Visceral Fat Accumulation and Its Relation to Plasma Hemostatic Factors in Healthy Men

Abstract

The associations between abdominal visceral fat and the plasma hemostatic system were examined in 38-year-old healthy men (n=52) with a wide range of fatness and fat distribution. Plasma hemostatic factors and metabolic parameters, including glucose tolerance, were measured, and body fatness and adipose tissue distribution were assessed by using computed tomography. The men with more visceral fat (ie, higher than the median value [n=26]) had a less favorable metabolic profile than the men with less visceral fat (n=26). They also had significantly (P<.05) higher plasma fibrinogen, factor VIII clotting activity, tissue-type plasminogen activator antigen, and plasminogen activator inhibitor-1 (PAI-1) activity (19.2+/-2.4 versus 8.5+/-1.6 AU/mL, P<.001) and lower basal tissue-type plasminogen activator activity. After adjustment for plasma insulin, the men with larger abdominal visceral fat area still had significantly higher plasma PAI-1 activity, but no difference was found in any of the other hemostatic factors. In multiple linear regression analysis, abdominal visceral fat area was a positive predictor of plasma PAI-1 activity, but it failed to show any significant association with other hemostatic factors after controlling for plasma insulin. These results suggest the presence of relationships between abdominal visceral fat and several plasma hemostatic factors that are largely mediated by concomitant alterations in plasma insulin concentration. In addition, our results suggest that abdominal accumulation of visceral fat is an independent predictor of plasma PAI-1 activity.

The impairment of flow-mediated vasodilatation in obese men with visceral fat accumulation

“…9,11,31 In our study, no signi®cant differences in plasma fasting glucose, IRI and haemoglobin A 1c levels were found among the three groups. Since we did not perform the oral glucose tolerance test with plasma IRI measurement or other insulin sensitivity tests, it is dif®cult to evaluate the role of insulin resistance in the impairment of¯ow-mediated vasodilatation.…”

“…Moreover, the mechanism responsible for impaired endothelial function in visceral fat accumulation is not fully understood. Evidence has accumulated that adipocytes synthesize some kinds of vasoactive substances such as tumor necrosis factor (TNF)-a, 36 plasminogen activator inhibitor (PAI)-1 31,37,38 and von Willebrand factor. 39 These may be involved in the mechanism of endothelial dysfunction.…”

The determinants of plasma plasminogen activator inhibitor-1 levels differ for American and Japanese men aged 40–49

“…Second, there may be the differences in the fat cell size between these two ethnic groups. Americans may have smaller fat cells 28 than the Japanese as smaller fat cells produce less PAI-1 compared to larger fat cells [30][31][32] . Third, it may be explained by the differences in genetic factors between these ethnic groups.…”

Visceral fat as a main determinant of plasminogen activator inhibitor 1 level in women

“…28±30 This work was intended to look at a relationship of PAI-1 levels with the amount of fat tissue, either visceral or subcutaneous, estimated by tomodensimetry in a group of premenopausal women with a wide range of body weight and to substantiate the association between VAT in PAI-1 levels, recently observed in Japanese subjects 27 and in men. 31 Additionally, to determine if the respective amounts of VAT and subcutaneous adipose tissue could be causally related to circulating PAI-1 levels, we compared the evolution of PAI-1 levels to that of fat tissue after a weight loss in a subgroup of these obese women.…”