT, compared to infants exposed to normal glucose tolerance (INGT). This suggests that IGDMtr may be characterised by excess fat accrual in internal adipose tissue. Given that intra-abdominal adiposity is a major risk factor for metabolic disorders, future studies should distinguish adipose tissue distribution of IGDMtr and INGT.

scholarly journals Cellular and Molecular Players in the Interplay between Adipose Tissue and Breast Cancer

2021 ◽  
Vol 22 (3) ◽  
pp. 1359
Author(s):  
Francesca Reggiani ◽  
Paolo Falvo ◽  
Francesco Bertolini
Keyword(s):  
Breast Cancer ◽  
Adipose Tissue ◽  
Metabolic Disorders ◽  
Current Knowledge ◽  
Therapeutic Interventions ◽  
Preclinical Research ◽  
The World ◽  
Adipose Cells

The incidence and severity of obesity are rising in most of the world. In addition to metabolic disorders, obesity is associated with an increase in the incidence and severity of a variety of types of cancer, including breast cancer (BC). The bidirectional interaction between BC and adipose cells has been deeply investigated, although the molecular and cellular players involved in these mechanisms are far from being fully elucidated. Here, we review the current knowledge on these interactions and describe how preclinical research might be used to clarify the effects of obesity over BC progression and morbidity, with particular attention paid to promising therapeutic interventions.

Evaluation of Biochemical Conditions Allowing Bypass of Confirmatory Testing in The Workup of Primary Aldosteronism: A Retrospective Study in a French Hypertensive Population

2019 ◽  
Vol 51 (03) ◽  
pp. 172-177 ◽  
Author(s):  
Maud Vivien ◽  
Emilie Deberles ◽  
Remy Morello ◽  
Aimi Haddouche ◽  
David Guenet ◽  
...  
Keyword(s):  
Primary Aldosteronism ◽  
Dynamic Testing ◽  
Challenge Test ◽  
Plasma Aldosterone ◽  
Aldosterone Secretion ◽  
Plasma Aldosterone Concentration ◽  
Hypertensive Patients ◽  
Hypertensive Population ◽  
Tertiary Center ◽  
Aldosterone To Renin Ratio

AbstractThe diagnostic workup for primary aldosteronism includes a screening step using the aldosterone-to-renin ratio (ARR) and a confirmatory step based on dynamic testing of aldosterone secretion autonomy. International guidelines suggest that precise clinical and biochemical conditions may allow the bypassing of the confirmatory step, however, data which validate hormone thresholds defining such conditions are lacking. At our tertiary center, we retrospectively examined a cohort of 173 hypertensive patients screened for PA by the ARR, of whom 120 had positive screening and passed a saline infusion test (SIT) or a captopril challenge test (CCT). Fifty-nine had PA, including 34 Conn adenomas and 25 with idiopathic aldosteronism (IA). Using a threshold of 160 pmol/l, post-SIT plasma aldosterone concentration (PAC) identified PA with 86.4% sensitivity, 94.7% specificity, and a negative predictive value of 92.3%. Of those subjects with a high ARR and a PAC above 550 pmol/l, 93% had a positive SIT, while 100% of subjects with a high ARR, but a PAC under 240 pmol/l had a negative SIT. Our results thus validate the biochemical conditions defined in the French and US guidelines for bypassing the confirmatory step in the workup for PA diagnosis.

Overexpression of hepatic 5α-reductase and 11β-hydroxysteroid dehydrogenase type 1 in visceral adipose tissue is associated with hyperinsulinemia in morbidly obese patients

Metabolism ◽  
2011 ◽  
Vol 60 (12) ◽  
pp. 1775-1780 ◽  
Author(s):  
René Baudrand ◽  
José Miguel Domínguez ◽  
Cristian A. Carvajal ◽  
Arnoldo Riquelme ◽  
Carmen Campino ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Visceral Adipose Tissue ◽  
Hydroxysteroid Dehydrogenase ◽  
Morbidly Obese ◽  
Obese Patients ◽  
Visceral Adipose

scholarly journals Chemotactic cytokines, obesity and type 2 diabetes:in vivoandin vitroevidence for a possible causal correlation?

2009 ◽  
Vol 68 (4) ◽  
pp. 378-384 ◽  
Author(s):  
Henrike Sell ◽  
Jürgen Eckel
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Low Grade ◽  
Obese Patients ◽  
Tissue Mass ◽  
Tissue Biology ◽  
Wide Range ◽  
Adipose Tissue Mass

A strong causal link between increased adipose tissue mass and insulin resistance in tissues such as liver and skeletal muscle exists in obesity-related disorders such as type 2 diabetes. Increased adipose tissue mass in obese patients and patients with diabetes is associated with altered secretion of adipokines, which also includes chemotactic proteins. Adipose tissue releases a wide range of chemotactic proteins including many chemokines and chemerin, which are interesting targets for adipose tissue biology and for biomedical research in obesity and obesity-related diseases. This class of adipokines may be directly linked to a chronic state of low-grade inflammation and macrophage infiltration in adipose tissue, a concept intensively studied in adipose tissue biology in recent years. The inflammatory state of adipose tissue in obese patients may be the most important factor linking increased adipose tissue mass to insulin resistance. Furthermore, chemoattractant adipokines may play an important role in this situation, as many of these proteins possess biological activity beyond the recruitment of immune cells including effects on adipogenesis and glucose homeostasis in insulin-sensitive tissues. The present review provides a summary of experimental evidence of the role of adipose tissue-derived chemotactic cytokines and their function in insulin resistancein vivoandin vitro.

scholarly journals Characterization of pendrin in urinary extracellular vesicles in a rat model of aldosterone excess and in human primary aldosteronism

2021 ◽  
Author(s):  
Fumika Ochiai-Homma ◽  
Emiko Kuribayashi-Okuma ◽  
Yuya Tsurutani ◽  
Kenichi Ishizawa ◽  
Wataru Fujii ◽  
...  
Keyword(s):  
Extracellular Vesicles ◽  
Rat Model ◽  
Primary Aldosteronism ◽  
Experimental Studies ◽  
Concomitant Administration ◽  
Therapeutic Interventions ◽  
Cross Sectional ◽  
Quantitative Changes ◽  
Highly Correlated ◽  
Sectional Analysis

AbstractPendrin is a Cl−/HCO3− exchanger selectively present in the intercalated cells of the kidney. Although experimental studies have demonstrated that pendrin regulates blood pressure downstream of the renin-angiotensin-aldosterone system, its role in human hypertension remains unclear. Here, we analyzed the quantitative changes in pendrin in urinary extracellular vesicles (uEVs) isolated from a total of 30 patients with primary aldosteronism (PA) and from a rat model of aldosterone excess. Western blot analysis revealed that pendrin is present in dimeric and monomeric forms in uEVs in humans and rats. In a rodent model that received continuous infusion of aldosterone with or without concomitant administration of the selective mineralocorticoid receptor (MR) antagonist esaxerenone, pendrin levels in uEVs, as well as those of epithelial Na+ channel (ENaC) and Na-Cl-cotransporter (NCC), were highly correlated with renal abundance. In patients with PA, pendrin levels in uEVs were reduced by 49% from baseline by adrenalectomy or pharmacological MR blockade. Correlation analysis revealed that the magnitude of pendrin reduction after treatment significantly correlated with the baseline aldosterone-renin ratio (ARR). Finally, a cross-sectional analysis of patients with PA confirmed a significant correlation between the ARR and pendrin levels in uEVs. These data are consistent with experimental studies showing the role of pendrin in aldosterone excess and suggest that pendrin abundance is attenuated by therapeutic interventions in human PA. Our study also indicates that pendrin analysis in uEVs, along with other proteins, can be useful to understand the pathophysiology of hypertensive disorders.

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