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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Both genetic and environmental factors contribute to adolescent obesity. Evidence of a genetic basis for obesity development is substantial, although the exact mechanism of action has yet to be identified. The purpose of this study was to document the circadian rhythmicity of the serum leptin level in young females and to assess the impact of the change in body fat stores during growth on the nocturnal rise in the serum leptin level with implications for obesity traits. There was a significant rise in serum leptin at midnight and 0400 h, suggesting a diurnal variation in serum leptin concentrations (ANOVA F ratio = 6.2; P < 0.0001). There was also a strong association between relative total body fat and the average daytime serum leptin level (r = 0.78; P < 0.0001). The percent increase in the nocturnal leptin concentration was inversely related to the percent gain in total body fat (r = 0.45; P < 0.024). Forward stepwise regression analysis selected the change in total body fat over a 6-month interval as the most powerful determinant of the percent increase in the nocturnal leptin concentration (partial R2 = 0.203; beta = -0.450; SE of beta = 0.186; t = -2.418; P < 0.024). If the lack of a nocturnal rise in serum leptin persists over a longer period of time, it may have implications for the development of obesity, presumably by inadequate suppression of nighttime appetite.
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PMID:Gain in body fat is inversely related to the nocturnal rise in serum leptin level in young females. 914 17

The effect of gender and degree of obesity on the size indicators V, used to normalize urea clearance (Kt/Vur), and body surface area (BSA), used to normalize creatinine clearance (Ccr), in peritoneal dialysis was studied by: (1) mathematical comparison of the formulae used to estimate V (Watson and Hume) with the Dubois formula used to estimate BSA in peritoneal dialysis; and (2) comparison of percent deviation of BSA (delta BSA%) and V (delta V%) from ideal weight estimates in 933 clearance studies performed in actual patients (555 in men and 378 in women on continuous ambulatory peritoneal dialysis). V was estimated by the Watson formulae and BSA by the Dubois formula in these studies. delta BSA% and delta V% were stratified in 10% increments in deviation of body weight from ideal (delta W%) in these studies. Mathematically, the relationship between V and BSA is not linear. In the same subject, as obesity develops (delta W% increases) and BSA increases in a linear manner, V increases exponentially. In addition, there are substantial differences in the relationship between V and BSA caused by gender. For the same height and BSA, men have a larger V than women. In the clearance studies performed in actual continuous ambulatory peritoneal dialysis patients, the difference between delta V% and delta BSA% increased significantly (P < 0.0001) from the wasted to the obese subjects by one-way ANOVA in both men and women. Normalization of urea and creatinine clearances by different size indicators creates two types of mathematical distortion in the relationship between the two clearances. One distortion is caused by the degree of obesity. The second distortion is caused by gender. Use of the same size indicator to normalize both urea and creatinine clearances would eliminate these distortions.
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PMID:Gender, degree of obesity, and discrepancy between urea and creatinine clearance in peritoneal dialysis. 951 14

Obese women are associated with clinical symptoms suggestive of abnormal reproductive functions including irregular menses and infertility. Previous studies of gonadotropin release in obese women, basal or after luteal hormone releasing hormone (LHRH) stimulation, are controversial. Obese women are also often characterized by glucose intolerance and hyperinsulinemia which might relate to their excessive body fat. To understand the link between abnormal gonadotropin release, carbohydrate metabolism and percent body fat, we examined 17 premenopausal morbid obese women with body mass index (BMI) 38.7 +/- 1.6 Kg/m2 (mean +/- SEM) and 16 age-matched lean controls with BMI 19.7 +/- 0.6 Kg/m2. Plasma glucose, insulin and C-peptide values were measured before and 30, 60, 90 and 120 min after a 75 gm oral glucose tolerant test (OGTT). Each individual also received LHRH test which involved determinations of serum LH and FSH values at basal, 15, 30 and 60 min after injection of LHRH for 0.1 mg intravenously. Women with morbid obesity had significantly greater responses of glucose, insulin and C-peptide values as compared with lean women (all p < 0.001, two-way ANOVA). Despite that basal concentrations were not different, serum LH, FSH and ratio of LH to FSH values in response to LHRH test showed significantly lesser increase in obese women than lean controls. Percent body fat, determined by bioelectrical impedance analysis, correlated positively with plasma glucose, insulin and C-peptide responses to OGTT while negatively with ratio of LH to FSH responses (r = -0.418, p < 0.01) to LHRH test. Body mass index also correlated inversely with ratio of LH to FSH responses (r = -0.472, p < 0.01). In conclusion, morbid obese women had glucose intolerance, hyperinsulinemia and lower responses of serum LH and FSH values as compared with lean women. Excessive body fat play an important role in mediating these carbohydrate and gonadotropin abnormalities.
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PMID:Abnormal gonadotropin release and carbohydrate metabolism in morbid obese women. 955 Dec 49

The alpha2-adrenergic receptors mediate part of the actions of the catecholamines noradrenaline and adrenaline on the regulation of energy balance. As part of an ongoing study on the genetics of obesity, the entire coding sequence of the alpha2B-adrenoceptor gene was screened in 58 obese, nondiabetic Finns by PCR-single stranded conformational analysis (PCR-SSCA). A polymorphism that leads to a deletion of 3 glutamic acids from a glutamic acid repeat element (Glu x 12, amino acids 297-309) present in the third intracellular loop of the receptor protein was identified. This repeat element has previously been shown to be important for agonist-dependent receptor desensitization. Of 166 genotyped subjects, 47 (28%) had 2 normal (long) alleles (Glu12/Glu12), 90 (54%) were heterozygous (Glu12/Glu9), and 29 (17%) were homozygous for the short (Glu9/Glu9) form. The basal metabolic rate, determined by indirect calorimetry and adjusted for fat-free body mass, fat mass, sex, and age, was 94 Cal/day (5.6%) lower (95% confidence interval for difference, 32, 156) in subjects homozygous for the short allele than in subjects with two long alleles (F = 4.84; P = 0.009, by ANOVA). Thus, a genetic polymorphism of the alpha2B-adrenoceptor subtype can partly explain the variation in basal metabolic rate in an obese population and may therefore contribute to the pathogenesis of obesity.
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PMID:Identification of a three-amino acid deletion in the alpha2B-adrenergic receptor that is associated with reduced basal metabolic rate in obese subjects. 1040 16

In adults, leptin seems to cross the blood-brain barrier by a saturable transporter. This may contribute to the development of obesity. The present study in healthy children investigates leptin levels in plasma and cerebrospinal fluid (CSF) in relation to body constitution. This prospective study analyzed leptin levels in plasma and CSF samples (stored at -80 C) of patients without CNS infection or blood-brain barrier dysfunction. Inclusion criteria included temperature less than 38.5 C, C-reactive protein levels below 10 mg/L, CSF leukocyte levels less than 10(7)/L, no need for neurosurgical or oncological treatment, and no history of trauma. Four groups were designated according to body mass index. Sixty-five children (28 girls and 37 boys) entered the study. Plasma leptin (median) was 7.4 in girls and 2.6 ng/mL in boys., CSF leptin was 0.273 and 0.204 ng/mL, respectively, leading to CSF/plasma ratios of 0.045 and 0.071, respectively. Ratios were clearly dependent on body mass index percentiles (r = -0.484; P < 0.01, significant differences between groups by ANOVA). Median plasma leptin levels in the 4 groups (body mass index, <10th, 10th-50th, 50th-90th, and >90th percentile) were 2.0, 2.3, 4.1, and 8.8 ng/mL; CSF/plasma ratios were inversely related: 8.2%, 7.6%, 5.5% and 3.6%. In healthy children, CSF leptin levels account for approximately 5% of plasma levels. CSF/plasma ratios in girls are lower than those in boys, explaining why calorie intake and energy expenditure are not grossly different despite large differences in circulating plasma leptin concentrations. CSF/plasma ratios of lean children are higher than those in obese children. The dynamic changes in the CSF/plasma ratios are more pronounced in lean children, i.e. the nonlinear transport characteristics of the leptin system amplifies the information about changes in body energy stores in this population, indicating that leptin is part of a mechanism to protect the body from critical weight loss rather than to avoid obesity.
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PMID:Lack of sex difference in cerebrospinal fluid (CSF) leptin levels and contribution of CSF/plasma ratios to variations in body mass index in children. 1048 58

Patterns of eating habits were analyzed to elucidate its relationship to the temporal change of body build from childhood through school age in subjects of the Toyama study. Survey questionnaires at the time of entrance to elementary school were used. Subjects were 6,452 (males 3,293, and females 3,159). Subjects were classified into 6 clusters among the males, 8 clusters among females based on the results of cluster analysis of eating habits. The cluster in males that preferred egg, milk, dairy products, fats, fish and shellfish, soybeans, fruits, green yellow vegetables indicated more frequent subjects whose BMI were less that 14. The cluster in girls that preferred fats indicated more frequent subjects whose BMI were more or equal to 18. The ANOVA showed significant relation of parental body build on their children. Even after grouping by parental body build, the cluster based on patterns of eating habits showed different frequencies of obese children. Preference for intake of milk indicated less frequent obese children among the similar parental body build for boys, while preference for intake of fats indicated more frequent obese children among a similar parental body build for girls. In conclusion, the obesity of a school child has a close relationship to parent's body build. However, the temporal changes of obesity were seen among eating habits clusters even if body builds of their parents are the same. It was shown that patterns of eating habit are important in school children's obesity development.
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PMID:[Relationship of dietary habits pattern and body build of parents to child obesity]. 1054 Aug 52

Insulin resistance is a common feature in obese patients. To evaluate the modifications in insulin sensitivity after a bariatric operation such as Bilio-pancreatic diversion (BPD), three groups of subjects (14 normal controls (N); seven ex-obese patients (X) with at least 2 years at weight-stable conditions after BPD surgery; and eight morbidly obese patients (0)) were studied with intravenous (IVGTT) and oral (OGTT) glucose tolerance tests. The ratio of the area under the curve (AUC) for glucose over that of insulin was used as a measure of insulin sensitivity. All the following tests were conducted as Bonferroni-corrected pairwise t-tests, in case overall ANOVA was significant. No significant difference was found between N and X subjects, while obese patients showed a reduced AUCg/AUCI ratio with respect to the normal controls (O vs N: 0.01164 +/- 0.00039 vs 0.02392 +/- 0.0039, p < 0.05). IVGTT, AUCS: significant differences were found in each case: N vs X: 0.0591 +/- 0.0075 vs 0.1402 +/- 0.0399, p < 0.05; N vs 0:0.0591 +/- 0.0075 vs 0.0223 +/- 0.0031, p < 0.01; X vs 0:0.1402 +/- 0.0399 vs 0.0223 +/- 0.0031, p < 0.05. IVGTT-derived data were also analyzed using the minimal model of glucose kinetics; with this method, glucose effectiveness was significantly different between normal subject and obese subjects (0.0248 +/- 0.00288 Vs 0.00906 +/- 0.00135 per min, p < 0.001). The insulin sensitivity index was not significantly different between normal and ex-obese subjects, while both of these groups were significantly different from obese patients (N vs 0: 12.04 x 10&sup5; +/- 2.61 x 10&sup5; vs 3.29 x 10&sup5; +/- 0.61 x 10&sup5;, p < 0.066; X vs 0: 16.42 x 10&sup5; +/- 4.23 x 10&sup5; vs 3.29 x 10(1)+/- 0.61 x 10&sup5; per min per pM, p < 0.02). In conclusion, the present study indicates that, after a body weight reduction operation capable of almost re-establishing ideal body weight like BPD, obese individuals with a family history of obesity show a normalization of insulin response to glucose load.
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PMID:Normalization of Insulin Sensitivity in the Obese Patient after Stable Weight Reduction with Biliopancreatic Diversion. 1074 75

Obesity and diet affect the incidence and severity of various types of cancer, including colon cancer. It is not known whether obesity, independent of diet, is a risk factor for colon adenocarcinoma. We used azoxymethane (AOM) to induce colon cancer in mature genetically obese male Zucker rats (fa/fa) on low-fat crude diet (LFC, 10% fat) and their lean counterparts (Fa/fa and Fa/fa) on high-fat crude diet (HFC, 40% fat) for three months. At death visible tumors, histopathology, and colonic aberrant crypt (AC) formation were studied by blinded investigators. At death the obese animals were heavier (719 +/- 19 g; mean +/- SEM) than lean animals regardless of diet or genotype (Fa/fa-LFC:451 = 6 g; Fa/fa-HFC:441 +/-10 g; Fa/Fa-HFC:412 +/- 9 g; P < 0.001 vs fa/fa by ANOVA). All AOM-treated rats developed AC, compared to none of the saline-injected controls. Macroscopic adenocarcinoma developed in 8/9 obese rats on LFC (P < 0.001), compared to none in lean rats regardless of diet. Obese rats had significantly more AC (876 +/- 116) than any of the lean rats (Fa/fa-LFC:550 +/- 99; Fa/fa-HFC:325 +/- 37; Fa/Fa-HFC:360 +/- 36; P < 0.05 vs fa/fa). We conclude that obesity more than exposure to high-fat diet was associated with colon carcinogenesis in these rats.
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PMID:Obesity potentiates AOM-induced colon cancer. 1079 50

Insulin resistance has been described as a possible underlying link for the clustering of Type 2 diabetes mellitus, hypertension, obesity, and dyslipidemia, known as the metabolic syndrome. Mutations within the insulin receptor have been associated with hypertension in some white and Oriental populations. We examined the relationship between the insulin receptor NsiI restriction fragment-length polymorphism (RFLP) and biochemical and anthropometric parameters associated with these disorders in 933 Chinese subjects. Of the 933 subjects, 117 were control subjects and 816 had one or more components of the metabolic syndrome: 59.7% hypertension, 64.6% glucose intolerance, 55.3% dyslipidemia, and 53.3% obesity. The prevalences of the N1 allele and N1N1 genotype were 74.4% and 55.8%, respectively, in the whole population. No differences were observed in the genotype and allele frequency distributions between the control group and the cohorts with glucose intolerance, hypertension, or dyslipidemia alone or in combination. Using one-way ANOVA, there was a weak relationship between the insulin receptor genotypes and diastolic blood pressure (DBP), P = .069. The DBP was significantly higher in subjects carrying the N1N1 genotype in both the total population (80 +/- 13 v 76 +/- 12 mm Hg, P = .038) and subjects with glucose intolerance (80 +/- 12 v 76 +/- 10 mm Hg, P = .048). Using stepwise multiple regression, the insulin receptor NsiI polymorphism was found to be an independent predictor of DBP in this Chinese population, P = .018. Age, gender, and body mass index (BMI) were also included in the analysis and were all significantly associated with diastolic DBP. To conclude, the insulin receptor gene NsiI RFLP is associated with DBP in these Chinese subjects.
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PMID:An insulin receptor gene polymorphism is associated with diastolic blood pressure in Chinese subjects with components of the metabolic syndrome. 1093 64

Many women associate one or more of their pregnancies with the development of adult obesity. Such an association has not been fully explored. This longitudinal study examines the changes in maternal anthropometric indices during pregnancy and postpartum. Seventy-seven pregnant subjects were investigated longitudinally at about 13, 25 and 36 weeks gestation, of whom forty-seven continued taking part into the postpartum period. Maternal weight, height and skinfold thickness (triceps, biceps, subscapular, suprailiac and mid thigh) were measured at each visit. Maternal fat mass was estimated from the conversion of the first four skinfold thicknesses. Maternal waist and hip circumferences were also measured at the first visit and 6 weeks and 6 months postpartum. Weight and fat gain during pregnancy (13-36 weeks gestation) was 10.9 (SD 4.7) kg and 4.6 (SD 3.3) kg (P < 0.001) respectively. A significant increase in fat mass from 13 weeks gestation to 6-months postpartum was observed (2.6 (SD 4.5), P < 0.001). The increased weight at 6-months postpartum, however, was not statistically significant (1.1 (SD 6.0) kg, P = 0.20). Based on BMI in early pregnancy, the subjects were divided into groups of underweight, normal weight, overweight and obese. The last three groups were compared using ANOVA. The obese group showed a significant difference in the pattern of changes in the skinfold thickness, waist:hip ratio and fat mass at the postpartum period, in comparison with the other two groups. In conclusion, there is a tendency in the obese group to develop central obesity at the postpartum period.
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PMID:A longitudinal study of maternal anthropometric changes in normal weight, overweight and obese women during pregnancy and postpartum. 1096 Nov 65


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