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April 2000, Volume 24, Number 4, Pages 502-507
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Preperitoneal fat thickness determined by ultrasonography is correlated with coronary stenosis and lipid disorders in non-obese male subjects
N Tadokoro1, S Murano1, T Nishide2, R Suzuki2, S Watanabe2, H Murayama2, N Morisaki1 and Y Saito1

1Second Department of Internal Medicine, School of Medicine, Chiba University, Chiba City, Japan

2Department of Internal Medicine, Matsudo Municipal Hospital, Chiba, Japan

Correspondence to: N Tadokoro, 2-1-16 Miyamoto, Funabashi City, Chiba, 273-0003, Japan.


OBJECTIVE: To investigate the relationship between preperitoneal fat thickness (PFT) determined by ultrasonography and the risk of coronary arterial disease, 130 non-obese patients with ischemic heart disease (77 men and 53 women) were examined.

RESULTS: There was a positive correlation between PFT and coronary artery stenosis score (r=0.212, P<0.05). After dividing the patients by gender, the correlation was recognized only in men (r=0.246, P<0.05). Also, PFT was positively correlated to serum total cholesterol (r=0.259, P<0.01), triglyceride (r=0.205, P<0.05) and low density lipoprotein (LDL)-cholesterol (r=0.205, P <0.05), and negatively correlated to serum high density lipoprotein (HDL)-cholesterol (r=-0.261, P<0.01). Again, these correlations were found only in men, not in women.

CONCLUSION: PFT shows good correlations with coronary artery stenosis score and dislipidemia, and may lead to the development of coronary artery disease in non-obese male subjects.

International Journal of Obesity (2000)24, 502-507


ultrasonography; preperitoneal fat thickness; visceral fat accumulation; lipid metabolism; ischemic heart disease


Recently, there has been a growing interest in regional body fat distribution rather than total body fat amount as a risk factor for metabolic disorders and cardiovascular disease. Recent observations strongly suggest that a metabolic abnormality in obesity is linked to intra-abdominal fat accumulation.1,2,3,4,5 Tokunaga et al classified obesity into two types, a visceral type and a subcutaneous type, using computed tomography (CT).6 They measured areas of visceral fat tissue and subcutaneous fat tissue on an axial CT section at the level of the umbilicus and calculated the ratio of visceral fat area to subcutaneous fat area (V/S ratio). Visceral type obesity has a higher incidence of complications, such as hyperlipidemia, abnormal glucose tolerance and hypertension, than subcutaneous type obesity.7 However, we still do not know in what manner and to what extent individual fat tissue contributes to abnormal metabolism and the resultant cardiovascular disease. Even though the V/S ratio has been shown to be an appropriate indicator of visceral adiposity for obese subjects, this does not seem to hold true in the case of non-obese subjects who have less fat tissue. According to a recently proposed hypothesis, visceral fat tissue causes alterations in metabolism through the hypersecretion of free fatty acids into the portal vein.8 Therefore, we suspect that, rather than the V/S ratio, the absolute intra-abdominal fat volume might be a more reliable indicator of metabolic and cardiovascular risks.

Previously, we developed a method to estimate the amount of visceral and subcutaneous fat tissues of obese subjects using ultrasonography.9 This method measures the thickness of fat tissue on the upper median abdomen by a linear-array probe. The thickness of fat tissue between the linea alba and visceral peritoneum is called preperitoneal fat thickness (PFT). PFT was correlated significantly with visceral fat area but not with the subcutaneous fat area, both of which were determined by CT scan. In this study, we utilized PFT as an indicator of visceral fat accumulation and observed the relationship between PFT and coronary artery stenosis and coronary risk factors such as plasma glucose, insulin and serum lipids.

Subjects and methods


One-hundred and thirty non-obese patients (77 men and 53 women) diagnosed with ischemic heart disease from a health checkup were the subject of this study. They had all been examined by coronary angiography. Their mean age and body mass index (BMI) were 56.7 y and 23.2 kg/m2, respectively (Table 1). The definition of 'non-obese' was based on that of the WHO, <30.0 kg/m2. The maximum BMI among the subjects was 26.1.9 Sixty percent of the patients were smokers and 45% of them were hypertensives under medical control.


Ultrasonography. Fat thickness was measured with Toshiba Sonolayer SSA-250 A or 270A ultrasonography equipment (Tokyo, Japan) by the method of Suzuki et al.10 In brief, the linear-array probe was kept perpendicular to the skin on the upper median abdomen in the supine position, and a longitudinal scan was done from the xiphoid process to the umbilicus. Scanning was performed while keeping the surface of the liver parallel to the skin as perfectly as possible by breath-holding. If the thickness was not even, we used the maximum thickness of preperitoneal fat as PFT, and the minimum thickness of abdominal wall subcutaneous fat as subcutaneous fat thickness (SFT) according to Suzuki et al.10 In the previous paper, PFT showed a positive correlation with visceral fat area obtained by CT scan (r=0.70, P<0.001).10

Coronary artery stenosis score. The severity of coronary artery stenosis was graded according to Gensini's scoring method; the roentgenographic appearance of the concentric lesions and eccentric plaques was judged as showing 25, 50, 75, 90, 99 or 100% obstruction of the lumen diameter. The relative severity of these lesions is shown using a score of 1 for the 25% obstruction, and doubling the score number with increasing severity of these obstructions in accordance with the reduction of the lumen diameter; this means that each step as indicated by the score is twice as large as the previous one. After the scores for each segment of the arteries were calculated, they were added together to produce a total severity score per artery; these scores were then summed up to obtain a total score for the entire coronary system.11

Glucose metabolism. Plasma glucose and insulin were assayed by glucose oxidase method12 and double-antibody radioimmunoassay,13 respectively.

Lipid metabolism. Serum total cholesterol and triglyceride concentrations were measured by enzyme assays14,15 after overnight fasting. Serum high-density lipoprotein (HDL)-cholesterol was determined by the precipitation method,16 and low-density lipoprotein (LDL)-cholesterol was calculated by the Friedewald formula.17

Statistics. Data analyses were conducted with Statview 4.5 programs. Data are given as mean±s.d. Statistically significant differences between groups were analyzed by applying the two-sample t-test; all tests were two-sided or non-parametric.


Physical and metabolic characteristics of the subjects are listed in Table 1. In both sexes, the mean values of BMI, fasting plasma glucose, serum total cholesterol, triglyceride and HDL-cholesterol were within normal limits. There was no statistical difference in any parameter between men and women, except in SFT. In the total patients, PFT showed a positive correlation with the coronary artery stenosis score, but SFT did not (Table 2). We also observed the relationships between PFT or SFT and coronary artery stenosis score by non-parametric Spearman's rank test. PFT showed a higher correlation with the coronary artery stenosis score than SFT (Table 3). When dividing the subjects according to gender, a significant positive correlation was apparent between PFT and coronary artery stenosis score in men, but not in women (Figure 1 and Table 2). However, even when we separated premenopausal from postmenopausal women, no correlation was found between PFT and coronary artery stenosis score in the two groups (premenopausal: r=0.246, P=0.426; postmenopausal: r=0.224, P=0.165). The correlation between SFT and coronary artery stenosis score was also recognized only in men. In these patients, there was a statistically positive correlation between PFT and SFT, and even after dividing the group into men and women, there was still a positive correlation between PFT and SFT, both in men and women (data not shown).

To assess the possible reasons why fat accumulation is related to coronary artery disease, we observed the relationships between PFT and plasma glucose, insulin and serum lipids. In these patients, PFT had positive correlations with serum total cholesterol, triglyceride and LDL-cholesterol, and a negative correlation with serum HDL-cholesterol (Table 4). SFT also had positive correlations with serum total cholesterol, and LDL-cholesterol, and a negative correlation with serum HDL-cholesterol, but there was no correlation with serum triglyceride.

Separating men and women, PFT showed positive correlations with serum total cholesterol, triglyceride, LDL-cholesterol, and a negative correlation with serum HDL-cholesterol in men, but not in women (Table 5). SFT also showed positive correlations with serum total cholesterol, LDL-cholesterol, and a negative correlation with serum HDL-cholesterol in men, but there was no correlation with serum triglyceride. We could not find a significant correlation between SFT and any serum lipids in women.

Concerning risk factors for atherosclerosis, 60% of the patients were smokers and 45% were hypertensives in this study. However, neither PFT nor SFT showed any significant differences between smokers and non-smokers and between hypertensives and normotensives.


Obesity and its complications are major classical risk factors for atherosclerosis. Reaven termed a combination of dyslipidemia, hypertension and impairment of glucose metabolism with hyperinsulinism on the basis of insulin resistance as 'Syndrome X'.3 Almost the same concept was advocated by Kaplan as 'Deadly Quartet', which was a combination of glucose intolerance, hypertriglyceridemia, hypertension and obesity.4 In further studies, visceral adiposity or intra-abdominal fat accumulation was shown to be much more related to a group of atherogenic disorders, hyperinsulinemia,18,19 hypertension,20 hyperlipidemia,21 and cardiovascular disease itself,22,23 rather than obesity per se. On the basis of these data, Matsuzawa et al proposed that a common pathology of the clustering of those risk factors for atherosclerosis might be intra-abdominal fat deposition.24

Many investigators have reported the relationship between intra-abdominal fat accumulation and the occurrence of cardiovascular disease,2,25,26,27,28 but most of the results were obtained from studies in obese subjects, and thus it is still unclear whether intra-abdominal fat accumulation has a relationship with cardiovascular disease in non-obese subjects. In a few studies, using groups consisting of mixtures of obese and non-obese men, a close relationship between the visceral fat area or V/S ratio and coronary risk factors was reported.29,30 In our study, we measured PFT as an index of visceral fat accumulation, and this parameter showed statistically significant correlations with the coronary artery stenosis score and serum lipids in non-obese patients. However, not only PFT, but also SFT showed positive correlations with serum total cholesterol and LDL-cholesterol and a negative correlation with HDL-cholesterol. We speculated that SFT showed these correlations with serum lipids because of its positive correlation with PFT in this study. Ideally, the significance of PFT should be proven by studies of subjects showing no correlation between PFT and SFT. The fact that PFT had a higher relevance to the coronary artery stenosis score than SFT suggested that visceral fat accumulation might play a more important role than SFT in the occurrence of ischemic heart disease. In this study, PFT but not SFT had a statistically significant correlation with serum triglyceride. Many studies have shown a univariate association between elevated plasma triglyceride concentration and subsequent coronary heart disease, particularly in subjects with normal or low serum total cholesterol levels.31 In one report, a high triglyceride level, increased plasma insulin concentration and low plasma HDL-cholesterol level were shown to increase the risk of coronary heart disease, and these characteristics were shown to cluster even in healthy individuals.32 Our results that PFT had positive correlations with serum total cholesterol and serum triglyceride and a negative correlation with serum HDL-cholesterol in patients with ischemic heart disease support our hypothesis that PFT could predict the risk for coronary heart disease in non-obese subjects.

The current working hypothesis receiving considerable attention proposes the mechanism that visceral adiposity induces insulin resistance, successive hyperinsulinemia, hyperlipidemia and hypertension by its resultant massive supply of free fatty acids to the liver and other organs via the portal vein.33 In addition, some substances secreted from the visceral adipose tissue, for example, plasminogen activator inhibitor-1, could be a cause of the atherogenicity.34,35 At present, although we do not know how regional body fat distribution is controlled, various types of growth factors and hormones have been shown to modulate the expression of genes involved in the proliferation and differentiation of pre-adipocytes in animals and humans.36,37,38 Such interactions within adipose tissue itself and the modulation by systemic hormones, cytokines and dietary and genetic factors should lead to studies in the near future that will reveal the reason why visceral fat tissue, but not subcutaneous fat tissue, is linked to this pathological condition.

Then, the question arises as to why PFT can in fact be a good indicator of visceral fat mass. Even though we did not have enough evidence, we suspected that PFT was positively correlated with the visceral fat area because preperitoneal fat tissue and mesenteric fat tissue had a close embryologic origin as fat tissue on the peritoneum, so that they responded similarly under the same metabolic circumstances.

Another interesting observation in our study was that PFT showed positive correlation with the coronary artery stenosis score and serum lipids only in men, and it remains unclear why this parameter showed no correlation with the coronary artery stenosis score in women. The smaller sample size of the female group may conceal correlations reported from the male group.

The distribution of fat is apparently different in men and women, and the morbidity of atherogenic diseases is higher in men than in women even after correcting the other risk factors of atherosclerosis. The essential differences between men and women are mainly derived from sex steroids, estrogen and testosterone. Estrogen is known to play a role in the delayed expression of coronary heart disease in women, and its supplement to postmenopausal women was reported to reduce the incidence of coronary heart disease.39,40 The precise mechanism(s) by which estrogen produces this benefit is unknown, although its effects on blood pressure, carbohydrate, lipid metabolism,41 and endothelial cell functions have been suggested.42 On the other hand, a hyperandrogenic state reflected by high testosterone, high free testosterone and low sex hormone-binding globulin levels was reported to be associated with abdominal obesity in women.43,44 However, men with excessive abdominal fat often have relatively low serum testosterone concentrations, despite a reduced level of sex hormone-binding globulin.45 Further, oral testosterone supplements were reported to decrease visceral fat mass in middle-aged abdominally obese men.46 It appears that the role of testosterone in abdominal fat accumulation might change in connection with other hormonal factors.

The plasma estrogen concentration changes drastically after menopause. First, we were afraid that the correlation between PFT and coronary artery stenosis score might have been obscured because of the menopausal heterogeneity of the women's group. However, even when we separated premenopausal women from postmenopausal ones, no correlation was found between PFT and coronary artery stenosis score in the two groups. Another explanation may be found in the relatively abundant subcutaneous fat in women compared to men. Larsson et al observed that subcutaneous fat mass in lower extremities was negatively correlated to coronary risk.47 The relatively dominant subcutaneous fat mass in women might keep the risk of visceral fat below the threshold level of atherogenesis.

Finally, we found that PFT was positively correlated with the coronary artery stenosis score in non-obese male subjects. This means that measurement of PFT could provide a simple and useful index of coronary risk for non-obese men. Even though it would be of little use for women, it is still clinically valuable because men are the dominantly vulnerable gender in coronary arterial disease.


We wish to thank Drs. Yasuo Hirai, Kazuhide Akiyama, Yasuhisa Matsushima, Hitoshi Ohshima and Yoichi Kuwabara for their valuable comments.


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Figure 1 Relationship between preperitoneal fat thickness and coronary artery stenosis score in patients with ischemic heart disease. (A) Men and women; (B) men; (C) women.


Table 1 Clinical characteristics

Table 2 Correlations between PFT and SFT and coronary artery stenosis score of men and women

Table 3 Spearman's correlation coefficients between PFT and SFT and coronary artery stenosis score

Table 4 Correlations between PFT and SFT, and plasma glucose, insulin and serum lipids

Table 5 Correlations between PFT and SFT, and plasma glucose, insulin and serum lipids of men and women

Received 27 April 1999; revised 27 September 1999; accepted 25 November 1999
April 2000, Volume 24, Number 4, Pages 502-507
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