An Adipocyte-Derived Plasma Protein, Adiponectin, Adheres to Injured Vascular Walls

Okamoto, Yoshihisa; Arita, Yukio; Nishida, Makoto; Muraguchi, Masahiro; Ouchi, Noriyuki; Takahashi, Masahiko; Igura, Takumi; Inui, Yukiharu; Kihara, Shinji; Nakamura, Tadashi; Yamashita, Shizuya; Miyagawa, J.; Funahashi, Tohru; Matsuzawa, Yasushi

doi:10.1055/s-2007-978586

Cited by 526 publications

(363 citation statements)

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“…Adiponectin suppresses TNF-ainduced endothelial adhesion molecule expression, the transformation of macrophages to foam cells, 10 and TNF-a expression in macrophages and adipose tissue. 22 In this study, plasma concentrations of VCAM-1 and E-selectin were elevated in preeclamptic women. Once cell adhesion molecules are expressed on the surface of endothelial cells or leukocytes following cytokine stimulation, they are shed within 24 h. In contrast to adiponectin, CRP induces adhesion molecule expression, 23 and elevated plasma levels of CRP may induce cell adhesion molecule expression in preeclamptic women.…”

Section: Discussionmentioning

confidence: 51%

Adipocytokines and endothelial function in preeclamptic women

et al. 2010

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Visceral fat accumulation stimulates the production of adipocytokines in patients with metabolic syndrome. Excess body weight gain during pregnancy is a risk factor for preeclampsia. To evaluate whether the pathogenesis of preeclampsia is similar to that of metabolic syndrome, we measured plasma adipocytokine concentrations and investigated the association between plasma adiponectin concentrations and body weight gain or endothelial function in preeclamptic women. We investigated 15 preeclamptic and 17 women with uncomplicated pregnancies. Women with preeclampsia had significantly lower plasma concentrations of adiponectin (10.2 ± 2.0 vs. 7.3 ± 2.2 lg ml À1 , Po0.01), but higher concentrations of leptin, plasminogen activator inhibitor-1, interleukin-6, vascular cell adhesion molecule-1, E-selectin and C-reactive protein. Plasma triglyceride levels were significantly higher in preeclamptic patients, but the levels of other lipids did not differ significantly between the two groups. We found that flow-mediated vasodilation was significantly decreased in preeclamptic women compared with controls (10.6 ± 6.4 vs. 3.8 ± 2.0%, Po0.001). Plasma adiponectin concentrations correlated negatively with body mass index (r¼À0.50, Po0.05) and body weight gain during pregnancy (r¼À0.63, Po0.01), and positively with flow-mediated vasodilation (r¼0.50, Po0.05) in preeclamptic women, but not in women with uncomplicated pregnancies. Similar to the patients with metabolic syndrome, we found that dysregulation of adipocytokines, such as low adiponectin levels and high levels of other adipocytokines, and excess body weight gain during pregnancy, may decrease plasma adiponectin concentrations that are associated with endothelial dysfunction in preeclamptic women.

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Section: Discussionmentioning

confidence: 51%

Adipocytokines and endothelial function in preeclamptic women

et al. 2010

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“…In addition, adiponectin strongly binds with subendothelial collagens such as collagen I, III, V, thus strengthening the sclerotic tissue plaque composition. 38 A possible mechanism of the prevention of atherosclerosis and acute coronary syndrome by adiponectin is shown in Figure 11. Adiponectin, abundantly present in the blood stream, may enter injured vascular walls by binding to subendothelial collagens and protecting against a variety of atherosclerotic cell phenomena as mentioned above.…”

Section: Fat Topography Y Matsuzawamentioning

confidence: 99%

The role of fat topology in the risk of disease

Matsuzawa

2008

Int J Obes

106

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Clustering of multiple risk factors such as impaired glucose metabolism, lipid disorders and hypertension has been shown to be the major background of atherosclerotic diseases, and disease entities such as the metabolic syndrome represent a highly atherogenic state. Although these common risks may generally co-exist by accident in one individual, clustering of multiple risk factors in the metabolic syndrome does not occur by accident, and there should be a key player for the syndrome. In 1983, we reported the method for fat analysis using computed tomography scan, which enables us to analyze intra-abdominal visceral adiposity as well as subcutaneous fat. Visceral fat accumulation has been shown to cause impaired glucose metabolism, lipid disorders, and hypertension, and therefore it is considered to be a key player in the metabolic syndrome. To clarify the mechanism by which visceral fat accumulation causes a variety of metabolic and vascular diseases, we studied the molecular characteristics of adipose tissue and adipocytes by investigating expressed genes in visceral and subcutaneous adipocytes and revealed that adipocytes, especially visceral adipocytes, secrete a variety of bioactive substances, the so-called adipocytokines. We showed that visceral fat accumulation causes abnormalities in adipocytokine secretion, such as hypersecretion of plasminogen activator inhibitor 1, which is related to thrombogenic vascular diseases. More importantly, we discovered an important benign adipocytokine named adiponectin, which protects against the development of diabetes mellitus, hypertension, inflammation, and atherosclerotic vascular diseases. Plasma levels of adiponectin decreased in individuals with visceral fat accumulation, and hypoadiponectinemia caused by visceral fat accumulation might be one of the major causes of metabolic syndrome.

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“…137,138 It can accumulate within injured vascular walls 139 and can suppress TNFa-induced expression of adhesion molecules in vascular endothelial cells. 137 This action is on the postreceptor part of TNF signalling, although the 'adiponectin receptor ' has not yet been identified.…”

Section: Adipocytokinesmentioning

confidence: 99%

Integrative physiology of human adipose tissue

et al. 2003

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Adipose tissue is now recognised as a highly active metabolic and endocrine organ. Great strides have been made in uncovering the multiple functions of the adipocyte in cellular and molecular detail, but it is essential to remember that adipose tissue normally operates as a structured whole. Its functions are regulated by multiple external influences such as autonomic nervous system activity, the rate of blood flow and the delivery of a complex mix of substrates and hormones in the plasma. Attempting to understand how all these factors converge and regulate adipose tissue function is a prime example of integrative physiology. Adipose tissue metabolism is extremely dynamic, and the supply of and removal of substrates in the blood is acutely regulated according to the nutritional state. Adipose tissue possesses the ability to a very large extent to modulate its own metabolic activities, including differentiation of new adipocytes and production of blood vessels as necessary to accommodate increasing fat stores. At the same time, adipocytes signal to other tissues to regulate their energy metabolism in accordance with the body's nutritional state. Ultimately adipocyte fat stores have to match the body's overall surplus or deficit of energy. This implies the existence of one (or more) signal(s) to the adipose tissue that reflects the body's energy status, and points once again to the need for an integrative view of adipose tissue function.

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An Adipocyte-Derived Plasma Protein, Adiponectin, Adheres to Injured Vascular Walls

Cited by 526 publications

References 1 publication

Adipocytokines and endothelial function in preeclamptic women

Adipocytokines and endothelial function in preeclamptic women

The role of fat topology in the risk of disease

Integrative physiology of human adipose tissue

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