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Journal ArticleDOI

Retroperitoneal adipose tissue denervation improves cardiometabolic and autonomic dysfunction in a high fat diet model.

TL;DR: In this paper, the effects evoked by bilateral white adipose tissue denervation in obese rats were evaluated, and it was shown that WAT denervation significantly attenuated these changes.
About: This article is published in Life Sciences.The article was published on 2021-07-21. It has received 3 citations till now. The article focuses on the topics: Denervation & White adipose tissue.
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Book ChapterDOI
01 Jan 2023
TL;DR: In this paper , the authors reviewed the actions of renin-angiotensins in WAT during the obese pathological remodeling, highlighting these molecules as a possible target to treat and prevent obesity.
Abstract: Obesity is defined as an increase in the amount of white adipose tissue (WAT) either in visceral (vWAT) or in subcutaneous (sWAT) pads, and it has increased worldwide, becoming an epidemic. Overweight/obese brings huge impacts, including health, social, and economic, to individuals and nations. It is already clear that the renin–angiotensin system (RAS) participates in the (patho)physiology of WAT, being involved in its remodeling in health and disease. Despite the angiotensin (Ang) II being the main biologically active metabolite of RAS, recent studies have demonstrated new peptides, enzymes, and arms acting through the systemic and local homeostasis of organs and tissues. The classical arm comprises the angiotensin-converting enzyme (ACE), the Ang II, and the angiotensin type 1 receptor (AT1R), which is upregulated in WAT of an obese individual, promoting inflammation, adipocyte hypertrophy, and impaired glucose metabolism. Alternatively, the Ang II can also bind to the AT2R promoting not only antagonism to the AT1R but also its own physiological actions. The counterregulatory arm comprises the ACE2, the Ang (1–7), and the Mas receptor (MasR), which antagonizes the classical arm and promotes antiinflammatory effects, decreases the adipocyte size, and improves glucose metabolism. Several studies have also demonstrated the relation between the angiotensins and the browning in WAT. Nonetheless, new peptides such as the Ang III, Ang IV, and alamandine have been described in the literature with some functions in WAT. In this chapter, we will review the actions of angiotensins in WAT during the obese pathological remodeling, highlighting these molecules as a possible target to treat and prevent obesity.
Journal ArticleDOI
TL;DR: In this paper , the authors investigated the effects of autocrine/paracrine effects on local resistance vessel function and morphology in human subcutaneous and omental adipose tissue (SAT and OAT): NE synthesis, angiogenesis, NE-mediated arteriolar vasoconstriction, the induction of collagen gene expression and its deposition in non-diabetic versus diabetic obese subjects.
Abstract: Norepinephrine (NE) is a known regulator of adipose tissue (AT) metabolism, angiogenesis, vasoconstriction and fibrosis. This may be through autocrine/paracrine effects on local resistance vessel function and morphology. The aims of this study were to investigate, in human subcutaneous and omental adipose tissue (SAT and OAT): NE synthesis, angiogenesis, NE-mediated arteriolar vasoconstriction, the induction of collagen gene expression and its deposition in non-diabetic versus diabetic obese subjects. SAT and OAT from obese patients were used to investigate tissue NE content, tyrosine hydroxylase (TH) density, angiogenesis including capillary density, angiogenic capacity and angiogenic gene expression, NE-mediated arteriolar vasoconstriction and collagen deposition. In the non-diabetic group, NE concentration, TH immunoreactivity, angiogenesis and maximal vasoconstriction were significantly higher in OAT compared to SAT (p < 0.05). However, arterioles from OAT showed lower NE sensitivity compared to SAT (10−8 M to 10–7.5 M, p < 0.05). A depot-specific difference in collagen deposition was also observed, being greater in OAT than SAT. In the diabetic group, no significant depot-specific differences were seen in NE synthesis, angiogenesis, vasoconstriction or collagen deposition. SAT arterioles showed significantly lower sensitivity to NE (10−8 M to 10–7.5 M, p < 0.05) compared to the non-diabetic group. SAT depot in non-diabetic obese patients exhibited relatively low NE synthesis, angiogenesis, tissue fibrosis and high vasoreactivity, due to preserved NE sensitivity. The local NE synthesis in OAT and diabetes desensitizes NE-induced vasoconstriction, and may also explain the greater tissue angiogenesis and fibrosis in these depots.
References
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Journal ArticleDOI
TL;DR: With prolonged obesity and development of target organ injury, obesity-associated hypertension becomes more difficult to control, often requiring multiple antihypertensive drugs and treatment of other risk factors, including dyslipidemia, insulin resistance and diabetes mellitus, and inflammation.
Abstract: Excess weight gain, especially when associated with increased visceral adiposity, is a major cause of hypertension, accounting for 65% to 75% of the risk for human primary (essential) hypertension. Increased renal tubular sodium reabsorption impairs pressure natriuresis and plays an important role in initiating obesity hypertension. The mediators of abnormal kidney function and increased blood pressure during development of obesity hypertension include (1) physical compression of the kidneys by fat in and around the kidneys, (2) activation of the renin-angiotensin-aldosterone system, and (3) increased sympathetic nervous system activity. Activation of the renin-angiotensin-aldosterone system is likely due, in part, to renal compression, as well as sympathetic nervous system activation. However, obesity also causes mineralocorticoid receptor activation independent of aldosterone or angiotensin II. The mechanisms for sympathetic nervous system activation in obesity have not been fully elucidated but may require leptin and activation of the brain melanocortin system. With prolonged obesity and development of target organ injury, especially renal injury, obesity-associated hypertension becomes more difficult to control, often requiring multiple antihypertensive drugs and treatment of other risk factors, including dyslipidemia, insulin resistance and diabetes mellitus, and inflammation. Unless effective antiobesity drugs are developed, the effect of obesity on hypertension and related cardiovascular, renal and metabolic disorders is likely to become even more important in the future as the prevalence of obesity continues to increase.

782 citations

Journal ArticleDOI
TL;DR: The occurrence of hypertension and its precursors is examined in the Framingham Offspring Study of 2,027 men and 2,267 women ages 20-49 years followed for 8 years and adiposity stands out as a major controllable contributor to hypertension.

716 citations

Journal ArticleDOI
TL;DR: Reduction in body weight induced by a hypocaloric diet with normal sodium content exerts a marked reduction in sympathetic activity owing to central sympathoinhibition, which can be due to the consequences of an increased insulin sensitivity but also to a restoration of the baroreflex control of the cardiovascular system with weight loss.
Abstract: Background —Previous studies have shown that sympathetic cardiovascular outflow is increased in obese normotensive subjects and that this increase is associated with a baroreflex impairment. The purpose of this study was to determine whether these abnormalities are irreversible or can be favorably affected by body weight reduction. Methods and Results —In 20 obese normotensive subjects (age, 31.3±1.7 years; body mass index, 37.6±0.9 kg/m 2 , mean±SEM), we measured beat-to-beat arterial blood pressure (Finapres technique), heart rate (ECG), postganglionic muscle sympathetic nerve activity (microneurography at a peroneal nerve), and venous plasma norepinephrine (high-performance liquid chromatography) at rest and during baroreceptor stimulation and deactivation induced by increases and reductions of blood pressure via stepwise intravenous infusions of phenylephrine and nitroprusside. Measurements were repeated in 10 subjects after a 16-week hypocaloric diet with normal sodium content (4600 to 5000 J and 210 mmol NaCl/d) and in the remaining 10 subjects after a 16-week observation period without any reduction in the caloric intake. The hypocaloric diet significantly reduced body mass index, slightly reduced blood pressure, and caused a significant and marked decrease in both muscle sympathetic nerve activity (from 50.0±5.1 to 32.9±4.6 bursts per 100 heart beats, P P P P P Conclusions —In obese normotensive subjects, a reduction in body weight induced by a hypocaloric diet with normal sodium content exerts a marked reduction in sympathetic activity owing to central sympathoinhibition. This can be due to the consequences of an increased insulin sensitivity but also to a restoration of the baroreflex control of the cardiovascular system with weight loss.

359 citations

Journal ArticleDOI
TL;DR: Results provide some support for the view that leptin stimulates the sympathetic nervous system, at least for renal sympathetic outflow, but do not confirm the concept of regulatory feedback inhibition of leptin release by the sympathetic nerve system.
Abstract: Results from animal experimentation suggest a 2-way interaction between leptin and the sympathetic nervous system, with leptin causing sympathetic activation and conversely, with the sympathetic system exercising regulatory feedback inhibition over leptin release. We have now tested this hypothesis in humans. In the absence of results from leptin infusions, to test for sympathetic stimulation of leptin release, we sought a quantitative naturalistic linkage of sympathetic activity with leptin plasma concentration across a broad range of leptin values in men of widely differing adiposity. Renal norepinephrine spillover was correlated with plasma leptin ( r =0.628, P 60 years and P

260 citations

Journal ArticleDOI
TL;DR: Transsynaptic viral tract tracers revealed WAT central sympathetic and sensory circuits including SNS-sensory feedback loops that may control lipolysis, and increases or decreases in WAT SNS drive/NE inhibit and stimulate white adipocyte proliferation, respectively.

248 citations