Effect of a conjugated linoleic acid and omega-3 fatty acid mixture on body composition and adiponectin

This study aimed to determine the effect of supplementation with conjugated linoleic acids (CLAs) plus n-3 long-chain polyunsaturated fatty acids (n-3 LC-PUFAs) on body composition, adiposity, and hormone levels in young and older, lean and obese men. Young (31.4+/-3.9 years) lean (BMI, 23.6+/-1.5 kg/m2; n=13) and obese (BMI, 32.4+/-1.9 kg/m2; n=12) and older (56.5+/-4.6 years) lean (BMI, 23.6+/-1.5 kg/m2; n=20) and obese (BMI, 32.0+/-1.6 kg/m2; n=14) men participated in a double-blind placebo-controlled, randomized crossover study. Subjects received either 6 g/day control fat or 3 g/day CLA (50:50 cis-9, trans-11:trans-10, cis-12) and 3 g/day n-3 LC-PUFA for 12 weeks with a 12-week wash-out period between crossovers. Body composition was assessed by dual-energy X-ray absorptiometry. Fasting adiponectin, leptin, glucose, and insulin concentrations were measured and insulin resistance estimated by homeostasis model assessment for insulin resistance (HOMA-IR). In the younger obese subjects, CLA plus n-3 LC-PUFA supplementation compared with control fat did not result in increased abdominal fat and raised both fat-free mass (2.4%) and adiponectin levels (12%). CLA plus n-3 LC-PUFA showed no significant effects on HOMA-IR in any group but did increase fasting glucose in older obese subjects. In summary, supplementation with CLA plus n-3 LC-PUFA prevents increased abdominal fat mass and raises fat-free mass and adiponectin levels in younger obese individuals without deleteriously affecting insulin sensitivity, whereas these parameters in young and older lean and older obese individuals were unaffected, apart from increased fasting glucose in older obese men.     

Is a small muscle mass index really detrimental for insulin sensitivity in postmenopausal women of various body composition status?

Objectives: We sought to determine if a small muscle mass index (MMI) is actually detrimental for insulin sensitivity when studying a large group of postmenopausal women displaying various body composition statuses and when age and visceral fat mass (VFM) are taken into account. Methods: A cross-sectional study was conducted in 99 healthy postmenopausal women with a BMI of 28?4 kg/m(2). Fat mass and total fat-free mass (FFM) were obtained from DXA and VFM and MMI were estimated respectively by the equation of Bertin and by: Total FFM (kg)/height (m)(2). Fasting plasma insulin and glucose were obtained to calculate QUICKI and HOMA as an insulin sensitivity index. Results: Total MMI and VFM were both significantly inversely correlated with QUICKI and positively with HOMA even when adjusted for VFM. A stepwise linear regression confirmed Total MMI and VFM as independent predictors of HOMA and plasma insulin level. Conclusions: A small muscle mass might not be detrimental for the maintenance of insulin sensitivity and could even be beneficial in sedentary postmenopausal women. The impact of muscle mass loss on insulin sensitivity in older adults needs to be further investigated.     

Effects of insulin therapy on liver fat content and hepatic insulin sensitivity in patients with type 2 diabetes

We determined whether insulin therapy changes liver fat content (LFAT) or hepatic insulin sensitivity in type 2 diabetes. Fourteen patients with type 2 diabetes (age 51+/-2 yr, body mass index 33.1+/-1.4 kg/m2) treated with metformin alone received additional basal insulin for 7 mo. Liver fat (proton magnetic resonance spectroscopy), fat distribution (MRI), fat-free and fat mass, and whole body and hepatic insulin sensitivity (6-h euglycemic hyperinsulinemic clamp combined with infusion of [3-(3)H]glucose) were measured. The insulin dose averaged 75+/-10 IU/day (0.69+/-0.08 IU/kg, range 24-132 IU/day). Glycosylated hemoglobin A1c (Hb A1c) decreased from 8.9+/-0.3 to 7.4+/-0.2% (P<0.001). Whole body insulin sensitivity increased from 2.21+/-0.38 to 3.08+/-0.40 mg/kg fat-free mass (FFM).min (P<0.05). This improvement could be attributed to enhanced suppression of hepatic glucose production (HGP) by insulin (HGP 1.04+/-0.28 vs. 0.21+/-0.19 mg/kg FFM.min, P<0.01). The percent suppression of HGP by insulin increased from 72+/-8 to 105+/-11% (P<0.01). LFAT decreased from 17+/-3 to 14+/-3% (P<0.05). The change in LFAT was significantly correlated with that in hepatic insulin sensitivity (r=0.56, P<0.05). Body weight increased by 3.0+/-1.1 kg (P<0.05). Of this, 83% was due to an increase in fat-free mass (P<0.01). Fat distribution and serum adiponectin concentrations remained unchanged while serum free fatty acids decreased significantly. Conclusions: insulin therapy improves hepatic insulin sensitivity and slightly but significantly reduces liver fat content, independent of serum adiponectin.     

Leptin in type 2 diabetic or myotonic dystrophic women.

BACKGROUND: Insulin resistance is an important determinant of circulating leptin concentrations in humans, but its independent contribution on plasma leptin levels are controversial. In the present study, we characterized plasma leptin levels and their regulation in women with 2 different insulin resistance states: type 2 diabetes and myotonic dystrophy disease, and in controls. MATERIAL AND METHODS: We studied 3 groups of women: 21 type 2 diabetic patients, 20 myotonic dystrophic patients and a control group of 20 normoglycemic subjects, matched in age and body mass index. Body composition, fasting glucose and insulin, IGF-I, IGF-binding protein-3 and leptin were studied. Body composition was measured using a bioelectrical impedance analyser. Insulin sensitivity (in percentage) was modeled according to a computer-based homeostasis model assessment model. Data are expressed in mean +/- SEM. RESULTS: In both groups of patients, glucose concentrations were higher in type 2 diabetic patients than in myotonic dystrophic patients, and insulin concentrations and insulin sensitivity were similar in the 2 groups of patients (82.4 +/- 18.6% in type 2 diabetic patients vs. 69.7 +/- 9.7% in myotonic dystrophic patients, p = 0.2) and lower than in controls. Serum leptin and leptin/fat mass ratio were higher in myotonic dystrophic patients than in type 2 diabetic patients (30 +/- 4.9 ng/ml vs. 17.7 +/- 2.6 ng/ml, p = 0.03 and 2.32 +/- 0.69 ng/ml/kg vs. 1.07 +/- 0.2 ng/ml/kg, p = 0.02, respectively) or those found in controls. In type 2 diabetic patients, leptin concentrations were correlated with body mass index and body fat, and in myotonic dystrophic patients leptin concentrations were correlated with age, body mass index, fasting insulin and lower insulin sensitivity, whereas leptin concentrations were not correlated with body fat. CONCLUSIONS: These findings suggest that leptin concentrations and regulation in myotonic dystrophic patients are different from type 2 diabetes.     

Racial differences in lipid metabolism in women with abdominal obesity

We evaluated palmitate rate of appearance (R(a)) in plasma during basal conditions and during a four-stage epinephrine infusion plus pancreatic hormonal clamp in nine white and nine black women with abdominal obesity, who were matched on fat-free mass, total and percent body fat, and waist-to-hip circumference ratio. On the basis of single-slice magnetic resonance imaging analysis, black women had the same amount of subcutaneous abdominal fat but less intra-abdominal fat than white women (68 +/- 9 vs. 170 +/- 14 cm(2), P < 0.05). Basal palmitate R(a) was lower in black than in white women (1.95 +/- 0.26 vs. 2.88 +/- 0.23 micromol. kg fat-free mass(-1). min(-1), P < 0.005), even though plasma insulin and catecholamine concentrations were the same in both groups. Palmitate R(a) across a physiological range of plasma epinephrine concentrations remained lower in black women, because the increase in palmitate R(a) during epinephrine infusion was the same in both groups. We conclude that basal and epinephrine-stimulated palmitate R(a) is lower in black than in white women with abdominal obesity. The differences in basal palmitate kinetics are not caused by alterations in plasma insulin or catecholamine concentrations or lipolytic sensitivity to epinephrine. The lower rate of whole body fatty acid flux and smaller intra-abdominal fat mass may have clinical benefits because of the relationship between excessive fatty acid availability and metabolic diseases.     

Insulin-like growth factor binding protein 1 (IGFBP-1) levels in Turner syndrome.

We tested whether IGFBP-1, a modulator of IGF-I action, would play a role in the pathogenesis of growth failure and metabolic picture of Turner syndrome. Fasting serum levels of IGFBP-1 were assessed in nineteen girls with Turner syndrome (aging 6.5 to 17.2 years) by radioimmunoassay. Our patients showed normal values of IGFBP-1 (mean +/- SD: 68.6 +/- 32.5 micrograms/l, range: 16 to 134 micrograms/l; range for age and pubertal stage-matched normal children: 15 to 180 micrograms/l). IGFBP-1 levels inversely correlated with bone age (p < 0.05), weight (p < 0.001), percentage of ideal body weight (p < 0.002) and body mass index (BMI) (p < 0.001). Our results seem to rule out a role of IGFBP-1 in the pathogenesis of growth failure in Turner syndrome. The close inverse relationship between IGFBP-1 levels and BMI suggests the serum concentrations of IGFBP-1 to be regulated by the nutritional status. Due to IGFBP-1 inhibiting action on IGF biological activity, the reduction of IGFBP-1 levels in overweight subjects might represent a mechanism to enhance the IGF insulin-like activity, thus supplementing the insulin action.     

Plasma adiponectin concentration in healthy pre- and postmenopausal women: relationship with body composition, bone mineral, and metabolic variables

The aim of the current investigation was to determine the possible relationships of fasting adiponectin level with body composition, bone mineral, insulin sensitivity, leptin, and cardiorespiratory fitness parameters in 153 women. Subjects were classified as premenopausal (n = 42; 40.8 +/- 5.7 yr) if they had regular menstrual periods, early postmenopausal (n = 49; 56.7 +/- 3.6 yr) if they had been postmenopausal for more than >1 yr but <7 yr (5.5 +/- 1.3 yr), and postmenopausal (n = 62; 72.2 +/- 4.5 yr) if they had been postmenopausal for >7 yr. All women studied had a body mass index (BMI) <30 kg/m(2). Adiponectin values were higher (P < 0.05) in middle-aged (12.0 +/- 5.1 microg/ml) and older (15.3 +/- 7.3 microg/ml) postmenopausal women compared with middle-aged premenopausal women (8.4 +/- 3.2 microg/ml). Mean plasma adiponectin concentration in the total group of women (n = 153) was 12.2 +/- 6.3 microg/ml and was positively related (P < 0.05) to age, indexes of overall obesity (BMI, body fat mass), and cardiorespiratory fitness (PWC) values. In addition, a negative association (P < 0.05) between adiponectin with central obesity (waist-to-hip and waist-to-thigh ratio), fat-free mass, bone mineral (bone mineral content, total and lumbar spine bone mineral density), and leptin and insulin resistance (insulin, fasting insulin resistance index) values was observed. However, multivariate regression analysis revealed that only age, fasting insulin resistance index, and leptin were independent predictors of adiponectin concentration. In conclusion, circulating adiponectin concentrations increase with age in normal-weight middle-aged and older women. It appears that adiponectin is independently related to age, leptin, and insulin resistance values in women across the age span and menstrual status.     

Blunted lipolysis and fatty acid oxidation during moderate exercise in HIV-infected subjects taking HAART

The protease inhibitor (PI) ritonavir (RTV) has been associated with elevated resting lipolytic rate, hyperlipidemia, and insulin resistance/glucose intolerance. The purpose of this study was to examine relationships between lipolysis and fatty acid (FA) oxidation during rest, moderate exercise and recovery, and measures of insulin sensitivity/glucose tolerance and fat redistribution in HIV-positive subjects taking RTV (n=12), HAART but no PI (n=10), and HIV-seronegative controls (n=10). Stable isotope tracers [1-(13)C]palmitate and [1,1,2,3,3-(2)H5]glycerol were continuously infused with blood and breath collection during 1-h rest, 70-min submaximal exercise (50% VO2 peak), and 1-h recovery. Body composition was evaluated using DEXA, MRI, and MRS, and 2-h oral glucose tolerance tests with insulin monitoring were used to evaluate glucose tolerance and insulin resistance. Lipolytic and FA oxidation rates were similar during rest and recovery in all groups; however, they were lower during moderate exercise in both HIV-infected groups [glycerol Ra: HIV+RTV 5.1+/-1.2 vs. HIV+no PI 5.9+/-2.8 vs. Control 7.4+/-2.2 micromol.kg fat-free mass (FFM)-1.min-1; palmitate oxidation: HIV+RTV 1.6+/-0.8 vs. HIV+no PI 1.6+/-0.8 vs. Control 2.5+/-1.7 micromol.kg FFM.min, P<0.01]. Fasting and orally-challenged glucose and insulin values were similar among groups. Lipolytic and FA oxidation rates were blunted during moderate exercise in HIV-positive subjects taking HAART. Lower FA oxidation during exercise was primarily due to impaired plasma FA oxidation, with a minor contribution from lower nonplasma FA oxidation. Regional differences in adipose tissue lipolysis during rest and moderate exercise may be important in HIV and warrant further study.     

Turner syndrome, insulin sensitivity and growth hormone treatment

Mild insulin resistance appears to be an early metabolic defect in girls with Turner syndrome (TS). Impaired glucose tolerance has been reported in 10-34% of patients with TS, and type 2 diabetes mellitus is 2-4 times more common and occurs at a younger age in girls with TS than in the general population. In a mixed longitudinal and cross-sectional study, we analysed carbohydrate tolerance and insulin sensitivity in 46 children and adolescents with TS who reached their final height after long-term treatment (mean 6.3 +/- 2.5 years) with growth hormone (GH: 0.33 mg/kg/week [0.05 mg/kg/day]), and in 36 of these patients who were followed-up after the cessation of GH therapy (mean follow-up, 2.6 +/- 2.5 years; range, 1-9.5 years). Patients with TS were compared with an age-matched female control group. Insulin sensitivity appeared to be lower in patients with TS than in controls, even before the start of GH therapy. As in controls, insulin sensitivity decreased with age in patients with TS, and levels were lower in those aged >12 years than in those aged <12 years. GH therapy resulted in good catch-up growth in patients with TS, with final height significantly higher than projected height evaluated before the initiation of GH therapy. Insulin sensitivity increased after 7-8 years of therapy and, on the cessation of GH therapy, returned to pre-treatment levels. The increase in insulin sensitivity seen on the cessation of GH therapy appeared to be influenced negatively by body mass index and triglyceride levels, and correlated positively with the number of years since cessation of GH therapy. As in the general population, excess weight and an abnormal lipid profile, in particular excess triglyceride levels, worsened insulin sensitivity. In conclusion, our study confirms that GH therapy reduces insulin sensitivity, but at its cessation there is a return to pre-therapy values. We therefore report a progressive improvement in carbohydrate tolerance and insulin function in patients with TS, despite an increase in age.     

The effect of weight loss on serum concentration of interleukine-6 (IL-6) and insulin resistance

INTRODUCTION: Interleukine-6 (IL-6) is one of the cytokines, excreting by adipocytes, which increases in obesity. These cytokines participate in very complicated mechanisms of developing insulin resistance that accompany obesity. The aim of the study was to: 1) evaluate the influence of weight loss on insulin resistance and serum concentration of IL-6, 2) evaluate the hypothetical association between serum concentration of IL-6 and the improvement of insulin sensitivity in obese women after weight loss. MATERIAL AND METHODS: The study involved 27 obese women (age 40.3 +/- 11.1 year; BMI 37.4 +/- 5.2 kg/m(2)) with insulin resistance diagnosed using HOMA index, without concomitant diseases and without any medication. All the patients participated in complex weight reduction treatment (diet, physical activity and psychotherapy). Before and after weight reduction therapy weight and height were measured, body composition was determined using bioimpedance analysis. Serum concentration of glucose was determined by enzymatic procedure, serum concentration of insulin was measured by radioimmunoassay, serum concentration of IL-6 was measured by ELISA. HOMA index was calculated with formula. RESULTS: The mean weight loss after 3-month was 9.2 +/- 4.5 kg (approximately 10% of initial weight). After weight reduction significant decreases in HOMA index, insulin and IL-6 concentrations was observed. However, no correlations between changes in insulin concentrations, HOMA index and decrease of IL-6 concentration were showed. We observed significant correlations between DeltaHOMA and DeltaBMI (r = 0.48; p = 0.012) and Delta percentage fat mass (r = 0.39; p < 0.05). CONCLUSIONS: A moderate weight loss improves insulin sensitivity and decreases serum concentrations of IL-6. However improvement of insulin sensitivity is the effect of fat mass reduction and does not change serum concentration of IL-6.     

Effects of HRT and exercise training on insulin action, glucose tolerance, and body composition in older women.

The independent and combined effects of exercise training and hormone replacement therapy (HRT) on body composition, fat distribution, glucose tolerance, and insulin action were studied in postmenopausal women, aged 68 +/- 5 yr, assigned to control (n = 19), exercise (n = 18), HRT (n = 15), and exercise + HRT (n = 16) groups. The exercise consisted of 2 mo of flexibility exercises followed by 9 mo of endurance exercise. HRT was conjugated estrogens 0.625 mg/day and trimonthly medroxyprogesterone acetate 5 mg/day for 13 days. Total and regional body composition were measured by dual-energy X-ray absorptiometry. Serum glucose and insulin responses were measured during a 2-h oral glucose tolerance test. There were significant main effects of exercise on reductions in total and regional (trunk, arms, legs) fat mass, increase in leg fat-free mass, and improvements in glucose tolerance and insulin action. There were significant main effects of HRT on the reduction of total fat mass (HRT, -3.0 +/- 4.0 kg; no HRT, -1.3 +/- 2.6 kg), with a strong trend for reductions in trunk and leg fat mass (both P = 0.07). There was also a significant improvement in insulin action in response to HRT. These results suggest that there are independent and additive effects of exercise training and HRT on the reduction in fat mass and improvement in insulin action in postmenopausal women; the effect of HRT on insulin action may be mediated, in part, through changes in central adiposity.     

Insulin sensitivity measured with the minimal model is higher in moderately overweight women with predominantly lower body fat.

Lower-body obesity is associated with a lower incidence of diabetes and high values of HDL2 cholesterol and thus seems to have a metabolic profile opposite to upper-body obesity. We measured insulin sensitivity by the minimal model procedure in 20 lower-body overweight women (age 40.3+/-2.3 years, waist-to-hip ratio WHR 0.75+/-0.01, body mass index BMI 29.9+/-0.7 kg/m2), compared to 18 women with a similar degree of upper-body obesity (age 40.4+/-3years, WHR 0.91+/-0.02, BMI 29.4+/-0.7 kg/m2) and 28 control women matched for age and height. Insulin sensitivity and basal insulin effect were higher in lower-body obesity (11.2+/-0.2 min-1/[microU/ml]x 10(-4) and 0.8+/-0.2 min(-1) x 10(-2), respectively) compared to upper-body obesity (2.6+/-0.4, p < 0.001 and 0.3+/-0.05, p < 0.01) and controls (6.1+/-0.7, p < 0.02 and 0.5+/-0.07, p < 0.02). It is suggested that lower-body obesity could be associated with a reduced free fatty acids-induced inhibition of insulin action by the Randle mechanism. This study confirms that body fat distribution is a more relevant determinant than obesity itself in the pathogenesis of insulin resistance. Contrary to upper-body obesity, moderate lower-body overweight seems to be associated with high values on insulin sensitivity.     

Improvements in cardiovascular risk profile with large-volume liposuction: a pilot study

In this study, the authors investigated the physiologic effects of the altered body composition that results from surgical removal of large amounts of subcutaneous adipose tissue. Fourteen women with body mass indexes of greater than > 27 kg/m2 underwent measurements of fasting plasma insulin, triglycerides, cholesterol, body composition by dual-energy x-ray absorptiometry (DXA), resting energy expenditure, and blood pressure before and after undergoing large-volume ultrasound-assisted liposuction.There were no significant intraoperative complications. Body weight had decreased by 5.1 kg (p < 0.0001) by 6 weeks after liposuction, with an additional 1.3-kg weight loss (p < 0.05) observed between 6 weeks and 4 months after surgery, for a total weight loss of 6.5 kg (p < 0.00006). Body mass index decreased from (mean +/- SEM) 28.8 +/- 2.3 to 26.8 +/- 1.5 kg/m2 (p < 0.0001). This change in body weight was primarily the result of decreases in body fat mass: as assessed by DXA, lean body mass did not change (43.8 +/- 3.1 kg to 43.4 +/- 3.6 kg, p = 0.80), whereas DXA total body fat mass decreased from 35.7 +/- 6.3 to 30.1 +/- 6.5 kg (p < 0.0001). There were significant decreases in fasting plasma insulin levels (14.9 +/- 6.5 mIU/ml before liposuction versus 7.2 +/- 3.2 mIU/ml 4 months after liposuction, p < 0.007), and systolic blood pressure (132.1 +/- 7.2 versus 120.5 +/- 7.8 mmHg, p < 0.0002). Total cholesterol, high-density lipoprotein cholesterol, plasma triglycerides, and resting energy expenditure values were not significantly altered after liposuction.In conclusion, over a 4-month period, large-volume liposuction decreased weight, body fat mass, systolic blood pressure, and fasting insulin levels without detrimental effects on lean body mass, bone mass, resting energy expenditure, or lipid profiles. Should these improvements be maintained over time, liposuction may prove to be a valuable tool for reducing the comorbid conditions associated with obesity.     

Thyroid volume as measured by ultrasonography in patients With type 1 diabetes mellitus without thyroid dysfunction.

The aim of this cross-sectional study was to assess and compare thyroid volume and its derminants in a cohort of type 1 diabetes mellitus (DM1) and compare the results to a healthy control group. We studied 65 DM1 patients treated with an intensive insulin regimen and 65 matched controls. In all participants we evaluated weight, height, BMI, waist-hip ratio, body surface area and body composition variables determined by using a bioelectrical impedance analyser. Thyroid size was estimated by ultrasonography. We determined basal TSH, anti-thyroid antibodies and urinary iodine excretion. Body weight, height, BMI and body surface area were similar in DM1 patients and in controls. Fat-free mass was higher in both male and female DM1 patients than in controls (64.4 +/- 6.9 vs. 60.4 +/- 8.2 kg, p=0.03 and 48.3 +/- 5.7 vs. 45.4 +/- 6, p=0.04, respectively), and fat mass was lower in male DM1 patients than in controls (9.7 +/- 7 vs. 14.2 +/- 8.1 kg, p=0.01). Thyroid volume was greater in both male and female DM1 patients than in controls (11.12 +/- 2.87 vs. 9.63 +/- 2.27 ml, p=0.0001 and 9.5 +/- 2.3 vs. 7.7 +/- 2 ml, p=0.002, respectively). Urinary iodine excretion was similar in the two groups. In both DM1 patients and controls, thyroid volume correlated with weight, height, BMI, waist-hip ratio, body surface area, fat-free mass and the multivariate linear regression analysis with thyroid volume as the dependent variable showed that fat-free mass in either group was the only significant determinant of thyroid volume. We conclude that DM1 patients had larger thyroid volume compared with healthy controls with similar anthropometry; body composition is different in DM1 patients and that the anthropometric and body composition variables, especially fat-free mass and body surface area, predict thyroid volume either in DM1 patients or in healthy controls.     

Insulin-like growth factor-1, leptin, body composition, and clinical status interactions in children with cystic fibrosis

BACKGROUND/AIMS: Children with cystic fibrosis (CF) are of increased risk of reduced fat body mass (FBM) and lean body mass (LBM). Serum concentrations of insulin-like growth factor-1 (IGF-1)and leptin could be markers of LBM and/or FBM depletion. To evaluate the relationships between disease activity, body composition, IGF-1 and leptin concentrations in CF children. METHODS: A cross-sectional study with 26 CF children aged 5.0-15.5 years and 33 healthy controls, mean age 9.4 years. Body composition was evaluated by dual-energy X-ray absorptiometry. Fasting blood samples were analyzed for leptin, IGF-1 and IGFBP-3. RESULTS: FBM standard deviation score (SDS; CF boys -0.02 +/- 0.88 vs. 0.78 +/- 0.65, p < 0.01; CF girls -0.37 +/- 1.15 vs. 0.70 +/- 0.97, p < 0.05), leptin concentration (CF boys 2.07 +/- 0.79 vs. 3.07 +/- 1.28 ng/ml, p < 0.05; CF girls 2.71 +/- 0.86 vs. 5.00 +/- 2.95 ng/ml, p < 0.05) and IGF-1SDS (CF boys -1.43 +/- 1.50 vs. -0.32 +/- 0.88, p < 0.05; CF girls -0.66 +/- 1.66 vs. 0.64 +/- 0.57, p < 0.01) were lower in CF children compared to controls. Shwachman score was the strongest predictor of lean body mass (R = 0.63). Leptin levels explain 60% of the variability in FBM. CONCLUSION: Serum concentrations of IGF-1 and leptin are decreased in children with CF and are associated with clinical conditions and body composition.     

Short-term fasting abolishes the sex-related difference in GH and leptin secretion in humans

We studied growth hormone (GH) and leptin secretion in eight male (age 29.3 +/- 1.2 yr, body mass index 22.2 +/- 0.5 kg/m(2)) and seven female normal subjects (28.0 +/- 0.8 yr, 20.1 +/- 0.7 kg/m(2)) before and after 36 h of fasting. In the fed state, 8-h mean GH and leptin concentrations were higher in females (P < 0.05 and P < 0. 0001, respectively). Fasting increased GH and decreased leptin in both sexes. There was significant interaction between gender and fasting (P < 0.05 for GH and P < 0.005 for leptin). Females showed a slighter increase in GH but a more marked decrease in leptin, so that there was no significant gender-related difference in GH and leptin after fasting. Fasting did not modify insulin-like growth factor (IGF) I, IGF binding protein (IGFBP)-3, acid-labile subunit, or GH binding protein; increased IGFBP-1 and free fatty acids (P < 0.0001) but decreased glucose (P < 0.001) and insulin levels (P < 0.05). In males, insulin levels were higher (P < 0.05) in the fed state and underwent deeper reduction after fasting (interaction P < 0.03). In conclusion, GH and leptin secretions are higher in women than in men in the fed but not in the fasting condition, which abolishes these gender-related differences in humans.     

Hyperinsulinemia and insulin insensitivity in women with nonclassical congenital adrenal hyperplasia due to 21-hydroxylase deficiency: the relationship between serum leptin levels and chronic hyperinsulinemia

BACKGROUND/AIM: Nonclassical congenital adrenal hyperplasia due to 21-hydroxylase deficiency (NC-CAH) is associated with hyperandrogenemia, chronic anovulation, hirsutism, acne and adrenal hyperplasia. A few studies have shown hyperinsulinemia and insulin insensitivity in NC-CAH. Hyperinsulinemia can stimulate leptin secretion, and androgens can inhibit leptin secretion. Thus, we designed a study to investigate the insulin levels and insulin sensitivity and the effect of chronic endogenous hyperinsulinemia and androgens on leptin in patients with NC-CAH. METHODS: Eighteen women with untreated NC-CAH and 26 normally cycling control women with a similar body mass index (BMI) were studied. Basal hormones, fasted and fed insulin levels, leptin and stimulated 17-hydroxyprogesterone (17-OHP) concentrations were studied. Homeostasis model assessment was used to assess insulin sensitivity. RESULTS: The basal 17-OHP, the free testosterone (fT) and dehydroepiandrosterone sulfate (DHEA-S) were significantly different in the 2 groups (p < 0.05). Fasting and fed insulin levels of the NC-CAH group were higher than those of the control group (p < 0.05) and insulin sensitivity was lower in NC-CAH than in controls (p < 0.05). Insulin levels were correlated with fT and 17-OHP (p < 0.05). Serum leptin levels for NC-CAH (25.9 +/- 12.5 microg/l) did not differ from the controls (25.4 +/- 12.06 microg/l) and were positively correlated with BMI (r = 0.725) and percent body fat (r = 0.710) for both groups (both p < 0.001). Leptin levels were not correlated with estrogen or androgens, gonadotropins or insulin levels. CONCLUSION: Hyperinsulinemia and insulin insensitivity associated with hyperandrogenism were detected in untreated NC-CAH patients as in previous reports, whereas serum leptin levels did not differ from those of controls.     

Comparison of short-term diet and exercise on insulin action in individuals with abnormal glucose tolerance.

The effects of a 10-day low-calorie diet (LCD; n = 8) or exercise training (ET; n = 8) on insulin secretion and action were compared in obese men (n = 9) and women (n = 7), aged 53 +/- 1 yr, with abnormal glucose tolerance by using a hyperglycemic clamp with superimposed arginine infusion and a high-fat drink. Body mass (LCD, 115 +/- 5 vs. 110 +/- 5 kg; ET, 111 +/- 7 vs. 109 +/- 7 kg; P < 0. 01) and fasting plasma glucose (LCD, 115 +/- 10 vs. 99 +/- 4 mg/dl; ET, 112 +/- 4 vs. 101 +/- 5 mg/dl, P < 0.01) and insulin (LCD, 23.9 +/- 5.6 vs. 15.2 +/- 3.9 microU/ml; ET, 17.6 +/- 1.9 vs. 13.9 +/- 2. 4 microU/ml; P < 0.05) decreased in both groups. There was a 40% reduction in plasma insulin during hyperglycemia (0-45 min) after LCD (peak: 118 +/- 18 vs. 71 +/- 14 microU/ml; P < 0.05) and ET (69 +/- 14 vs. 41 +/- 7 microU/ml; P < 0.05) and trends for reductions during arginine infusion and a high-fat drink. The 56% increase in glucose uptake after ET (4.95 +/- 0.90 vs. 7.74 +/- 0.82 mg. min-1. kg fat-free mass-1; P < 0.01) was significantly (P < 0.01) greater than the 19% increase (5.72 +/- 1.12 vs. 6.80 +/- 0.94 mg. min-1. kg fat-free mass-1; P = not significant) that occurred after LCD. The marked increase in glucose disposal after ET, despite lower insulin levels, suggests that short-term exercise is more effective than diet in enhancing insulin action in individuals with abnormal glucose tolerance.     

Insulin resistance (HOMA) in relation to plasma cortisol,IGF-I and IGFBP-3. A study in normal short-statured and GH-deficient children

OBJECTIVE: To investigate the possible contribution of plasma cortisol and growth hormone (GH) as reflected by insulin-like growth factor-I (IGF-I)/insulin-like growth factor-binding protein-3 (IGFBP-3) on insulin action in short-statured children. METHODS: In this study, insulin resistance (HOMA) was determined in 34 normal short-statured (age 9.4 +/- 3.5 years) and in 19 GH-deficient children (age 10.4 +/- 2.2 years). HOMA was examined in relation to fasting plasma cortisol, IGF-I, IGFBP-3 and in addition to birthweight and body mass index (BMI). RESULTS: Birthweight was not correlated to insulin resistance. In GH-deficient children, BMI was significantly augmented and was associated with HOMA (p < 0.02). In both groups of patients, fasting plasma cortisol was related to HOMA (normal: r = 0.295, p < 0.05, GH-deficient: r = 0.495, p < 0.02). Only in normal short-statured children IGF-I (r = 0.338, p < 0.03) and IGFBP-3 (r = 0.493, p < 0.002) were associated with insulin resistance. CONCLUSION: The results indicated that at a young age cortisol contributed to insulin resistance in short-statured children. In normal short-statured children HOMA was associated with IGF-I and IGFBP-3. Possibly GH, a known cause of insulin resistance, contributed to HOMA as IGF-I and IGFBP-3 do not mediate insulin resistance but reflect growth hormone secretion. The results in GH-deficient children supported this conclusion as in the absence of GH insulin resistance was not associated with IGF-I/IGFBP-3.     

Fat mass deposition during pregnancy using a four-component model.

Estimates of body fat mass gained during human pregnancy are necessary to assess the composition of gestational weight gained and in studying energy requirements of reproduction. However, commonly used methods of measuring body composition are not valid during pregnancy. We used measurements of total body water (TBW), body density, and bone mineral content (BMC) to apply a four-component model to measure body fat gained in nine pregnant women. Measurements were made longitudinally from before conception; at 8-10, 24-26, and 34-36 wk gestation; and at 4-6 wk postpartum. TBW was measured by deuterium dilution, body density by hydrodensitometry, and BMC by dual-energy X-ray absorptiometry. Body protein was estimated by subtracting TBW and BMC from fat-free mass. By 36 wk of gestation, body weight increased 11.2 +/- 4.4 kg, TBW increased 5.6 +/- 3.3 kg, fat-free mass increased 6.5 +/- 3.4 kg, and fat mass increased 4.1 +/- 3.5 kg. The estimated energy cost of fat mass gained averaged 44,608 kcal (95% confidence interval, -31, 552-120,768 kcal). The large variability in the composition of gestational weight gained among the women was not explained by prepregnancy body composition or by energy intake. This variability makes it impossible to derive a single value for the energy cost of fat deposition to use in estimating the energy requirement of pregnancy.