Vascular Endothelial Growth Factor Is the Major Angiogenic Factor in Omentum: Mechanism of the Omentum-Mediated Angiogenesis

Zhang, Qingxue; Magovern, Christopher J.; Mack, Charles A.; Budenbender, Kurt T.; Ko, Wilson; Rosengart, Todd K.

doi:10.1006/jsre.1996.4983

Cited by 336 publications

(237 citation statements)

References 2 publications

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“…This assumption is supported by a recent study showing that, in patients with coronary artery diseases, the degree of hypoxic induction of VEGF correlates with the extent of collateral vessel formation. 30 In one animal study, omental adipocytes were shown to have significantly greater in vitro rates of VEGF release compared with epididymal fat 31 and another animal study indicated cultured omental stromal cells had similar rates of VEGF secretion to those of epididymal fat stromal cells. 8 However, in our study, serum levels of VEGF positively correlated with S area but not with V area.…”

Section: Discussionmentioning

confidence: 99%

Serum bFGF levels are reduced in Japanese overweight men and restored by a 6-month exercise education

et al. 2003

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OBJECTIVE:To investigate whether the changes in vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) concentrations before and after weight reduction in Japanese overweight men are associated with changes in body mass index (BMI), visceral, subcutaneous fat, VO 2 and work rate (WR) at ventilatory threshold (VT). DESIGN: Cross-sectional and longitudinal clinical intervention study with exercise education. SUBJECTS: In total, 30 Japanese overweight men (BMI, 29.072.2 kg/m 2 ) and 31 normal-weight men (BMI, 22.571.6 kg/m 2 ) at baseline were enrolled: 30 overweight men (BMI, 29.072.2 kg/m 2 ) were further enrolled into a 6-month exercise program. MEASUREMENTS: Fat distribution evaluated by visceral fat (V) and subcutaneous fat (S) areas measured with computed tomography scanning at umbilical levels, angiogenic peptides including VEGF and bFGF, exercise tests at baseline and after 6 months. RESULTS: In normal-weight and overweight subjects at baseline, VEGF positively correlated with S area (r ¼ 0.350, P ¼ 0.007) but not with V area. In contrast, bFGF negatively correlated with BMI (r ¼ À0.619, Po0.001), S (r ¼ À0.457, Po0.001) and V areas (r ¼ À0.466, Po0.001). By intervention with exercise education, 30 overweight subjects showed reduction in BMI (29.072.2 to 28.072.0, Po0.001), V and S areas, increase in VO 2 and WR at VT, increase in bFGF (9.2175.82-21.277.04 ng/ ml, Po0.001), and no change in VEGF (1.4570.72-1.8870.52 ng/ml, P ¼ 0.016). The stepwise multiple regression analysis revealed that DBMI (b ¼ À6.052) and DVO 2 (b ¼ 2.806) were independently related to DbFGF (Po0.001) and all other variables including DS area, and DV area, and DWR did not enter the equation at significant levels. CONCLUSION: The present study indicated a negative correlation between serum bFGF levels and BMI at baseline as well as an association of DBMI and DVO 2 with DbFGF after exercise intervention. The exercise-induced elevation of bFGF may be beneficial in the prevention of the atherosclerosis in overweight subjects.

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Section: Discussionmentioning

confidence: 99%

Serum bFGF levels are reduced in Japanese overweight men and restored by a 6-month exercise education

et al. 2003

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“…VEGF-A exhibits predominantly pro-angiogenic activity in AT (78). Furthermore, VEGF levels are known to be regulated by hypoxia, insulin stimulation, certain growth factors, and specific cytokines (79) and vary during adipogenesis (80).…”

Section: Angiogenesis a Rate-limiting Step For At Expansion And Remomentioning

confidence: 99%

Adipose tissue remodeling and obesity

Sun¹,

Kusminski²,

Scherer³

2011

J. Clin. Invest.

1,585

1,381

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To fulfill its role as the major energy-storing tissue, adipose has several unique properties that cannot be seen in any other organ, including an almost unlimited capacity to expand in a non-transformed state. As such, the tissue requires potent mechanisms to remodel, acutely and chronically. Adipocytes can rapidly reach the diffusional limit of oxygen during growth; hypoxia is therefore an early determinant that limits healthy expansion. Proper expansion requires a highly coordinated response among many different cell types, including endothelial precursor cells, immune cells, and preadipocytes. There are therefore remarkable similarities between adipose expansion and growth of solid tumors, a phenomenon that presents both an opportunity and a challenge, since pharmacological interventions supporting healthy adipose tissue adaptation can also facilitate tumor growth. IntroductionAdipose tissue (AT) can respond rapidly and dynamically to alterations in nutrient deprivation and excess through adipocyte hypertrophy and hyperplasia, thereby fulfilling its major role in wholebody energy homeostasis. AT remodeling is an ongoing process that is pathologically accelerated in the obese state, and thus, features such as reduced angiogenic remodeling, ECM overproduction, a heightened state of immune cell infiltration and subsequent proinflammatory responses prevail in many obese fat-pads (1). However, not all AT expansion is necessarily associated with pathological changes. The concept of the "metabolically healthy obese" state (2) suggests that some individuals can preserve systemic insulin sensitivity on the basis of "healthy" AT expansion, bypassing all of the aforementioned pathological consequences associated with obesity (3), thereby also avoiding the obesity-associated lipotoxic side effects. Many physiologically relevant processes important for human AT remodeling can be studied in rodent models, with the added advantage that processes related to AT expansion and reduction can occur at an extremely rapid rate. A 24-hour fast in a mouse is associated with a dramatic loss of AT mass and an acute remodeling process that involves rapid infiltration of macrophages; moreover, merely 24 to 48 hours of exposure to a high-fat diet (HFD) can cause a prompt increase in adipocyte size (4). AT is therefore an ideal model system to study rapid alterations in tissue expansion and reduction, as it adapts to a differential nutrient supply. Here, we will focus on key aspects of the intricate dynamics of AT remodeling and subsequent inflammatory consequences that arise from obesity.

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“…Loss of a single VEGF-A allele causes embryonic vascular defects, while reduction of VEGF-A levels by only 25% impairs spinal cord perfusion, resulting in motor neuron degeneration reminiscent of amyotrophic lateral sclerosis (Carmeliet et al, 1996;Ferrara et al, 1996;Oosthuyse et al, 2001). VEGF-A is believed to be responsible for most of adipose tissue's angiogenic capacity (Zhang et al, 1997). VEGF-B (21 kDa) is 43% identical to VEGF-A165; it also promotes angiogenesis and is implicated in ECM degradation via regulation of plasminogen activation (Olofsson et al, 1998).…”

Section: Vascular Endothelial Growth Factors and Placental Growth Factormentioning

confidence: 99%

Angiogenesis and development of adipose tissue

Christiaens

Lijnen

2010

Molecular and Cellular Endocrinology

195

159

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Vascular Endothelial Growth Factor Is the Major Angiogenic Factor in Omentum: Mechanism of the Omentum-Mediated Angiogenesis

Cited by 336 publications

References 2 publications

Serum bFGF levels are reduced in Japanese overweight men and restored by a 6-month exercise education

Serum bFGF levels are reduced in Japanese overweight men and restored by a 6-month exercise education

Adipose tissue remodeling and obesity

Angiogenesis and development of adipose tissue

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