Insulin misuse by women with type 1 diabetes mellitus complicated by eating disorders does not favorably change body weight, body composition, or body fat distribution.
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The aim of this work was to evaluate the prevalence of microalbuminuria in an obese population and to study the relation between albumin excretion rate (AER), various clinical (body mass index, adipose tissue distribution) nutritional (macronutrient intake) and metabolic parameters. A cross-sectional study was carried out, and AER was evaluated in 182 obese subjects (BMI > 27) with no medication, no intercurrent disease, no cardiac, pulmonary or endocrinological disorders (including diabetes and hypertension) and also in 31 control subjects at the outpatient clinic of the department of Nutrition, Hôtel Dieu, Paris, France. The following were measured: BMI, waist/hip ratio (WHR), urinary AER, blood glucose, insulin and C peptide levels, cholesterol (CT), triglycerides, HDL cholesterol (HDL-CT), apoprotein A1 and B. In the obese population, 18 subjects (9.9%) were found to have an increased AER: 13 subjects (7.1%) with microalbuminuria (AER between 30 to 300 mg/24 h) and five with AER over 300 mg/24 h. AER was normal in all control subjects but one, who was found to have microalbuminuria. Log AER was positively correlated to WHR (P < 0.001), blood pressure (P < 0.05), cholesterol (P < 0.05), Apo B levels (P < 0.01) and with fasting Insulin levels and protein intake (P < 0.001). Positive association between log AER and protein intake, insulin levels, Apo B and blood pressure were found independently of BMI and WHR. It is suggested that abdominal obesity may be associated with incipient nephropathy in some obese subjects without diabetes and hypertension. Microalbuminuria may be included among metabolic abnormalities connected with abdominal-type excess weight distribution.(ABSTRACT TRUNCATED AT 250 WORDS)
OBJECTIVE: To examine and compare in vitro basal and insulin-stimulated glucose uptake in human omental and subcutaneous adipose tissue derived from lean, overweight or obese individuals, and in those with central or peripheral obesity. DESIGN: In vitro study of basal and insulin-stimulated 2-deoxyglucose uptake in human omental and subcutaneous adipose tissue explants derived from patients undergoing elective abdominal surgery. SUBJECTS: Fourteen lean (average age 47 y, average body mass index (BMI) 22 kg/m(2)), 12 overweight (average age 51 y, average BMI 27 kg/m(2)), and 15 obese subjects (average age 45 y, average BMI 39 kg/m(2)). Ten peripherally obese (average age 43 y, average WHR 0.76) and 17 centrally obese (average age 50 y, average waist-to-hip ratio (WHR) 0.92). MEASUREMENTS: Fatness and fat distribution parameters (by anthropometry), basal and insulin stimulated [(3)H]-2-deoxyglucose uptake in omental and subcutaneous adipose tissue explants. RESULTS: In adipose tissue from lean subjects transport of 2-deoxyglucose over basal was stimulated approximately two-fold by insulin. In contrast, 2-deoxyglucose transport in adipose tissue of obese or overweight subjects was not responsive to insulin. Following incubation with 100-nM insulin for 35 min, insulin-stimulated 2-deoxyglucose transport was significantly lower in both omental and subcutaneous adipose tissue of obese and overweight compared to lean subjects. Basal 2-deoxyglucose uptake was also significantly reduced in omental and subcutaneous tissue in obese compared to lean subjects. Depot-specific differences in 2-deoxyglucose uptake were also seen. Overall 2-deoxyglucose uptake was greater in omental than subcutaneous adipose tissue but this was due to increased basal levels rather than increased insulin action. The reduction in insulin-stimulated 2-deoxyglucose uptake seen in overweight and obese subjects was relatively similar in both depots. However, insulin responsive 2-deoxyglucose transport was significantly lower in the omental adipose tissue of subjects with central obesity, as compared to that of subjects with peripheral obesity. No difference in insulin induced 2-deoxyglucose transport was observed in the subcutaneous adipose tissue explants of subjects with either central or peripheral obesity. CONCLUSION: In lean individuals insulin responsiveness of omental and subcutaneous adipose tissue was similar, but basal glucose uptake was significantly higher in omental adipose tissue. Adipose tissue obtained from overweight as well as obese individuals is insulin resistant. This insulin resistance occurs at a lower BMI than previously expected and is not adipose-depot specific. However, in obese subjects with a central distribution of adiposity insulin resistance occurs at the site of omental adipose tissue, in contrast to those with peripheral obesity.
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When bone mineral content (BMC) is measured by dual X-ray absorptiometry (DXA), the X-ray beam is attenuated by bone and soft tissue. Since the component of the attenuation caused by the soft tissue overlying bone cannot be measured, the attenuation caused by soft tissue adjacent to bone is measured and is used in the calculation of BMC. the assumption underlying this approach is that the amount and composition of this adjacent soft tissue is the same as overlying bone. The aim of this study was to examine the validity of this assumption by determining whether fat distribution over and adjacent to bone differ and whether this introduces accuracy errors in the measurement of BMC by postero-anterior (PA) and lateral scanning. BMC (posterior processes plus vertebral body, g) of the third lumbar vertebra was 17.3 +/- 0.7 by PA and 17. +/- 0.7 by lateral scanning in 27 premenopausal women (p = NS), but 2.7 g or 20% higher by PA than scanning in 27 postmenopausal women (14.4 +/- 0.7, 11.7 +/- 0.5, p<0.01). Thus, the respective diminutions across age by PA scanning was about half that by lateral scanning (16.8 +/- 3.9%, 31.2 +/- 3.0%, p<0.01). Percent fat in the soft tissue baseline (anterior to bone, ST-ant) used to derive BMC by lateral scanning by 2.6 +/- 0.7% in premenopausal women and 7.5 +/- 1.0% in postmenopausal women (both p<0.01). After adjusting for these differences in percent fat, BMC by PA and lateral scanning no longer differed.
BACKGROUND: Uterine leiomyomata are a major source of morbidity in black women. We prospectively investigated the risk of self-reported uterine leiomyomata in relation to body mass index (BMI), weight change, height, waist and hip circumferences, and waist-to-hip ratio in a large cohort of U.S black women. METHODS: Data were derived from the Black Women's Health Study, a U.S. prospective cohort study of black women who complete biannual mailed health questionnaires. From 1997 through 2001, we followed 21,506 premenopausal women with intact uteri and no prior diagnosis of uterine leiomyomata. Cox regression models were used to estimate incidence rate ratios (IRRs) and 95% confidence intervals (CIs). RESULTS: After 70,345 person-years of follow up, 2146 new cases of uterine leiomyomata confirmed by ultrasound (n = 1885) or hysterectomy (n = 261) were self-reported. Compared with the thinnest women (BMI <20.0 kg/m), the multivariate IRRs for women with BMIs of 20.0-22.4, 22.5-24.9, 25.0-27.4, 27.5-29.9, 30.0-32.4, and 32.5+ kg/m were 1.34 (95% CI = 1.02-1.75), 1.39 (1.07-1.81), 1.45 (1.12-1.89), 1.47 (1.11-1.93), 1.36 (1.02-1.80), and 1.21 (0.93-1.58), respectively. IRRs were larger among parous women. Weight gain since age 18 was positively associated with risk, but only among parous women. No other anthropometric measures were associated with risk. CONCLUSIONS: BMI and weight gain exhibited a complex relation with risk of uterine leiomyomata in the Black Women's Health Study. The BMI association was inverse J-shaped and findings were stronger in parous women. Weight gain was positively associated with risk among parous women only.
The interaction between environmental and genetic factors in the alterations of glucose-insulin homeostasis was studied in 104 non-diabetic men. Family history of diabetes mellitus was used as an index of genetic predisposition to diabetes. Body composition was measured by underwater weighing whereas subcutaneous and visceral adipose tissue areas were measured at the abdominal and femoral levels by computed tomography. The sample was first divided into two groups. The first group included subjects with "normal" glycaemic and insulinaemic responses during a 75 g oral glucose tolerance test. The second group was composed of subjects either with a high glucose response or high insulin response or both. Men included in the second group were different from the "normal" subjects for almost all body fatness variables. They also presented a prevalence of a positive family history of diabetes which was significantly higher than "normal" subjects. The second group was then divided into three distinct subgroups based on insulin and glucose responses of the subjects during the oral glucose tolerance test. Subjects with high insulin but "normal" glucose responses were characterized by significantly higher levels of total body fat and deep abdominal adipose tissue when compared to the "normal" group (p less than 0.05). Men with both high insulinaemic and glycaemic responses displayed higher body fatness values and higher deep and subcutaneous abdominal adipose tissue areas (p less than 0.05) in comparison with "normal" subjects. They also had a higher body mass index at age 20 years than control subjects and subjects with high insulin but "normal" glucose responses.(ABSTRACT TRUNCATED AT 250 WORDS)
BACKGROUND: Smoking is reported to be positively related to abdominal fat in young and middle-aged persons; however, it is unclear whether this relationship exists in elderly persons. Behavioral influence on fat distribution is of importance because of the accumulation of abdominal fat with age and its associated health risks. METHODS: The relationship was investigated in a population-based sample of 1,178 men and 1,163 women aged 55-85 years, representative of the Dutch older population in 1992-1993. Waist and hip circumference and their ratio were used as indices of fat distribution. Past and current smoking habits were obtained by questionnaire. RESULTS: Smoking was associated with waist/hip-ratio (WHR) in men, with current smokers having the highest WHR and never smokers the lowest. A dose-response relationship between the daily number of cigarettes smoked and WHR was observed in men. These associations remained significant after adjustment for confounding due to age, education, body mass index, health status, alcohol intake, and sports activity. The dose-response relationship did not change after additional adjustment for duration of smoking. Among former male smokers, recent quitters had a higher WHR compared to long-term quitters. Additional analysis showed that smoking was more strongly associated with waist than with hip circumference. In women the relationship between smoking and fat distribution was not clear. CONCLUSIONS: Past and current smoking habits are positively associated with abdominal fat in older men, but not in older women.
Urinary cortisol output and serum cortisol concentrations were measured in the steady state, under "field" conditions, and during standardized inhibitory and stimulatory tests in premenopausal, obese women, and were analyzed in relation to adipose tissue distribution. Urinary cortisol output was increased under field conditions in women with an elevated waist to hip circumference ratio (WHR) and, in particular, in women with a large abdominal sagittal diameter, indicating visceral fat accumulation. However, dexamethasone inhibition of cortisol secretion was normal. Stimulation with corticotropin analogue and with physical (cold-pressor test) or mental (color-word or mathematic) stress tests also showed elevated responses of serum cortisol, but not of prolactin or growth hormone concentrations. It is suggested that women with visceral fat accumulation have elevated cortisol secretion due to an increased sensitivity along the hypothalamic-pituitary-adrenal axis, and that this may be causing their abnormal fat depot distribution.
In a prospective study of risk factors for ischemic heart disease, 792 54-yr-old men selected by year of birth (1913) and residence in Göteborg, Sweden, agreed to attend for questioning and a number of anthropometric and other measurements in 1967. Thirteen and one-half years later, these baseline findings were reviewed in relation to the number of men who had subsequently developed diabetes mellitus. This analysis focused on the importance of abdominal adipose tissue distribution, measured as the waist-to-hip circumference ratio, as a predictor for development of diabetes. Even when the confounding effect of body mass index, as a measure of the total body fat mass, was accounted for, the waist-to-hip ratio was positively and significantly associated with the risk for diabetes. These results from a prospective study strongly support previous cross-sectional findings indicating that not only the degree of obesity but also the localization of fat is a risk factor for diabetes.
All women aged 45-64 (n = 1084) in the community of Strömstad, Sweden, were invited to a health survey aimed at identifying cardiovascular risk factors. Adiposity as a risk factor was defined as body mass index (BMI: kg/m2) greater than or equal to 30 or waist-to-hip ratio (W/H ratio; cm/cm) greater than or equal to 0.82 or both. All persons who fulfilled these criteria for adiposity (n = 208) were invited to an educational programme. Of these 208 women, 31 per cent were willing to take part in the educational programme. Participants with W/H ratio greater than or equal to 0.82 but BMI less than 30 reduced their body weight, BMI, waist circumference. W/H ratio and serum triglyceride levels significantly, compared to the corresponding non-participants. Their triglyceride levels were reduced by 21 per cent. Participants with BMI greater than or equal to 30 and W/H less than 0.82 only reduced their body weight and BMI significantly. It seems justified to pay special attention to subjects with abdominal adiposity when planning for preventive work in women.
Body fat distribution, its continuity from childhood (4-6 years) to 30 years of age, and its link to that of parents is described in a longitudinal study population. A computer-assisted image analysis technique was used to measure body fat distribution (as measured by waist and hip diameters) from somatotype photographs. Pearson correlation coefficients were used to assess the association between the waist/hip diameter ratio (WHDR) and the body mass index (BMI) at all ages and between the WHDR of parents and offspring. Both Pearson correlation coefficients and the Foulkes-Davis tracking index were used to assess tracking of the WHDR from childhood to age 30 years. Stepwise regression analyses were performed to determine the predictability of the WHDR at age 30 years from WHDRs in childhood and adolescence. Among both sexes the WHDR decreased and BMIs increased with age from childhood to 18 years, then both increased from age 18 to 30 years. The correlation between the WHDR and BMI was significant only at 30 years for males (r = 0.37; p < 0.05) and during all stages of adolescence in females (p < 0.05). Age-to-age correlations were high for both sexes (p < 0.0001), and remained significant over a span of up to 25 years. Using the Foulkes-Davis tracking index, tracking from the year of peak height velocity to 30 years (a span of approximately 20 years) was strong for both sexes. Parent and child WHDRs were correlated and differed by sex. Father-son correlations were not significant in childhood, but reached significance in early adolescence (2 years before the year of peak velocity) and remained significant to 30 years (p < 0.05). Mother-daughter correlations were significant at all ages (p < 0.05). The level of the WHDR at the peak of the pubertal growth spurt (year of peak height velocity) predicted up to 58% of the variance in males and 51% of the variance in females of the WHDR at 30 years. We conclude that the adult WHDR (a proxy for the waist/hip ratio) becomes evident by the year of the pubertal growth spurt in height.
The GNB3 825T allele encodes a product that has enhanced activation of heterotrimeric G proteins in vitro and could play a role in adipogenesis. We therefore evaluated the possibility that the GNB3 825T allele was associated with obesity in a sample of 213 healthy Canadian Inuit. We found that body weight, body mass index, waist girth, hip girth, subscapular skinfold thickness, and triceps skinfold thickness were significantly higher in subjects with the GNB3 825T/T genotype than in subjects with other genotypes. Furthermore, two anthropometric ratios, namely that of waist to hip circumference and that of subscapular to triceps skinfold thickness, were not significantly different across genotypes. This suggested that the increased deposition of fat in subjects with the GNB3 825T/T genotype was generalized and not localized to particular subregions. There was no association of this genetic variation with blood pressure. The GNB3 825T/T genotype accounted for between 1.6% and 3.3% of the total variation (< or =13% of attributable variation) of the obesity-related traits. The potential for a genetic marker of obesity creates opportunities for future studies in the Inuit, not just to confirm the associations, but also to examine prospectively the influence of interventions and possible relationships between GNB3 825T and longer term complications of obesity.
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BACKGROUND: It has been previously shown that food intake elevates circulating ACTH and cortisol levels, but no report has been published regarding the changes in circulating dehydroepiandrosterone (DHEA). DHEA was originally described as a weak androgen, but more recently it has been associated with a wide range of metabolic functions. In addition, previous studies have described a hyper-responsive hypothalamo-pituitary-adrenal axis in obese subjects in response to various stimuli, but the specific response to food has not been studied. SUBJECTS AND DESIGN: We studied the effect of food on the hypothalamo-pituitary-adrenal axis in 20 subjects of normal body mass index (BMI range 18-25) and also in a group of 12 obese subjects (BMI range 34-61). Levels of glucose, insulin, ACTH, cortisol and dehydroepiandrosterone were measured every 20 minutes. RESULTS: A small rise in DHEA accompanies the rise in circulating ACTH and cortisol in response to food in both lean and obese subjects, but DHEA rose independently of cortisol and ACTH on the fasting day. In the obese subjects, food induced a significantly greater change in serum cortisol (peak cortisol rise (mean +/- SEM); normal-weight group, 169 +/- 14%; obese group, 294 +/- 23%) and in the cortisol/DHEA ratio (area under the curve; normal-weight group, 202 +/- 15%; obese group, 292 +/- 29%) than in the normal-weight subjects. This difference was particularly notable in those with central-type obesity (waist/hip ratio > 0.80). A group of the normal, jean female subjects showed no cortisol rise after food intake. CONCLUSION: Our results suggest that DHEA may vary independently of circulating cortisol, and that the cortisol response to food is enhanced in obese subjects, particularly in those with central obesity. We speculate that there may be a caused connection between the cortisol response to food in normal subjects, and the subsequent distribution of fat if such subjects overeat sufficiently to become obese.
Although many studies have suggested that increased androgenicity is associated with insulin resistance and hyperinsulinemia in both pre- and postmenopausal women, relatively few data are available on this relationship in men. We examined the association of body mass index (BMI), waist-to-hip ratio (WHR), sex hormone-binding globulin (SHBG), total and free testosterone, dehydroepiandrosterone sulfate (DHEA-SO4), and estradiol with insulin concentrations and whole-body glucose disposal in 87 men from a population-based study in Kuopio, Finland. BMI was significantly correlated with fasting insulin (r = 0.46), total whole-body glucose disposal (r = -0.30), glucose oxidation (r = -0.21), and nonoxidative glucose disposal (r = -0.25). WHR also was significantly associated with fasting insulin (r = 0.61), total whole-body glucose disposal (r = -0.54), glucose oxidation (r = -0.23), and nonoxidative whole-body glucose disposal (r = -0.50). SHBG and total and free testosterone were significantly associated with insulin concentrations and total and nonoxidative glucose disposal but not with glucose oxidation. DHEA-SO4 and estradiol were not associated with insulin, glucose concentrations, or whole-body glucose disposal in univariate analysis. In multivariate analysis, total whole-body glucose disposal was associated negatively with WHR and positively associated with total testosterone and SHBG; nonoxidative whole-body glucose disposal was associated negatively with WHR and positively associated with total and free testosterone. Glucose oxidation was significantly associated only with WHR. In conclusion, higher WHR and lower testosterone were strongly associated with a decrease in total and nonoxidative whole-body glucose disposal in men.
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