73. Liver steatosis and its relation to haemostatic factors in healthy males

Targher, G.; Agostino, G.; Tonoli, M.; Deorsola, B.; Muggeo, Michele; Sandre, G. De; Cigolini, M.

doi:10.1016/s0268-9499(96)80650-3

Cited by 12 publications

(17 citation statements)

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“…17 Many studies in healthy subjects have suggested that beside visceral fat accumulation, other elements of the insulin resistance syndrome are associated with increased plasma PAI-1 levels. PAI-1 levels were reported to be positively correlated with increased insulin levels, 9,10,[12][13][14]16,43 decreased insulin sensitivity, 10,13,14,19,43 increased plasma triglyceride levels, 11,12,14,15,43 and increased blood pressure. 16,43 However, these associations could well be indirect and, at least in part, depend on the relationship between PAI-1 and visceral fat, because visceral fat is associated with insulin resistance 44 and increased glucose, insulin, and triglyceride levels.…”

Section: -42mentioning

confidence: 99%

“…4 The exact origin of plasmatic PAI-1 is unknown, but in vitro studies show that it is produced by a wide variety of cell types, 4 including endothelial cells, vascular smooth muscle cells, hepatocytes, 5 and adipocytes. [6][7][8] Correlations have been found between plasma PAI-1 levels and visceral fat accumulation measured by means of the waist-to-hip ratio (WHR), 9 -14 ultrasonographic techniques, 15 or CT. 7,16 It is unknown, however, whether this association already exists in young, nonobese subjects, since previous studies included middle-aged subjects, 7,9 -16 obese subjects, 9 -16 or subjects with essential hypertension.…”

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confidence: 99%

“…17 Therefore, it is unknown whether the association between plasma PAI-1 levels and visceral fat accumulation is independent of these disturbances. 18 Previous studies either did not include all of these elements of the insulin resistance syndrome in one statistical model 7,9,10 or used indirect or crude estimates, such as WHR, to estimate fat distribution, 9,[11][12][13][14]19 and insulin levels after a glucose tolerance test, 12,15,16 the minimalmodel method, 11,13 or a hyperglycemic clamp 14 to estimate insulin sensitivity.…”

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Visceral Fat Accumulation Is an Important Determinant of PAI-1 Levels in Young, Nonobese Men and Women

Giltay

Elbers

Gooren

et al. 1998

ATVB

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Abstract-Increased plasminogen activator inhibitor type-1 (PAI-1) levels, leading to impaired fibrinolysis, are associated with increased visceral fat in middle-aged and obese subjects. It is unknown, however, whether this association is independent of other disturbances clustered in the insulin resistance syndrome. We analyzed this association in young, nonobese transsexual men and women before and after administration of cross-sex steroids, which potentially influence many elements of the insulin resistance syndrome, including PAI-1 levels and visceral fat accumulation. We assessed the visceral fat area (by MRI); total body fat; insulin sensitivity (with a glucose clamp technique); and plasma levels of PAI-1, insulin, and triglycerides in young (Ͻ37 years old), nonobese (body mass index Ͻ28 kg/m 2 ), healthy men (nϭ18) and women (nϭ15) before and after 12 months of cross-sex hormone administration. Men were treated with ethinyl estradiol 100 g/d plus cyproterone acetate 100 mg/d, and women were treated with testosterone esters 250 mg IM every 2 weeks. At baseline, only visceral fat area was significantly correlated with plasma PAI-1 levels in both men (rϭ0.57, Pϭ0.03) and women (rϭ0.59, Pϭ0.03). In multivariate linear regression analysis, this association was independent of total body fat, insulin sensitivity, and plasma levels of triglycerides and insulin. After 12 months of cross-sex hormone administration, the plasma PAI-1 levels were no longer correlated with visceral fat (which had increased).We conclude that in young, nonobese men and women, visceral fat area is an important determinant of plasma PAI-1 levels. After cross-sex hormone administration, this association was no longer demonstrable.

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Visceral Fat Accumulation Is an Important Determinant of PAI-1 Levels in Young, Nonobese Men and Women

Giltay

Elbers

Gooren

et al. 1998

ATVB

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“…1,2 Interestingly, some reports have underlined the independent association of body adiposity and plasma PAI-1 levels, mainly visceral fat, in mice 3,4 and in humans. [5][6][7][8][9] PAI-1 expression has been reported to be upregulated in adipose tissue from obese mice and humans concomitantly with increased plasma PAI-1 levels, 10 -12 and it has been proposed that the increase in adipose tissue PAI-1 observed in obesity could be the result of tumor necrosis factor-␣ disturbance, which specifically accompanies insulin resistance. 13 The precise origin of PAI-1 expression in adipose tissue is not definitively established, because PAI-1 synthesis has been attributed or not to adipocytes, depending on which model was used.…”

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“…Several studies have emphasized the relationship between visceral fat and plasma PAI-1. [5][6][7][8][9] In mice, Shimomura 4 described a strong PAI-1 expression in visceral fat. Using human adipose tissue explants maintained in culture or differentiating adipocytes, we and others have observed a higher PAI-1 secretion by the visceral fat.…”

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Stromal Cells Are the Main Plasminogen Activator Inhibitor-1-Producing Cells in Human Fat

Bastelica

Morange

Berthet

et al. 2002

ATVB

170

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Abstract-Elevated plasma plasminogen activator inhibitor (PAI)-1 observed during insulin resistance has been connected with an excessive PAI-1 adipose tissue secretion mainly by visceral fat. Our aim was to compare the localization of PAI-1 in human visceral and subcutaneous fats. PAI-1 secretion was also investigated in vitro during human adipocyte differentiation. PAI-1 antigen and mRNA were localized in the stromal area of the tissue and were also present in a few CD14-positive monocytes, in direct contact with adipocytes. In addition, in subcutaneous tissue, PAI-1 mRNA contents, determined by using real-time polymerase chain reaction, were higher in the stromal fraction than in the adipocyte fraction. PAI-1 mRNA-positive cells were 5-fold more frequent in the visceral area than in the subcutaneous stromal area (Pϭ0.004). Such a difference was also observed for PAI-1 mRNA content between both whole adipose tissues. In contrast to leptin, during adipocyte differentiation, PAI-1 secretion did not follow adipocyte maturation. In situ hybridization in culture did not reveal PAI-1 mRNA in lipid-filled cells. Our results demonstrate that PAI-1 production is mainly due to stromal cells, which were more numerous in the visceral than in the subcutaneous depot. These results could explain the strong relationship observed between circulating PAI-1 levels and the accumulation of visceral fat.

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Noninvasive Evaluation of Abdominal Fat and Liver Changes Following Progressive Weight Loss in Severely Obese Patients Treated with Laparoscopic Gastric Bypass

Genio

Genio²,

Sio³

et al. 2009

OBES SURG

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73. Liver steatosis and its relation to haemostatic factors in healthy males

Cited by 12 publications

References 0 publications

Visceral Fat Accumulation Is an Important Determinant of PAI-1 Levels in Young, Nonobese Men and Women

Visceral Fat Accumulation Is an Important Determinant of PAI-1 Levels in Young, Nonobese Men and Women

Stromal Cells Are the Main Plasminogen Activator Inhibitor-1-Producing Cells in Human Fat

Noninvasive Evaluation of Abdominal Fat and Liver Changes Following Progressive Weight Loss in Severely Obese Patients Treated with Laparoscopic Gastric Bypass

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