Human Adipose Tissue Cells Keep Tight Control on the Angiotensin II Levels in Their Vicinity

Schling, Petra; Schäfer, Thorsten

doi:10.1074/jbc.m204058200

Cited by 60 publications

(48 citation statements)

References 46 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…17 It has previously been shown that Ang II concentrations are B2-3-fold higher in the incubation medium of (pre)adipocytes than in the circulation. 4,7 Because stimulation of adipocytes with physiological concentrations of Ang II evoked near-maximal inhibition of lipolysis in the present experiments, Ang II may not play an important role in the regulation of adipocyte lipolysis. Instead, Ang II may exert a tonic suppression of adipocyte lipolysis.…”

Section: Resultsmentioning

confidence: 74%

“…Part of this association may be explained by adipose tissue products that exert autocrine, paracrine and/ or endocrine effects that may affect metabolism. [1][2][3] A functional renin-angiotensin system (RAS) is present in human adipose tissue, [4][5][6] and local generation of angiotensin II (Ang II), the effector molecule of the RAS, by human (pre)adipocytes has been demonstrated. 7 The adipose tissue RAS may be involved in obesity-related disorders, such as insulin resistance, 8,9 possibly through an effect on adipocyte differentiation.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Angiotensin II: a hormone that affects lipid metabolism in adipose tissue

et al. 2006

View full text Add to dashboard Cite

Background: Alterations in adipose tissue lipolysis may contribute to the pathophysiology of obesity and insulin resistance. We examined the effects of angiotensin II (Ang II) on abdominal subcutaneous adipose tissue lipolysis in humans. Methods and results: First, adipocytes obtained from nine normal weight and seven obese subjects were stimulated with Ang II (10 À14 -10 À6 M). Glycerol concentration in the medium, used as an indicator of adipocyte lipolysis, was significantly reduced (B20%) after Ang II stimulation in adipocytes from normal weight (P ¼ 0.04) and obese subjects (Po0.001). Based on these observations, adipocytes of seven additional obese subjects were stimulated with lower doses of Ang II (10 À17 -10 À6 M) in the presence and absence of Ang II type 1 (AT 1 ) receptor blockade. Lipolysis was dose dependently inhibited by B20 to 25% after Ang II stimulation (P ¼ 0.001). AT 1 receptor blockade completely abolished the Ang II-induced effects (P ¼ 0.35). Conclusion: Ang II directly inhibits abdominal subcutaneous adipocyte lipolysis in normal weight and obese subjects via the AT 1 receptor.

show abstract

Section: Resultsmentioning

confidence: 74%

Section: Introductionmentioning

confidence: 99%

Angiotensin II: a hormone that affects lipid metabolism in adipose tissue

et al. 2006

View full text Add to dashboard Cite

show abstract

“…Therefore, Ang II secretion from these tissues cannot explain the increased Ang II concentrations observed in obese subjects during ␤-adrenergic stimulation. Because it is well established that Ang II is produced by human adipocytes, 28 our data suggest that locally produced Ang II in adipose tissue acts as an autocrine and/or paracrine hormone and does not exert endocrine effects. The present findings seem to be in contrast with a recent study demonstrating Ang II secretion from adipose tissue in vivo in overweight/obese subjects.…”

Section: Endocrine Function Of the Local Ras In Adipose Tissue And Skmentioning

confidence: 62%

Endocrine Role of the Renin-Angiotensin System in Human Adipose Tissue and Muscle

et al. 2007

View full text Add to dashboard Cite

Abstract-The renin-angiotensin system has been implicated in obesity-related hypertension and insulin resistance. We examined whether locally produced components of the renin-angiotensin system in adipose tissue and skeletal muscle play an endocrine role in vivo in humans. Furthermore, the effects of ␤-adrenergic stimulation on plasma concentrations and tissue release of renin-angiotensin system components were investigated. Systemic renin-angiotensin system components and arteriovenous differences of angiotensin II (Ang II) and angiotensinogen (AGT) across abdominal subcutaneous adipose tissue and skeletal muscle were assessed in combination with measurements of tissue blood flow before and during systemic ␤-adrenergic stimulation in 13 lean and 10 obese subjects. Basal plasma Ang II and AGT concentrations were not significantly different between lean and obese subjects. Ang II concentrations were increased in obese compared with lean subjects during ␤-adrenergic stimulation (12.6Ϯ1.5 versus 8.1Ϯ1.0 pmol/L; Pϭ0.04), whereas AGT concentrations remained unchanged. Plasma renin activity increased to a similar extent in lean and obese subjects during ␤-adrenergic stimulation (both PϽ0.01). No net Ang II release across adipose tissue and skeletal muscle could be detected in both groups of subjects. However, AGT was released from adipose tissue and muscle during ␤-adrenergic stimulation in obese subjects (both PϽ0.05). In conclusion, locally produced Ang II in adipose tissue and skeletal muscle exerts no endocrine role in lean and obese subjects. In contrast, AGT is released from adipose tissue and muscle in obese subjects during ␤-adrenergic stimulation, which may contribute to the increased plasma Ang II concentrations during ␤-adrenergic stimulation in obese subjects. Key Words: angiotensin Ⅲ ␤-adrenergic receptors Ⅲ obesity Ⅲ renin Ⅲ sympathetic nervous system A bdominal obesity plays a central role in the metabolic syndrome and is a major risk factor for chronic diseases, such as type 2 diabetes mellitus and cardiovascular disease. 1 Although abdominal obesity is frequently accompanied by hypertension, the mechanisms by which an excess fat mass may lead to hypertension are not fully understood. The reninangiotensin system (RAS) has been established as a major determinant of blood pressure and cardiovascular disease. 2 Furthermore, recent clinical trials suggest that blockade of RAS may reduce the incidence of type 2 diabetes. 3 Angiotensin II (Ang II), the main effector component of RAS, is produced in the circulation from angiotensinogen (AGT) because of the action of the enzymes renin and angiotensinconverting enzyme. In addition, it has become evident that several components of RAS are present in a variety of tissues, including adipose tissue and skeletal muscle (reviewed in Reference 4), implying that these tissues have the ability to produce Ang II.There is substantial evidence that circulating RAS components are increased in (hypertensive) obese subjects. [5][6][7][8] In line with this, it has been shown t...

show abstract

“…20 To show that Ang II also stimulates IL-6 secretion at lower concentrations, we performed additional experiments in which we added Ang II at a concentration of 10 Ϫ9 M every 6 hours for 24 hours. The stimulation of IL-6 protein release was similar as compared with 10 Ϫ5 M Ang II administered once (Table 2).…”

Section: The Effect Of Repetitive Addition Of Ang II On Il-6 Release mentioning

confidence: 99%

Angiotensin II Stimulates the Release of Interleukin-6 and Interleukin-8 From Cultured Human Adipocytes by Activation of NF-κB

Skurk

Harmelen

Hauner

2004

ATVB

119

View full text Add to dashboard Cite

Objective-Several proinflammatory cytokines including IL-6 and IL-8 are produced by human adipocytes, but it is still unclear how this process is regulated. Angiotensin (Ang) II, which is also produced by adipocytes, might play a role as a regulator. In the present study, we investigated the effect of Ang II on the production of IL-6 and IL-8 in in vitro differentiated human adipocytes. Methods and Results-Isolation of preadipocytes and differentiation of these cells into adipocytes, Real-time quantitative reverse-transcriptase polymerase chain reaction, Western-blot, enzyme-linked immunosorbent assay, and electromobility shift assay. Ang II-stimulated IL-6 and IL-8 mRNA expression and protein release in a time-and concentrationdependent way. This action of Ang II was completely blocked by the NF-B-blocker Bay 117082 and the AT 1 blocker candesartan, but only partially by the AT 2 -blocker PD 123 319. Incubation of adipocytes with Ang II resulted in an increased phosphorylation of the p65 subunit of NF-B and an increased translocation of NF-B to the nucleus. Conclusion-Ang II stimulates IL-6 and IL-8 production and release from human adipocytes by a NF-B-dependent pathway. This proinflammatory action of Ang II seems to be mediated by the AT 1 and less by the AT 2 receptor subtype.

show abstract

Human Adipose Tissue Cells Keep Tight Control on the Angiotensin II Levels in Their Vicinity

Cited by 60 publications

References 46 publications

Angiotensin II: a hormone that affects lipid metabolism in adipose tissue

Angiotensin II: a hormone that affects lipid metabolism in adipose tissue

Endocrine Role of the Renin-Angiotensin System in Human Adipose Tissue and Muscle

Angiotensin II Stimulates the Release of Interleukin-6 and Interleukin-8 From Cultured Human Adipocytes by Activation of NF-κB

Contact Info

Product

Resources

About