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PubMedDate not supplied

Modification of corporal weight, body fat distribution, blood lipids and glucose levels in oral contraceptive users.

The association between oral contraceptives and the modification of corporal weight and body fat distribution is controversial. The characteristics of the menstrual cycle, lipids and glucose levels were also analyzed. Thirty women who received ethinylestradiol 0.035 mg and norethindrone 0.400 mg for one year were studied. The following variables were analyzed every 3 months: weight, body mass index (BMI), hip perimeter, waist perimeter, waist-hip ratio (WHR), duration of menstrual cycle, quantity of uterine bleeding, as well as blood levels of cholesterol, triglycerides and glucose. Waist and hip perimeters increased during the third evaluation; as well as the BMI starting from the second evaluation. The triglycerides levels rose from the first evaluation. No modifications were found in the WHR, glucose and cholesterol levels and the duration of the menstrual cycle, but the quantity of uterine bleeding decreased from the third month. The oral contraceptive significantly increased BMI and triglycerides level, but no changes were detected in body fat distribution, cholesterol and glucose levels. Uterine bleeding decreased from the first evaluation.

Adipose Tissue↗
PubMed2003

Body fat distribution and cortisol metabolism in healthy men: enhanced 5beta-reductase and lower cortisol/cortisone metabolite ratios in men with fatty liver.

In Cushing's syndrome, cortisol causes fat accumulation in specific sites most likely to be associated with insulin resistance, notably in omental adipose and also perhaps in the liver. In idiopathic obesity, cortisol-metabolizing enzymes may play a key role in determining body fat distribution. Increased regeneration of cortisol from cortisone within adipose by 11beta-hydroxysteroid dehydrogenase (HSD) type 1 (11HSD1) has been proposed to cause visceral fat accumulation, whereas decreased hepatic 11HSD1 may protect the liver from glucocorticoid excess. Increased inactivation of cortisol by 5alpha- and 5beta-reductases in the liver may drive compensatory activation of the hypothalamic-pituitary-adrenal axis, hence increasing adrenal androgens and 'android' central obesity. This study aimed to examine relationships between these enzymes and detailed measurements of body fat distribution. Twenty-five healthy men (age, 22-57 yr; body mass index, 20.6-35.6 kg/m(2)) were recruited from occupational health services. Body composition was assessed by anthropometric measurements, bioimpedance, and cross-sectional abdominal magnetic resonance imaging scans. Liver fat content was assessed by magnetic resonance imaging spectroscopy. Insulin sensitivity was measured in a euglycemic hyperinsulinemic clamp. Cortisol metabolites were measured in a 24-h urine sample by gas chromatography-mass spectrometry. In vivo hepatic 11HSD1 activity was measured by generation of plasma cortisol after an oral dose of cortisone. In vitro 11HSD1 activity and mRNA were measured in 18 subjects who consented to provide abdominal sc adipose biopsies. Indices of obesity (body mass index, whole-body percentage fat, waist/hip ratio) were associated with higher urinary excretion of 5alpha- and 5beta-reduced cortisol metabolites (for percentage fat, P < 0.05 and P < 0.01, respectively) and increased adipose 11HSD1 activity (P < 0.05). Liver fat accumulation was associated with a selective increase in urinary excretion of 5beta-reduced cortisol and cortisone metabolites (P < 0.01) and a lower ratio of cortisol/cortisone metabolites in urine (P < 0.001) but no difference in in vivo cortisone-to-cortisol conversion or in vitro adipose 11HSD1. Higher excretion of 5beta-reduced cortisol metabolites was independently associated with insulin resistance and hypertriglyceridemia. Lower conversion of cortisone to cortisol was associated with lower fasting plasma cortisol (P < 0.01). However, visceral adipose fat mass was not associated with indices of cortisol metabolism; indeed, after adjusting for the effects of whole-body and liver fat, increased visceral fat was associated with lower cortisol metabolite excretion. We conclude that alterations in 11HSD1 and hepatic 5alpha-reductase activity are associated with generalized, rather than central, obesity in humans. Activation of 5beta-reductase in men with fat accumulation in the liver may confound the interpretation of cortisol metabolite excretion when liver fat content is unknown, and may contribute to altered bile acid and cholesterol metabolism in nonalcoholic steatohepatitis.

11-beta-Hydroxysteroid Dehydrogenase Type 1↗
PubMed1987

Body circumferences as alternatives to skinfold measurements of body fat distribution in Mexican-Americans.

The ratios of circumferences (waist/hip, waist/thigh) have been proposed in lieu of skinfold measurements for studies of obesity and body fat distribution. The purpose of this paper is to present our experience in measuring a series of body circumferences and skinfolds in an obese population, and seek the relationship between these two kinds of variables as indicators of fatness and body fat distribution using canonical correlation analysis. With this method, weighted vectors of circumferences on the one hand and skinfolds on the other, are formed in such a way that the correlation between the two sets of variables is maximized. The weights (regression coefficients) and their signs help us select the best combination of circumferences which describe a component of centralized obesity. Our experience showed that 21 percent of women would have been excluded from this multivariate analysis due to skinfolds what could not be measured (mainly due to poor fold definition). Few men were so excluded (6 per cent), and almost all circumferences could be measured in both sexes. A first canonical correlation was substantial (0.84 in women, 0.89 in men) and appeared to relate to level of fatness. A second canonical correlation was moderate (0.59 in women, 0.42 in men) and statistically significant (P less than 0.01) in both sexes. Only in women was it independent of age, but in both sexes it reflected differences in central and peripheral (especially lower limb) fat. The simple waist/thigh ratio correlated well with the second canonical variate (0.79 in women, 0.67 in men).(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue↗
PubMed1996

Body mass index and body fat distribution in newly-arrived Vietnamese refugees in Sydney, Australia.

Body mass index (BMI), body fat distribution and some behavioural variables were examined in an ethnic Vietnamese population newly arrived in Australia. The age range was 23 to 74 years for males (n = 246, mean = 38.8) and 24 to 66 for females (n = 165, mean = 36.4). Mean BMI was 20.62 +/- 2.65 (male) and 21.25 +/- 3.16 (female). Waist-to-hip ratio (WHR) was 0.844 (males) v 0.802 (females), p < 0.0001: waist was 73.7 cm (males) v 71.7 cm (females), (p = 0.007). Male smoking was 69%, female, 1%; the BMI of male non-smokers was higher than that of smokers 21.22 v 20.35 (p = 0.0017). Exercise patterns, diet or alcohol intake did not appear to affect BMI. The mean BMI of this refugee Vietnamese population is low by comparison with the Australian population. Vietnamese females although of lower mean BMI, have higher WHR than Australian females.

Adipose Tissue↗
PubMed1991

Effect of obesity and body fat distribution on sex hormones and insulin in men.

To investigate the relationship between body fat distribution, sex hormones, and hyperinsulinemia in male obesity, we examined 52 obese men (body mass index [BMI], 35.0 +/- 6.1, mean +/- SD) and 20 normal-weight controls. Their waist to hip circumference ratio (WHR), which was used as an index of fat distribution, was 0.985 +/- 0.052 and 0.913 +/- 0.061 (P less than .005), respectively. Compared with controls, obese men presented significantly lower levels of total (357 +/- 132 v 498 +/- 142 ng/dL; P less than .005) and free testosterone (14.2 +/- 2.9 v 17.1 +/- 2.6 pg/mL; P less than .05) and sex hormone-binding globulin (SHBG; 41.7 +/- 31.9 v 66.2 +/- 18.6 nmol/L; P less than .001) without any significant difference on the other sex steroid or on gonadotropin concentrations. Fasting and glucose-stimulated insulin and C-peptide levels were significantly higher in obese than in controls, and in obese with the WHR value greater than 0.97 (corresponding to the distribution median) than in those with WHR lower or equal to 0.97. BMI was negatively correlated with testosterone (P less than .005), free testosterone (P less than .01), and SHBG (P less than .001) and positively with fasting (P less than .001) and glucose-stimulated (P less than .005) C-peptide concentrations, whereas no relationship was found between these variables and WHR values. On the contrary, WHR was significantly correlated with fasting and post-glucose insulin levels (P less than .05), but not with those of sex steroids.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue↗
PubMed2005

Obesity, regional body fat distribution, and the metabolic syndrome in older men and women.

BACKGROUND: The metabolic syndrome is a disorder that includes dyslipidemia, insulin resistance, and hypertension and is associated with an increased risk of diabetes and cardiovascular disease. We determined whether patterns of regional fat deposition are associated with metabolic syndrome in older adults. METHODS: A cross-sectional study was performed that included a random, population-based, volunteer sample of Medicare-eligible adults within the general communities of Pittsburgh, Pa, and Memphis, Tenn. The subjects consisted of 3035 men and women aged 70 to 79 years, of whom 41.7% were black. Metabolic syndrome was defined by Adult Treatment Panel III criteria, including serum triglyceride level, high-density lipoprotein cholesterol level, glucose level, blood pressure, and waist circumference. Visceral, subcutaneous abdominal, intermuscular, and subcutaneous thigh adipose tissue was measured by computed tomography. RESULTS: Visceral adipose tissue was associated with the metabolic syndrome in men who were of normal weight (odds ratio, 95% confidence interval: 2.1, 1.6-2.9), overweight (1.8, 1.5-2.1), and obese (1.2, 1.0-1.5), and in women who were of normal weight (3.3, 2.4-4.6), overweight (2.4, 2.0-3.0), and obese (1.7, 1.4-2.1), adjusting for race. Subcutaneous abdominal adipose tissue was associated with the metabolic syndrome only in normal-weight men (1.3, 1.1-1.7). Intermuscular adipose tissue was associated with the metabolic syndrome in normal-weight (2.3, 1.6-3.5) and overweight (1.2, 1.1-1.4) men. In contrast, subcutaneous thigh adipose tissue was inversely associated with the metabolic syndrome in obese men (0.9, 0.8-1.0) and women (0.9, 0.9-1.0). CONCLUSION: In addition to general obesity, the distribution of body fat is independently associated with the metabolic syndrome in older men and women, particularly among those of normal body weight.

Adipose Tissue↗
PubMed1993

[Body fat distribution: independent factor affecting the blood lipid profile].

The association of life style factors with profiles of blood lipids is described in a cohort of 75 middle aged (41.2 +/- 7.8 years) physically inactive, nonsmoking employees. The importance of body fat distribution in relation to relative body weight and the lipid profiles was also studied. The strongest possible predictor for an atherogenic lipid fraction was the quotient of abdominal and hip circumferences indicating an abdominal fat accumulation. In the group with the lowest quotient (< 0.84) the triglyceride and cholesterol values were lower by 43% and 13% respectively than in that with the highest quotient (< 0.88). The body mass index (BMI) gave the best inverse correlation with HDL-c and Apo A-I: Men with a BMI < 23.7 kg/m2 had in the average a HDL-c concentration 0.2 mmol/l higher than slightly overweighted men (BMI > 25 kg/m2). Physical inactivity and a reduced physical endurance were both associated with significantly higher total cholesterol and Apo B values. In a multivariate analysis the quotient of abdominal and hip circumferences, physical activity and endurance together with adherence to recommended nutritional behaviour explained approximately one third of the variations in LDL and Apo-B concentrations. This study thus confirms in a cohort of non smoking middle aged employees the predictive character of unfavorable life style for an atherogenic lipid profile. The assessment of body fat distribution added further information on the lipid profile that could not be detected by body size and weight determination alone.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue↗
PubMed2003

Relationships of body fat distribution, insulin sensitivity and cardiovascular risk factors in lean, healthy non-diabetic Thai men and women.

In order to study the relationships of body fat distribution, insulin sensitivity and cardiovascular risk factors in lean, healthy non-diabetic Thai men and women, 32 healthy, non-diabetic subjects, 16 men and 16 women, with respective mean age 28.4+/-6.6 (S.D.) and 32.8+/-8.9 years, mean BMI 21.0+/-2.8 and 21.2+/-3.7 kg/m(2), were measured for total body fat and abdominal fat by dual energy X-ray absorptiometry (DEXA), anthropometry and insulin sensitivity by euglycemic hyperinsulinemic clamp. Cardiovascular risk factors included fasting and post-glucose challenge plasma glucose and insulin, blood pressure, lipid profile, fibrinogen and uric acid. For similar age and BMI, men had a lower amount and percent of total body fat, but had a higher proportion of abdominal/total body fat than women. In men, insulin sensitivity, as determined by glucose infusion rate during euglycemic hyperinsulinemic clamp, was inversely correlated with total body fat, abdominal fat, BMI and waist circumference, whereas only total body fat, but not abdominal fat, BW and hip circumference were inversely correlated with insulin sensitivity in women. No cardiovascular risk factors, except area under the curve (AUC), of plasma insulin in women correlated with insulin sensitivity when adjusted for total body fat. After age adjustment, total body fat was better correlated with fasting and AUC of plasma glucose and insulin in men and with systolic blood pressure as well as triglyceride levels in women. Only HDL-C in men was better correlated with abdominal fat. In conclusion, there were sex-differences in body fat distribution and its relationship with insulin sensitivity and cardiovascular risk factors in lean, healthy non-diabetic Thai subjects. Total body fat was a major determinant of insulin sensitivity in both men and women, abdominal fat may play a role in men only. Body fat, not insulin sensitivity, was associated with cardiovascular risk factors in these lean subjects.

Absorptiometry, Photon↗
PubMedDate not supplied

Body fat distribution and hyperinsulinemia as risk factors for diabetes and cardiovascular disease.

Differences in body fat distribution between diabetics and nondiabetics have been recognized for several decades; diabetics have a more centralized or upper body fat pattern than nondiabetics. Recently, attention has focused on fat patterning and also on hyperinsulinemia as possible risk factors for cardiovascular disease, as well. The case for insulin as a cardiovascular risk factor is bolstered by theoretical considerations related to its possibly atherogenic effects on serum and arterial wall lipids. Empirical evidence for fat patterning and hyperinsulinemia as cardiovascular risk factors rests on six prospective epidemiologic studies, three on fat patterning and three on insulin. Although provocative, none of these studies can be regarded as definitive. In none was a dose-response effect demonstrated, and there are various inconsistencies within and across the studies. Moreover, in none of the studies were hyperinsulinemia and fat patterning evaluated simultaneously. This is of particular importance in view of the well-documented interrelationships between these two variables. For example, insulin resistance and hyperinsulinemia have been found to be greater in women with upper body obesity compared to women with lower body obesity of equivalent degree. Considerable progress has been made recently in understanding the mechanisms of the differential metabolic effects of these two types of obesity. The extent to which fat patterning and hyperinsulinemia are genetic or acquired has received relatively little attention. Further research on this question is warranted since elucidation of any environmental influences on these variables might suggest new clinical and public health control measures.

Adipose Tissue↗
PubMed2003

[Influence of body fat distribution on the prevalence of arterial hypertension and other cardiovascular risk factors in obese patients].

INTRODUCTION: Obese people are at higher cardiovascular risk than people with normal body weight. The objective of this study was to establish the relationship between obesity, body fat distribution and cardiovascular risk factors. METHODS: Body mass index (BMI), waist-hip ratio (WHR) systolic (SBP) and diastolic blood pressure (DBP), plasma cholesterol, triglycerides and glucose levels were determined in a population of 499 overweight and obese patients (432F/67M; age 39 12.9y). RESULTS: High prevalence of abnormal glucose tolerance or diabetes (21.8%), hypercholesterolenemia (49.1%), hypertri glyceridemia (21.3%) and hypertension (43.8%) were found in this population. The prevalence of hypertension increased from 23% in patients with BMI 25-29.9 kg/m to 67.1% (p<0.05) in those with BMI > 40kg/m and also from 35.7% in patients with WHR between 0.73 and 0.88 to 66.6% in those with WHR >0.97 (p<0.05). In addition, a correlation was found between the waist circumference and SBP (r=0.35; p<0.0001). In the hypertensive group, but not in the normotensive, SBP increased with BMI, from 150 12 mmHg in the overweight group to 161 18mmHg in that with BMI > 40kg/m , (p<0.05). CONCLUSION: Our data reinforce the association between obesity and high cardiovascular risk. In addition, our findings suggested a role for body fat distribution in the development of hypertension in obese patients.

Adult↗
PubMed2000

Oestrogen and progestogen hormone replacement therapy for peri-menopausal and post-menopausal women: weight and body fat distribution.

BACKGROUND: Hormone replacement therapy (HRT) is commonly prescribed to treat menopausal symptoms and to prevent post-menopausal bone loss. However, many women are concerned about hormonal replacement therapy because they believe that such treatment will result in weight gain. The effect of HRT on weight and body fat distribution has not yet been examined in systematic reviews. It is an important topic since many women decline oestrogen therapy due to their concerns about resultant weight gain, and thus forego its potential therapeutic benefits. OBJECTIVES: To evaluate the effect of unopposed oestrogen or combined oestrogen and progestogen hormone replacement therapy (HRT) upon the weight and body fat distribution of perimenopausal and postmenopausal women. SEARCH STRATEGY: The search strategy of the Menstrual Disorders and Subfertility Group was used for the identification of randomised controlled trials (RCTs). Computerised searches of MEDLINE, EMBASE, Current Contents, Biological Abstracts and CINAHL were performed. Attempts were made to identify trials from citation lists of review articles and relevant papers already obtained. In most cases, first authors of each eligible trial were contacted for additional information. All those trials that had been located as at August 1998 were examined for eligibility. SELECTION CRITERIA: All randomised, placebo or no treatment controlled trials that detailed the effect of HRT on weight or body fat distribution, including studies where HRT was combined with other therapy such as diet, supplements or exercise. Studies were eligible for consideration even though the main focus of the trial may have been on another aspect of HRT. Previous HRT use should have ceased at least one month (in the case of patches, cream or gel) or three months (for oral preparations or subcutaneous pellets) before commencement of the study. DATA COLLECTION AND ANALYSIS: Twenty two RCTs were identified that fulfilled the inclusion criteria for this review. The results of one trial were not available in a form that allowed it to be included in the meta-analysis; however, it has been included in the text of the review for discussion. Twenty four RCTs are awaiting assessment pending additional information from first authors. Two reviewers extracted the data independently, and the weighted mean differences for continuous outcomes were estimated from the data. Results for unopposed oestrogen and combined oestrogen were analysed separately, and the effect of each treatment regimen on body weight, BMI, waist-hip ratio, fat mass and skinfold measurement was examined where available. The effect of differing dosage levels on these parameters was also examined. MAIN RESULTS: Outcomes were evaluated separately for unopposed oestrogen and oestrogen/progestogen regimens. Statistical analysis was performed using the weighted mean difference for continuous outcomes as recommended by the Cochrane Menstrual Disorders and Subfertility Group. No statistically significant difference was found in mean weight gain between those using unopposed oestrogen and non-HRT users (0.66 kg, 95% CI -0.62, 1.93). No significant difference was found in mean weight gain between those using oestrogen/progestogen therapy and non-HRT users (-0.47 kg, 95% CI -1.63, 0.69). Insufficient data exist to enable meta-analysis of the effect of unopposed oestrogen on BMI. The reviewers found no statistically significant difference in mean BMI increase between those using oestrogen/progestogen and non-HRT users (-0.50, 95% CI -1.06, 0.06). Insufficient data exist to enable meta-analysis of the effect of HRT on waist-hip ratio, fat mass or skinfold thickness. REVIEWER'S CONCLUSIONS: There is evidence of no effect of unopposed oestrogen or combined oestrogen on body weight, indicating that these regimens do not cause extra weight gain in addition to that normally gained at menopause. (ABSTRACT TRUNCATED)

Body Mass Index↗
PubMed1998

Are leptin levels dependent on body fat distribution in obese men and women?

Leptin levels are strongly related to total body fat. It is however not yet clear if leptin is also related to visceral fat accumulation or not. In this study, we investigated whether leptin is also associated with body fat distribution and if this association is different in men and women. Leptin was measured in 143 obese subjects (118 women and 25 men) with a body mass index (BMI) greater than 28. Also weight, skinfolds, waist-to-hip ratio (WHR), fat mass by bioimpedance analysis (BIA) were measured, and abdominal visceral and subcutaneous fat were determined by CT scan. Leptin levels were significantly related with BMI, with fat mass (in kg and percentage body fat) as measured by BIA and skinfolds, and with total abdominal fat mass and subcutaneous fat measured by CT scan. No association was found with visceral fat, waist circumference or WHR. In men and women separately, however, a correlation with visceral fat existed. After correction for total body fat, the correlation remained significant only with subcutaneous fat in women. Multiple regression analyses pointed out that percentage body fat was the most important determinant of leptin for all subjects, while for women subcutaneous fat was the most important parameter, and for men alone total abdominal fat. These results suggest that subcutaneous fat seems to be an important factor related to leptin levels.

Adipose Tissue↗
PubMed1999

Effect of troglitazone on body fat distribution in type 2 diabetic patients.

OBJECTIVE: Troglitazone was recently reported to specifically promote the differentiation of pre-adipocytes into adipocytes in vitro in subcutaneous fat only, indicating a relation to insulin-resistance-improving action of troglitazone. To expand on this finding, we investigated at the clinical level how long-term administration of troglitazone influences the body fat distribution in type 2 diabetic patients. RESEARCH DESIGN AND METHODS: Troglitazone (400 mg/day) was administered for 6 months to 30 type 2 diabetic patients whose glycemic control was poor. A total of 18 patients received diet therapy alone (in the single-treatment group, BMI 26.0 +/- 4.6, HbA1c 8.2 +/- 1.7%), and 12 patients concomitantly received glibenclamide (1.25-7.5 mg/day) (in the concomitant sulfonylurea group, BMI 25.4 +/- 4.7, HbA1c 9.2 +/- 1.2%). BMI, HbA1c, serum lipid level, and body fat distribution, which were determined by computed tomography (CT) scan at the umbilical level, were measured and compared before and after troglitazone treatment. RESULTS: During the 6-month troglitazone treatment, HbA1c levels decreased and BMI increased in both groups. As for body fat distribution in the single-treatment group, visceral fat area (VFA) decreased (from 118.3 +/- 54.3 to 101.1 +/- 50.8 cm2; P < 0.001), and subcutaneous fat area (SFA) increased (from 189.7 +/- 93.3 to 221.6 +/- 101.6 cm2; P < 0.001), resulting in a decrease in visceral/subcutaneous (V/S) ratio (from 0.74 +/- 0.48 to 0.50 +/- 0.32; P < 0.001). In the concomitant sulfonylurea group, VFA was unchanged (from 108.1 +/- 53.5 to 112.5 +/- 59.9 cm2), while SFA increased (from 144.6 +/- 122.0 to 180.5 +/- 143.5 cm2; P < 0.01), thereby decreasing the V/S ratio (from 0.91 +/- 0.46 to 0.77 +/- 0.44; P < 0.01). The serum triglyceride level and the area under glucose curve during the 75-g oral glucose tolerance test decreased significantly in the single-treatment group. CONCLUSIONS: According to our data, troglitazone appears to promote fat accumulation in the subcutaneous adipose tissue rather than in the visceral adipose tissue in mildly obese Japanese people with type 2 diabetes. This shift of energy accumulation from the visceral to subcutaneous adipose tissue may greatly contribute to the troglitazone-mediated amelioration of insulin resistance.

Abdomen↗
PubMed2000

Android obesity at diagnosis and breast carcinoma survival: Evaluation of the effects of anthropometric variables at diagnosis, including body composition and body fat distribution and weight gain during life span,and survival from breast carcinoma.

BACKGROUND: Although a large body of research exists concerning pathologic prognostic indicators of the rate of incidence and survival from breast carcinoma, to the authors' knowledge very few studies have examined the effects of anthropometric variables such as height, obesity, weight gain in adulthood, timing of weight gain, and body composition to survival, although these variables are related to the incidence rate. METHODS: The survival status of 166 patients diagnosed with primary breast carcinoma and followed for at least 10 years was obtained from the Cancer Center's registry, and significant anthropometric and other known prognostic indicators regarding survival after diagnosis were determined by Cox proportional hazards analysis. RESULTS: Eighty-three of 166 breast carcinoma patients (50%) with up to 10 years of follow-up died of disease. Android body fat distribution, as indicated by a higher suprailiac:thigh ratio, was a statistically significant (P < 0.0001) prognostic indicator for survival after controlling for stage of disease, with a hazards ratio of 2.6 (95% confidence interval [95% CI], 1.63-4.17). Adult weight gain, as indicated specifically by weight at age 30 years, was a statistically significant (P < 0.05) prognostic indicator for survival with a hazards ratio of 1.15 (95% CI, 1.0-1.28). In addition, the authors observed the Quatelet Index, a negatively significant (P < 0.01) prognostic indicator for survival with a hazards ratio of 0.92 (95% CI, 0.87-0.98). Other markers of general obesity such as weight at diagnosis, percent body fat, and body surface area were not significant markers influencing survival. Similarly, height; triceps, biceps; subscapular, suprailiac, abdominal, and thigh skinfolds; waist and hip circumferences; family history; and reproductive and hormonal variables at the time of diagnosis showed no apparent significant relation to survival. CONCLUSIONS: The results of the current study provide some evidence that android body fat distribution at diagnosis and increased weight at age 30 years increases a woman's risk of dying of breast carcinoma.

Adult↗
PubMed1997

Birth weight and body fat distribution in adolescent girls.

OBJECTIVE: To examine the association between birth weight and body fat distribution in a group of adolescent girls. DESIGN: A total of 216 white girls who were born in Southampton had their heights, weights, waist and hip circumferences, and skinfold thicknesses measured when they were aged between 14 and 16 years. RESULTS: The girls who were smallest at birth, but who were fattest at time of measurement were the most centrally obese. In girls whose body mass index was above the median (21 kg/m2), the subscapular to triceps skinfold ratio rose by 9% for every kilogram decrease in birth weight. Among overweight girls, with a body mass index over 25, the ratio rose by 27% for every kilogram decrease in birth weight. CONCLUSION: In adolescent girls, the tendency to store fat on the trunk rather than the limbs, seems to be programmed by growth in fetal life, and is most evident in those who are overweight.

Adipose Tissue↗
PubMed2004

Body fat distribution, relative weight, and liver enzyme levels: a population-based study.

Regional body fat distribution may represent an independent risk factor for several conditions, especially metabolic and cardiovascular diseases; recent findings have shown that abdominal fat accumulation can be an independent predictor of hepatic steatosis. Very few studies, mostly using selected clinical samples, have focused on the relationship between indices of abdominal visceral fat accumulation and the most commonly used biochemical liver tests, such as alanine aminotransferase (ALT), aspartate aminotransferase (AST), and gamma-glutamyltransferase (GGT). The aim of the present study was to evaluate the relation between central fat accumulation, as assessed by abdominal height, relative weight, as determined by body mass index (BMI), and liver function tests (ALT, AST, and GGT) in a random sample of 2,704 residents of Erie and Niagara Counties in New York State, 35-80 years of age and free from known hepatic disease. Multiple linear regression models were used, with liver enzymes as dependent variables with abdominal height and BMI as independent variables, and the inclusion of several covariates (age, race, education, smoking status, pack-years of smoking, drinking status, and total ounces of ethanol in the past 30 days). Abdominal height was consistently a better correlate of ALT and GGT levels than BMI in both sexes. In addition, abdominal height was the most powerful independent predictor of ALT in both sexes as well as of GGT among women. In conclusion, these findings support a role for central adiposity independent from BMI in predicting increased levels of hepatic enzymes, likely as a result of unrecognized fatty liver.

Abdomen↗
PubMed1991

Relationship of absence or presence of a family history of diabetes to body weight and body fat distribution in type 2 diabetes.

In a study sample of second generation Japanese American men (age range 45-74 years), family history of diabetes in a sibling or parent was present in 69 men (24 of 79 normal men and 45 of 78 type 2 diabetic men, P less than 0.001). Both general adiposity and body fat distribution have been associated with type 2 diabetes. Our hypothesis was that the association of both overall adiposity and of larger specific regional fat deposits with type 2 diabetes would differ depending upon family history. The relationships between diabetes and differences in general adiposity (whether current or maximum lifetime body mass index or BMI, sum of skinfolds, or sum of computed tomography or CT fat areas) and between diabetes and body fat distribution (measured as abdominal and thigh circumferences, cross-sectional body fat areas by CT of thorax, abdomen, and thigh, and skinfold thicknesses of triceps, biceps, forearm, chest, subscapula, abdomen, and thigh) were more apparent in those men without a family history of diabetes than in those with a family history. In men without a family history, diabetic men had significantly higher values for several variables which assessed overall adiposity: current BMI (P less than 0.001), maximum lifetime BMI (P less than 0.001), sum of skinfolds (P less than 0.006), and sum of CT fat areas (P less than 0.015). In addition several measurements of upper truncal adiposity were significantly increased in diabetic men: abdominal circumference (P less than 0.004), thoracic (P less than 0.015) and abdominal (P less than 0.03) subcutaneous CT fat areas, intra-abdominal CT fat areas (P less than 0.001), and chest (P less than 0.03) and subscapular (P less than 0.0002) skinfold thicknesses. The results pertaining to those without a family history appear to be due to increased adiposity and associated larger specific regional fat depots leading to diabetes and lesser adiposity and smaller amounts of fat in the same regional depots protecting against diabetes.

Adipose Tissue↗
PubMed1987

Relation of body fat distribution to hyperinsulinemia in children and adolescents: the Bogalusa Heart Study.

The relation of body fat distribution to plasma levels of glucose and insulin during an oral glucose tolerance test was examined in 355 Black and White school-age children. Both central and peripheral fat were similarly related to fasting, 30-min, and 1-h glucose. Unlike peripheral fat, central body fat was more strongly related to the 1-h insulin response (r = 0.35 vs 0.26); this association remained significant for central fat independent of peripheral fat (r = 0.18). The strong relation of central fat to insulin response was noted in both races and sexes but not in either sexually immature or relatively thin children. These findings indicate that, even in early life, a central body fat pattern relates positively to insulin response to glucose load. Thus, knowledge of body fat localization may help identify persons most susceptible to hyperinsulinemia in early life.

Adipose Tissue↗