Regulation of vascular tone by adipocytes

Maenhaut, Nele; Voorde, Johan Van de

doi:10.1186/1741-7015-9-25

Cited by 132 publications

(95 citation statements)

References 144 publications

(212 reference statements)

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“…Moreover, this group observed that leptin levels were positively correlated with TG, lipoprotein (a) [Lp (a)], Apo-A1, glucose, systolic blood pressure and diastolic blood pressure levels, and negatively with HDL-C levels in DM2 patients. Also, it has been proposed that the increased levels of leptin observed in obesity deregulates blood pressure control and results in hypertension, suggesting that leptin may also be a potential promoter of hypertension [38].…”

Section: The Role Of Leptin In Metabolic Syndrome and Diabetesmentioning

confidence: 99%

The role of leptin/adiponectin ratio in metabolic syndrome and diabetes

López‐Jaramillo¹,

Gómez-Arbeláez²,

López‐López

et al. 2013

Hormone Molecular Biology and Clinical Investigation

347

299

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Abstract:The metabolic syndrome comprises a cluster of cardiometabolic risk factors, with insulin resistance and adiposity as its central features. Identifying individuals with metabolic syndrome is important due to its association with an increased risk of coronary heart disease and type 2 diabetes mellitus. Attention has focused on the visceral adipose tissue production of cytokines (adipokines) in metabolic syndrome and type 2 diabetes mellitus, as the levels of the anti-inflammatory adipokine adiponectin are decreased, while proinflammatory cytokines are elevated, creating a proinflammatory state associated with insulin resistance and endothelial dysfunction. In this review, we will give special attention to the role of the leptin/adiponectin ratio. We have previously demonstrated that in individuals with severe coronary artery disease, abdominal obesity was uniquely related to decreased plasma concentrations of adiponectin and increased leptin levels. Leptin/adiponectin imbalance was associated with increased waist circumference and a decreased vascular response to acetylcholine and increased vasoconstriction due to angiotensin II. Leptin and adiponectin have opposite effects on subclinical inflammation and insulin resistance. Leptin upregulates proinflammatory cytokines such as tumor necrosis factor-α and interleukin-6; these are associated with insulin resistance and type 2 diabetes mellitus. In contrast, adiponectin has anti-inflammatory properties and downregulates the expression and release of a number of proinflammatory immune mediators. Therefore, it appears that interactions between angiotensin II and leptin/adiponectin imbalance may be important mediators of the elevated risk of developing type 2 diabetes mellitus and cardiovascular diseases associated with abdominal obesity.

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Section: The Role Of Leptin In Metabolic Syndrome and Diabetesmentioning

confidence: 99%

The role of leptin/adiponectin ratio in metabolic syndrome and diabetes

López‐Jaramillo¹,

Gómez-Arbeláez²,

López‐López

et al. 2013

Hormone Molecular Biology and Clinical Investigation

347

299

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“…Specifically, adiponectin reduces hepatic gluconeogenesis, increases glucose uptake by muscle and adipocytes, and reduces liver and muscle triacylglyceride accumulation while increasing fatty acid oxidation in these tissues (6). Along with these insulin-sensitizing actions, adiponectin exhibits cardioprotective and anti-inflammatory properties by acting directly on cardiomyocites, vascular cells, and macrophages, which has been proposed to underlie its beneficial effects on cardiovascular disorders (7)(8)(9)(10). Recent studies demonstrated that adiponectin also promotes cell survival of pancreatic ␤-cells (11) and may also play a role in the development and progression of distinct malignancies associated with obesity and insulin resistance, including breast cancer and colon cancer (12,13).…”

mentioning

confidence: 99%

Adiponectin Receptors Form Homomers and Heteromers Exhibiting Distinct Ligand Binding and Intracellular Signaling Properties

Almabouada

Díaz‐Ruiz

Rabanal-Ruíz

et al. 2013

Journal of Biological Chemistry

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Background: Adiponectin receptors (AdipoR1 and 2) mediate the effects of adiponectin, which possesses insulin sensitizing and anti-inflammatory properties. Results: AdipoRs organize into oligomers exhibiting distinct interaction and signaling properties. Conclusion:The cellular response to adiponectin depends on the specific AdipoR repertoire. Significance: To envisage novel therapeutic strategies, the capacity of AdipoRs to form oligomeric complexes must be taken into consideration.

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“…ROS are known to induce inflammatory cytokines and, conversely, the cytokines also increase the ROS generation, thereby potentially forming a vicious cycle. [8][9][10][11][12][13][14]16,[19][20][21] Furthermore, a recent study by Banday and Lokhandwala 22 indicates that ROS increase the expression of Ang II receptors. Interestingly, the suppression of ROS production during the Ang II infusion almost completely abolished the persistent changes in the cytokines, Rac-1 and TBARS, following the discontinuation of Ang II infusion (Figures 2 and 3).…”

Section: Discussionmentioning

confidence: 99%

“…[8][9][10][11][12][13][14]16 However, how the upregulation of these proteins decays after the withdrawal of RAS activation has remained unclear.…”

Section: Discussionmentioning

confidence: 99%

“…The rationale for this hypothesis is three-fold. Activation of the AT 1 receptor has been shown to activate multiple signaling pathways, leading to inflammatory reactions in blood vessels, 8,9 adipose tissue 10,11 and skeletal muscles. 12,13 Second, inflammatory reactions are often self-perpetuating 14 and are maintained even after the initial stimuli are withdrawn.…”

Section: Introductionmentioning

confidence: 99%

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Angiotensin II receptor activation in youth triggers persistent insulin resistance and hypertension—a legacy effect?

et al. 2011

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Although the involvement of angiotensin II (Ang II) in insulin resistance and hypertension has been established, the temporal relationships between Ang II receptor activation and changes in insulin sensitivity and blood pressure are not clear. To better understand this issue, we infused rats with Ang II (200 ng kg À1 min À1 ) or vehicle for 4 weeks and assessed the residual effects after the discontinuation of the infusion on blood pressure, insulin sensitivity and tissue parameters of inflammation. Four weeks after the discontinuation of the Ang II infusion, the blood pressure was higher by 12.8 mm Hg, and insulin sensitivity as determined by a euglycemic hyperinsulinemic glucose clamp was reduced (glucose infusion rate: 11.1 ± 0.7 vs. 17.6±0.5 mg kg À1 min À1 ) in the Ang II-treated group compared with controls. The persistent hypertension and insulin resistance were associated with greater than two-fold increases in macrophage chemoattractant protein-1, tumor necrosis factor-a and thiobarbituric acid-reactive substrates in the soleus muscle. Furthermore, total and activated forms of Rac-1, a regulatory subunit of the NADPH oxidase complex, were increased by 144 ± 14% and 277 ± 82%, respectively, in the skeletal muscle of Ang II-treated rats. These residual effects after Ang II infusion were all attenuated by the co-administration of tempol, a free radical scavenger, or candesartan with Ang II. The effects of candesartan were not mimicked by hydralazine at an equidepressant dose. These findings suggest that Ang II receptor activation in youth triggers the upregulation of inflammatory cytokines and the production of reactive oxygen species, thereby inducing later insulin resistance and hypertension. INTRODUCTIONEvidence from patients and animal models has indicated that the angiotensin II (Ang II) type 1 receptor (AT 1 receptor) has a major role in the development of insulin resistance and hypertension. 1-4 However, the relationship between timing of the AT 1 receptor activation and the development (and persistence) of changes in insulin sensitivity and blood pressure has not been fully elucidated. Interestingly, the Trial of Preventing Hypertension Study showed that the treatment of prehypertensive patients with the AT 1 receptor blocker (ARB) candesartan for 2 years significantly delayed the progression from pre-hypertension to stage 1 hypertension during the following 2 years. 5 This finding suggests long-lasting effects of transitory activation of the AT 1 receptor in the development of hypertension. The results of the Trial of Preventing Hypertension Study bear certain similarities to those of a study by Holman et al. 6 (United Kingdom Prospective Diabetes Study), indicating the so-called 'legacy effect' . These authors found that the reduction of microvascular events continued for 10 years, in spite of the loss of differences in glycemic control after 10 years of intensive glycemic control had been discontinued. Furthermore, such 'legacy

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Regulation of vascular tone by adipocytes

Cited by 132 publications

References 144 publications

The role of leptin/adiponectin ratio in metabolic syndrome and diabetes

The role of leptin/adiponectin ratio in metabolic syndrome and diabetes

Adiponectin Receptors Form Homomers and Heteromers Exhibiting Distinct Ligand Binding and Intracellular Signaling Properties

Angiotensin II receptor activation in youth triggers persistent insulin resistance and hypertension—a legacy effect?

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