Interrelationships between weight loss, body fat distribution and sex hormones in pre- and postmenopausal obese women

Objectives. Relationships between regional body fat distribution and sex hormones as well as changes in sex hormones after weight loss were evaluated. Setting. All subjects were hospitalized in the Institute of Internal Medicine of the University of Verona. Subjects. Twenty-six premenopausal (age 33.7± 10.2 years) and 15 postmenopausal (age 57.9±5.9 years) obese women. Interventions. Body weight, body-mass index, waist and hip circumferences, visceral fat by computed tomography and sex hormones were evaluated before and after 4 weeks on a very low energy diet. Results. Body-mass index was higher in pre- than in postmenopausal women, although the difference was not significant. Total and free testosterone were significantly higher in the pre- than in the postmenopausal group (P<0.001). Significant negative correlations were found between age and total testosterone (r=?0.65; P<0.001), free testosterone (r=?0.54; P<0.001), androstenedione (r=?0.46; P<0.01) and urinary cortisol excretion (r=?0.50; P<0.01). A negative correlation was found between visceral fat and total testosterone (r=?0.41; P<0.01). After adjusting for age, the negative correlation between total testosterone and visceral fat encountered both in the subject group as a whole and in premenopausal women was no longer significant, whilst a significant negative association between visceral fat and sex hormone binding globulin (SHBG) (r=?0.56; P<0.001) was always found. When step-down regression analysis was used to evaluate the joint effect of age, menopausal status, and anthropometric and metabolic variables on sex hormones, age was the most powerful independent variable for predicting total testosterone, free testosterone and androstenedione levels, whilst menopausal status was the most powerful predictor of FSH and LH levels. Changes in hormones after VLED were analysed separately in pre- and postmenopausal women. None of the hormones changed significantly after VLED in the postmenopausal group, except for FSH values. LH, free testosterone and urinary cortisol excretion values decreased significantly after VLED in the premenopausal group. Conclusions. Our data show that age, to a greater extent than visceral fat, seems to be negatively associated with steroid sex hormones. Weight loss seems to be associated with changes in sex hormones only in premenopausal women.     

The relationship between body fat distribution and weight loss in obese adolescent girls.

Recent studies have demonstrated an association between the pattern of body fat distribution and the occurrence of cardiovascular risk factors. In this study, we evaluated changes in body fat distribution as defined by several anthropometric criteria during a six week weight reduction programme in 110 obese adolescent girls (mean age 15.2 +/- 0.4 years). The standardized regimen included a mixed diet of 1032 kcal/day and a daily exercise programme of 1-2 h duration. The mean weight loss was 8.6 +/- 2.8 kg, decreasing the body mass index (BMI) from 31.4 +/- 4.7 to 28.2 +/- 4.9 kg/m2 (P < 0.01). The reduction in body weight was accompanied by a significant decrease in the waist-to-hip ratio (WHR) from 0.86 +/- 0.06 to 0.81 +/- 0.05 (P < 0.01). The initial WHR was correlated with the degree of weight loss independent of the initial weight (r = 0.34, P < 0.001). Categorized according to the waist-to-hip ratio girls in the upper tertile (WHR > 0.88) lost significantly more weight than girls in the lower tertile (WHR < 0.80) (9.8 +/- 2.7 vs. 6.8 +/- 2.5 kg, P < 0.01). These findings suggest that girls with an abdominal type of obesity benefit more from a weight reduction programme than girls with a gluteal-femoral type of obesity.     

Differences in insulin resistance do not predict weight loss in response to hypocaloric diets in healthy obese women

The current study was initiated to determine whether insulin resistance and/or hyperinsulinemia affected the ability of obese individuals to lose weight in response to hypocaloric diets. Thirty-one obese, nondiabetic women, with values for body mass index ranging from 28.0-35.0 kg/m2, volunteered for this program. Resistance to insulin-mediated glucose disposal was assessed by determining their steady state plasma insulin and glucose concentration during the last 30 min of a 180-min infusion of somatostatin, insulin, and glucose. The total integrated insulin response to breakfast and lunch was also determined. After the baseline measurements, volunteers were placed on a hypocaloric diet calculated to lead to a minimum weekly loss of 1% of ideal body weight. Individuals who met the criteria after 30 days of dieting were defined as weight loss successes (n = 20) and continued on the diet for another 30 days. Individuals not meeting the criteria were designated as weight loss failures (n = 12) and were discharged from the study. There was a mean (+/-SEM) weight loss at 60 days of 9.2 +/- 0.4 kg in the 20 individuals defined as weight loss successes, but there was no correlation between weight loss and either steady state plasma glucose or the total integrated insulin response (r < 0.1; P > 0.83). Furthermore, using the same criteria to define insulin sensitivity and insulin resistance as those for therapeutic successes, the therapeutic failures comprised six insulin-sensitive and five insulin-resistant subjects. In summary, insulin-mediated glucose disposal varied widely in nondiabetic, obese women, and there was no relationship between baseline insulin resistance or total integrated insulin response and weight loss. It is concluded that the ability to lose weight on a calorie-restricted diet over a short time period does not vary in obese, healthy women as a function of insulin resistance or hyperinsulinemia.     

Relationship between hormone replacement therapy use with body fat distribution and insulin sensitivity in obese postmenopausal women.

The aim of this study was to compare the effect of hormone replacement therapy (HRT) on insulin resistance and central adiposity in obese postmenopausal women. Forty-five obese postmenopausal women (16 HRT users and 29 nonusers), with a mean age of 56.6 +/- 5.3 years and duration of current, continuous HRT use of 4.7 +/- 2.9 years, were included in the study. Subjects were studied using oral glucose tolerance tests, euglycemic clamping, dual photon x-ray absorptiometry, computed tomography, doubly labeled water, and treadmill testing. Insulin sensitivity, total fat, visceral fat, subcutaneous abdominal fat, thigh muscle attenuation, daily physical activity energy expenditure, peak oxygen consumption (Vo(2)) were measured. HRT users had lower body weight (88.0 +/- 11.0 v 98.2 +/- 15.0 kg, P =.05), lower body mass index (33.1 +/- 3.5 v 36.8 +/- 5.2 kg/m(2), P =.05), lower fat mass (38.3 +/- 7.3 v 44.1 +/- 10 kg, P =.05), less visceral adipose tissue (157 +/- 47 v 211 +/- 81 cm(2); P =.05), and higher peak Vo(2) (21.1 +/- 4.6 v 17.6 +/- 2.2 mL/kg/min, P =.001) than nonusers. After adjustment for total fat, we noted a trend for decreased visceral adipose tissue in HRT users (P =.09). After adjustment for peak Vo(2), the decreased visceral adipose tissue persisted in HRT users (P <.01). Insulin sensitivity per kilogram of lean body mass did not differ between HRT users (0.51 +/- 0.22 mmol/kg/min) and nonusers (0.49 +/- 0.22 mmol/kg/min). It was concluded that obese postmenopausal women using HRT have a more favorable body composition and fat distribution pattern than nonusers. Although visceral adipose tissue is decreased in HRT users, insulin sensitivity does not differ between HRT users and nonusers.     

Adiponectin before and after weight loss in obese children

Adiponectin is decreased in obesity and seems to be involved in insulin resistance. The influences of age, gender, puberty, and weight loss on adiponectin have not been studied in obese children. We measured body fat mass based on skinfold thickness, age, pubertal stage, gender, adiponectin, and insulin resistance (homeostasis model assessment) in 42 obese children. We analyzed adiponectin and homeostasis model assessment 1 yr later in these obese children and separated them into two groups according to degree of weight loss (decrease in sd score for body mass index, >or=0.5 vs. <0.5). Adiponectin was negatively correlated to percentage body fat (r = -0.44; P = 0.002), insulin resistance (r = -0.33; P = 0.016), and age (r = -0.41; P = 0.003). Adiponectin levels were significantly (P = 0.017) higher in pubertal girls compared with boys, but there was no significant difference in prepubertal children in respect to gender (P = 0.833). Adiponectin was significantly (P < 0.001) lower in pubertal compared with prepubertal children. The significant weight loss in 16 children was associated with a significant increase in adiponectin (P = 0.010) and a decrease in insulin resistance (P = 0.013), whereas there were no changes in the 26 children without significant weight loss. Adiponectin levels in obese children were negatively correlated to age, body fat, and insulin resistance and were decreased in puberty. Significant weight loss led to an increase in adiponectin levels and an improvement of insulin resistance.     

Androgens before and after weight loss in obese children

CONTEXT: Little information is available on androgens in obese children, and it is unknown whether these hormones change after weight loss. OBJECTIVE: The objective of this study was to compare androgens between obese and normal-weight children and to study the effect of weight loss on androgens. DESIGN: The design was a cross-sectional comparison between obese and normal-weight children separated according to pubertal stage and longitudinal 1-yr follow-up study in obese children participating in a weight-loss intervention. SETTING: The setting of this study was a primary care facility. PATIENTS: A total of 273 obese and 79 lean children (aged 4-14 yr) were studied, including a subgroup of 155 obese children for the longitudinal study. INTERVENTION: The intervention program was an outpatient 1-yr intervention program based on exercise, behavior, and nutrition therapy (high-carbohydrate low-fat diet). MAIN OUTCOME MEASURES: The outcome measures included testosterone and dehydroepiandrosterone sulfate (DHEAS) at baseline and 1 yr later. RESULTS: The obese prepubertal children and the obese pubertal girls showed significantly (P < 0.01) higher testosterone and DHEAS levels, whereas obese pubertal boys did not significantly differ in androgens from their lean counterparts. Significant correlations with body mass index were demonstrated in multivariate regression analyses for DHEAS in all children and for testosterone in prepubertal children and in pubertal girls. The obese prepubertal children and obese girls losing substantial weight showed a significant (P < 0.05) decrease in their testosterone concentrations. CONCLUSIONS: Moderately increased testosterone and DHEAS levels were found in obese prepubertal children and in obese pubertal girls, whereas androgen concentrations did not differ between obese and normal-weight pubertal boys. Weight loss induced a decrease in testosterone in obese prepubertal children and pubertal girls pointing to a reversible increase of androgens.     

Levels of acylation stimulating protein in obese women before and after moderate weight loss

Acylation stimulating protein (ASP) is a small (MW 14,000) basic (pI 9.0) protein which has only recently been purified from human plasma. Since ASP is the most potent known stimulant of triglyceride synthesis in human adipose tissue, the present study was designed to determine if plasma ASP was elevated in patients with moderate obesity, and if so, whether this level changed with weight loss. Fasting plasma ASP levels were determined by competitive ELISA immunoassay in 10 obese women before weight loss, immediately after weight loss, and 3 months after maintaining weight reduction. Their plasma ASP results were compared to 17 age and sex-matched lean controls. With weight loss, plasma ASP decreased significantly: 19.6 +/- 10.7 mg/dl before weight loss vs 15.0 +/- 9.5 mg/dl after weight loss vs 13.8 +/- 7.7 mg/dl 3 months after being weight stable, P less than 0.05 initial vs final value. Nevertheless, plasma ASP was significantly higher than the control value at all three times. Thus, before weight loss, the average ASP in the obese group was four times that in the control group (19.6 +/- 10.7 vs 5.1 +/- 3.6 mg/dl, P less than 0.0005) while even 3 months after weight loss, it remained almost three times above the control group (13.8 +/- 7.7 vs 5.1 +/- 3.6 mg/dl, P less than 0.0005). The data suggest, therefore, that an elevated plasma level of ASP is common in obesity, that the level of plasma ASP may reflect the fat cell mass present in an individual, and raises the possibilities that ASP may play a role in initiation or maintenance of the obese state.     

Circulating soluble leptin receptor, leptin, and insulin resistance before and after weight loss in obese children

OBJECTIVE: To study the relationships between leptin, soluble leptin receptor (sOB-R), and insulin resistance in obese children before and after weight reduction. METHODS: We determined fasting serum leptin, sOB-R, and insulin resistance index (Homeostasis model assessment (HOMA)) in 36 obese children at baseline and 1 y later and compared them to 72 lean children matched for age, gender, and pubertal stage. The changes of leptin (Deltaleptin) and sOB-R (DeltasOB-R) over the 1 y period were correlated to the changes of HOMA (DeltaHOMA), the changes of weight status, and the changes of percentage body fat (Delta%BF) based on skinfold measurements. Multiple linear regression analyses were conducted for the dependent variables Deltaleptin and DeltasOB-R, including DeltaBMI and DeltaHOMA as independent variables adjusted for age, gender, and pubertal stage. Changes of leptin and sOB-R levels were analyzed in 11 obese children after they had lost weight substantially (decrease SDS-BMI>0.5) and compared to 11 obese children without substantial weight loss matched for age, gender, and pubertal stage. RESULTS: Obese children showed significantly (P<0.001) higher leptin and lower sOB-R levels. Deltaleptin correlated significantly to DeltaSDS-BMI (r=0.28, P<0.05), Delta%BF (r=0.44, P<0.05), and DeltaHOMA (r=0.42, P<0.01), while DeltasOB-R correlated significantly to DeltaSDS-BMI (r=-0.42, P<0.01) and Delta%BF (r=-0.47, P<0.01), but not to DeltaHOMA. In contrast to DeltasOB-R, Deltaleptin correlated significantly to DeltaHOMA (P=0.02) in multiple linear regression analysis. Substantial weight loss led to a significant increase in sOB-R (P=0.02) and to a decrease in HOMA (P=0.02). In children without substantial weight loss, there were no changes in sOB-R, while HOMA (P=0.04) and leptin (P=0.02) increased significantly. CONCLUSIONS: The decrease of sOB-R and the increase of leptin levels in obese children normalized after weight loss. Therefore, these changes are consequences rather than the cause of overweight. In contrast to sOB-R, leptin levels are associated with insulin resistance.     

Decrease in visceral fat following diet-induced weight loss in upper body compared to lower body obese premenopausal women

BACKGROUND: Obesity is associated with numerous metabolic disturbances, such as insulin resistance, diabetes mellitus type 2, dyslipidemia, and hypertension. An excess of fat within the abdomen, so-called visceral adiposity, confers a greater and independent health risk of metabolic and cardiovascular complications than does adipose tissue accumulation elsewhere. The present study aimed to investigate a possible differential effect of diet-induced weight loss in visceral fat mass and metabolic parameters in obese individuals with the upper body (UBO) and lower body (LBO) obese phenotype. METHODS: The obese subjects were prescribed a liquid, very-low calorie diet to reduce 50% of their overweight (15% body weight loss). Specific body fat measurements (MRI, BIA), anthropometrics, and fasting metabolic parameters were obtained in control subjects and two groups of obese subjects (UBO and LBO) before and after weight loss. RESULTS: Weight loss was accompanied by significant decreases in total, subcutaneous, and visceral fat in both UBO and LBO women. The largest reduction in visceral fat mass was found in the UBO women (absolute decrease 223+/-32 cm(2) vs 122+/-91 cm(2) in LBO women; P=0.01), while the amount of visceral fat was reduced to normal levels in LBO women (155+/-25 cm(2) after weight loss vs 143+/-17 cm(2) in controls; P=NS). Furthermore, weight loss significantly lowered fasting glucose, total cholesterol, and LDL cholesterol concentrations in UBO women. CONCLUSION: The obese phenotype is preserved after body weight loss. UBO women have to lose a larger amount of overweight in order to bring the amount of fat in the visceral depot down to normal levels and to obtain normalization of their cardiovascular risk profile.     

Effect of weight loss and regional fat distribution on plasma leptin concentration in obese women.

OBJECTIVES: To investigate how circulating leptin concentrations are related to regional fat distribution and whether moderate weight loss alters these relationships. DESIGN: A 6 month, clinical weight reduction trial with measurements before and after weight loss. SUBJECTS: 38 healthy, obese women (age: 44.3+/-9.9 y, BMI: 34.0+/-4.0 kg/m2). MEASUREMENTS: The following measurements were made. 1. indices of obesity and fat distribution: weight, body mass index (BMI), hip circumference (peripheral fat), waist circumference, total body fat (bioelectrical impedance), abdominal fat distribution: visceral fat and abdominal subcutaneous fat (ultrasonography); and 2. Biochemical measurements: plasma leptin and serum insulin. RESULTS: Baseline plasma leptin concentrations were three-fold higher in obese women than in normal weight controls. After weight loss averaging 8.4 kg (9.0%), plasma leptin decreased by a mean of 22.3% (P < 0.001), corresponding to body fat decrease of 16.6% (P < 0.001), abdominal subcutaneous fat decrease of 17.4% (P < 0.001) and visceral fat decrease of 18.7% (P < 0.001). The total amount of body fat correlated with plasma (serum) leptin before (r = 0.64, P < 0.001) and after (r = 0.75, P < 0.001) weight loss. Plasma leptin concentrations expressed per kg of body fat did not change significantly during weight loss. After controlling for body fat, baseline leptin concentrations were significantly associated with hip circumference (r = 0.57, P < 0.001) but not with any indices of abdominal fat distribution. After weight loss the associations became significant for hip and waist circumference as well as for visceral and abdominal subcutaneous fat. Changes in leptin correlated with changes in all indices of obesity except visceral fat. CONCLUSIONS: Plasma leptin concentrations reflect not only total fat mass but also adipose tissue distribution, especially peripheral fat. Plasma leptin values per kilogram of fat mass do not change significantly with modest weight loss.     

Clinical and hormonal characteristics of obese amenorrheic hyperandrogenic women before and after weight loss

We studied a group of obese hyperandrogenic amenorrheic women to determine the effects of weight loss on anthropometry, hormonal status, menstrual cycles, ovulation, and fertility. Fourteen women had polycystic ovaries, two the hyperandrogenism-insulin resistance-acanthosis nigricans syndrome, one hirsutism of adrenal origin, and three idiopathic chronic anovulation. The duration of amenorrhea before the study ranged from 3-17 months [mean, 8.6 +/- 4.5 (+/- SD)]. All women ate a hypocaloric diet for a period of 8.0 +/- 2.4 months. Weight loss ranged from 4.8 to 15.2 kg (mean, 9.7 +/- 3.1 kg; 1.35 +/- 0.56 kg/month) and the waist to hip ratio, which was used as a measurement of body fat distribution, decreased from 0.86 +/- 0.1 to 0.81 +/- 0.06 (P less than 0.0001). The women's mean plasma testosterone and LH concentrations decreased significantly (P less than 0.001 and P less than 0.005, respectively). A significant positive correlation was found between the decreases in plasma testosterone levels and the decreases in glucose-stimulated insulin levels. Moreover, the decreases in the waist to hip ratio correlated positively with the decreases in glucose-stimulated insulin levels and inversely with the decreases in plasma 17 beta-estradiol. No relationships were found between weight loss and the changes in plasma insulin, steroid, and gonadotropin concentrations. The responsiveness to the weight reduction program was evaluated by comparing the number of menstrual cycles during the study period with the number reported before it. Eight women had significantly improved menstrual cyclicity (responders), while 12 did not (nonresponders). The clinical characteristics and hormone values were similar in responder and nonresponder women. In the group as a whole, 33% of the menstrual cycles during the study were ovulatory, and 4 pregnancies occurred. Hirsutism improved significantly in more than half of the women, as did acanthosis nigricans when present. We conclude that weight loss is beneficial in all obese hyperandrogenic women regardless of the presence of polycystic ovaries, the degree of hyperandrogenism, and the degree and distribution of obesity.     

Resistin concentrations before and after weight loss in obese children

OBJECTIVE: The influences of gender, puberty, and obesity on resistin levels and the longitudinal relationships between insulin resistance, weight loss, and resistin have not yet been studied in childhood. METHODS: Age, pubertal stage, gender, weight status (standard deviation score-body mass index (SDS-BMI)), resistin levels, and insulin resistance index calculated by homeostasis model assessment (HOMA) were evaluated in 63 obese children and compared to 36 lean children of same age, gender, and pubertal stage. Furthermore, we analyzed the changes of weight status (SDS-BMI, percentage body fat based on skinfold measurements), waist-to-hip ratio, resistin, and HOMA over a 1-year period in 38 obese children. RESULTS: The resistin levels did not significantly (P = 0.079) differ between obese (median resistin 8.7 ng/ml) and lean children (median resistin 9.7 ng/ml). Resistin concentrations were independent of age and pubertal stage, but girls demonstrated significantly higher resistin levels than boys (P = 0.021). There were no significant correlations between changes of resistin and changes of SDS-BMI (r = 0.14, P = 0.198), changes of percentage body fat (r = -0.01, P = 0.466), changes of waist-to-hip ratio (r = 0.17, P = 0.141), and changes of insulin resistance index (r = 0.01, P = 0.472) over the 1-year period. The weight loss of > or = 0.5 SDS-BMI in 16 children was associated with a significant decrease in HOMA (P = 0.030), while there was no significant change in resistin levels (P = 0.878). CONCLUSIONS: Girls demonstrated higher resistin concentrations than boys. Our data do not support a relationship between resistin, insulin resistance index, and weight status in childhood.     

Pancreatic polypeptide in obese children before and after weight loss

OBJECTIVE: Little is known concerning pancreatic polypeptide (PP) in weight loss and in childhood obesity. METHODS: Fasting PP, leptin and insulin concentrations were determined in 38 obese children and compared with 35 lean children of the same age, gender and pubertal stage. Furthermore, changes of PP concentrations over a 1-year period were analyzed in the obese children participating in a weight loss intervention program. RESULTS: Obese children had significantly (P<0.01) lower PP, and higher leptin and insulin levels compared to lean children. In multiple linear regression analysis, PP was significantly negatively correlated to body mass index (P<0.01), but not to leptin, insulin, age, gender and pubertal stage. Changes of PP did not significantly correlate to changes of insulin (r=0.07, P=0.343) and leptin (r=-0.02, P=0.459). The substantial weight loss in 17 children led to a significant (P<0.05) increase in PP and decrease in insulin and leptin. In the 21 children without substantial weight loss, there were no significant changes in PP, insulin and leptin. CONCLUSIONS: PP concentrations are decreased in obese children and independent of age, gender, pubertal stage, leptin and insulin. The decrease of PP in obese children normalized after weight loss. Therefore, low PP concentrations reflect the overweight status, rather than cause it.     

Short-term weight loss and exercise training effects on glucose-induced thermogenesis in obese adolescent males during hypocaloric feeding

Our purpose was to examine the effect of short-term weight loss and exercise training on the thermic effect of a glucose load in lean and obese adolescents. Nine obese (age 14.3 +/- 0.3 years, mean +/- s.e.m.) boys were examined during the first (Ob-pre) and sixth (Ob-post) week of caloric restriction (1300-1500 kcal/day, 5441-6279 kJ/day) and aerobic exercise conditioning (walk/jog/swim/calisthenics), and compared to age-matched lean controls (Con). A 100-g oral glucose tolerance test (OGTT) was administered while simultaneously measuring energy expenditure by indirect calorimetry every 30 min for 3 h. Posttest results revealed a decrease in body weight and body fatness in obese boys, but not to the level of that in lean controls (P less than 0.01). The thermic effect of glucose, calculated as the area under the response curve for three hours in excess of resting metabolic rate, was similar in Ob-pre and Con (0.77 +/- 0.14 vs. 0.57 +/- 0.28 kcal/kg lbm/3h), but decreased in Ob-post (0.29 +/- 0.08 kcal/kg lbm/3h, P less than 0.01). The area under the response curve for glucose was elevated in Ob-pre (328.1 +/- 12.2 mg/dl/3h) compared to Con (270.4 +/- 21.4 mg/dl/3h). The insulin response was similar in Ob-pre and Con (120.4 +/- 11.3 vs 125.6 +/- 12.4 mU/ml/3h), but decreased in Ob-post (89.6 +/- 15.1 mU/ml/3h, P less than 0.05). Thus, the improvement in peripheral insulin sensitivity with short-term exercise and weight loss was unaccompanied by favorable alterations in carbohydrate-induced thermogenesis in obese adolescents.     

Excess body fat distribution and glucose homeostasis in obese Arab women

The relationship of body fat distribution to glucose intolerance and non-insulin-dependent diabetes mellitus in Arab women was studied in 102 obese non-diabetic and 40 obese women with diabetes. The obese women underwent a glucose tolerance test. Linear regression analysis revealed a significant correlation between the waist/hip ratio and the plasma glucose concentration at 120 min. When divided into two groups according to the median of their waist/hip ratio (0.815), obese women without history of diabetes but with high waist/hip ratio (0.86 +/- 0.07, mean +/- SD) had significantly higher prevalence of glucose intolerance and of diabetes mellitus than those with the low ratio (0.78 +/- 0.03, chi 2 = 9.32, p less than 0.001). The highest ratio (0.89 +/- 0.06) was observed in the obese women with known diabetes mellitus.     

The effects of two different hypocaloric diets on glucagon-like peptide 1 in obese adults, relation with insulin response after weight loss

ObjectiveFew studies have investigated the effect of type of diets on GLP-1 concentrations. The aim of this study was to compare the effect of two diets on circulating GLP-1 levels and the relation with insulin response after weight loss.MethodsA population of 118 obese patients were analyzed. Patients were randomly allocated to two groups: (a) Diet I (low carbohydrate) and (b) Diet II (low fat). Biochemical and anthropometric parameters were measured before and after 3 months of hypocaloric diet.ResultsFifty-two patients (12 male/40 female) were treated with Diet I and 66 patients (21 male/45 female) with Diet II. In Group I, basal GLP-1 levels did not change after dietary treatment (9.4±3.3 vs. 9.9±3.1 ng/ml; ns). In Group II, GLP-1 levels decreased significantly (8.4%) (9.2±3.3 vs 8.7±3.1 ng/ml; P<.05). In the multivariate analysis with a dependent variable (levels of GLP-1), only insulin levels remained as an independent predictor in the model (F=5.9; P<.05), with an increase of 0.6 ng/ml (95% CI 0.1–1.1) GLP-1 concentrations with each increase of 1 mUI/ml of insulin.ConclusionA hypocaloric diet with a low fat percentage decreased GLP-1 levels with a direct correlation with insulin levels. Nevertheless, patients with a hypocaloric diet with a low carbohydrate percentage treatment did not change GLP-1 levels. Diet macronutrient manipulation on GLP-1 response could be useful in an obesity nutrition therapy.     

A prospective study of body fat distribution and weight loss

Previous studies have suggested an association between adipose tissue cellularity and body fat distribution, and between adipose tissue cellularity and ability to lose weight. To determine whether there was an association between body fat distribution and ability to lose weight, we prospectively studied 187 severely obese women. The women were all 50 percent or more above ideal body weight, with personal physician documentation of no known major illnesses. Weights were recorded at the beginning and end of a 3-week hospitalization and every 3 months following hospitalization, for up to 2 years. The ratio of waist girth to hip girth (WHR) was used as an index of body fat distribution. A statistical analysis which adjusted for age and weight on admission did not find any association between WHR and weight loss during hospitalization, or at any time up to 2 years after hospital discharge. We conclude that the WHR index of body fat distribution is not a useful prognostic indicator of weight change for severely obese women with refractory obesity.     

Relationship between insulin resistance, weight loss, and coronary heart disease risk in healthy, obese women.

Several popular books have recently been published stating that being insulin-resistant favors weight gain and/or prevents weight loss. Because this view seems to have gained widespread support in the general population, we thought it important to perform the current study testing the hypothesis that differences in insulin-mediated glucose disposal do not affect weight loss in response to calorie-restricted diets. For this purpose, we studied the change in weight and risk factors for coronary heart disease (CHD) in healthy women volunteers, defined as being obese on the basis of a body mass index (BMI) greater than 30.0 kg/m(2). The insulin suppression test was used to stratify obese women at baseline into insulin-resistant and insulin-sensitive subgroups on the basis of their steady-state plasma glucose (SSPG) concentration at the end of a 180-minute infusion of octreotide, exogenous insulin, and glucose. They were then instructed on a calorie-restricted diet plus sibutraminine (15 mg/day) for a total period of 4 months. Baseline measurements also included determination of fasting lipid and lipoprotein concentrations, and hourly (8 AM to 4 PM) determinations of plasma glucose and insulin concentrations before and after breakfast and lunch. Twenty-four women completed the 4-month period of calorie restriction: 13 classified as insulin-resistant (SSPG = 219 +/- 7 mg/dL) and 11 as insulin-sensitive (SSPG = 69 +/- 6 mg/dL). The insulin-resistant group also had higher (P =.03) plasma triglyceride (TG) concentrations and a higher ratio of total to high-density lipoprotein (HDL) cholesterol concentration (P =.02) at baseline. Both groups lost a significant amount of weight during the study, and there was no difference between the weight loss in the insulin-resistant (8.6 +/- 1.3 kg) and insulin-sensitive (7.9 +/- 1.4 kg) groups. Weight loss in the insulin-resistant group was also associated with a significant decrease in SSPG concentration (219 +/- 7 to 144 +/- 14 mg/dL), associated with significantly lower fasting TG concentrations (P <.001) and day-long concentrations of plasma glucose and insulin (P <.005). None of these variables changed in the insulin-sensitive group. These results indicate that: (1) CHD risk factors in obese women vary as a function of being insulin-resistant or insulin-sensitive; (2) dramatic variations in insulin-mediated glucose disposal do not modulate weight loss in response to calorie-restricted diets, and (3) weight loss is effective in reducing CHD risk in insulin-resistant, obese women. Given these data, it seems obvious that attempts to reduce CHD risk factors by weight loss should focus on obese individuals who are also insulin-resistant.     

Effects of a community risk factor reducing programme on weight, body fat distribution, and lipids in obese women

All women aged 45-64 (n = 1084) in the community of Str?mstad, 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.