Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of ACP1 phenotype on birth weight, neonatal jaundice, and obesity in children are dependent on ADA genotype. These phenomena may represent a clinical counterpart of the in vitro biochemical interactions between the two systems recently observed by our group.
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PMID:Interaction at clinical level between erythrocyte acid phosphatase and adenosine deaminase genetic polymorphisms. 273 33

The effects of polymorphism of aldehyde dehydrogenase (ALDH) and obesity (body weight/lean body mass) on the rate of ethanol elimination were studied. One hundred and forty subjects of healthy Japanese male volunteers who ingested 0.4 g/kg of ethanol were divided into two groups, i.e., a normal ALDH group with a low Km isozyme of ALDH and a deficient group. They were further divided into three groups in which the obesity increased in the order group A, B, C. Ethanol elimination (ER) and beta were significantly higher in the normal ALDH group than in the deficient group. In the normal ALDH subjects, beta of group C(0.187 mg/ml/hr) was higher than that of group B(0.155 mg/ml/hr). No difference in ER was observed among the three groups of the obesity in each ALDH group. Distribution volume of ethanol, r, estimated by Watson's method (0.65 to 0.89) was more accurate than Widmark's r(0.5 to 1.00). Ethanol elimination rate in the normal ALDH subjects was greater than that in Caucasian reported by other authors. Body weight was correlated well with liver weight in 135 autopsy materials.
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PMID:Individual and ethnic differences in ethanol elimination. 342 6

Chromosomal synteny between the mouse model and humans was used to map a gene for the complex trait of obesity. Analysis of NZB/BINJ x SM/J intercross mice located a quantitative trait locus (QTL) for obesity on distal mouse chromosome 2, in a region syntenic with a large region of human chromosome 20, showing linkage to percent body fat (likelihood of the odds [LOD] score 3.6) and fat mass (LOD score 4.3). The QTL was confirmed in a congenic mouse strain. To test whether the QTL contributes to human obesity, we studied linkage between markers located within a 52-cM region extending from 20p12 to 20q13.3 and measures of obesity in 650 French Canadian subjects from 152 pedigrees participating in the Quebec Family Study. Sib-pair analysis based on a maximum of 258 sib pairs revealed suggestive linkages between the percentage of body fat (P < 0.004), body mass index (P < 0.008), and fasting insulin (P < 0.0005) and a locus extending approximately from ADA (the adenosine deaminase gene) to MC3R (the melanocortin 3 receptor gene). These data provide evidence that a locus on human chromosome 20q contributes to body fat and insulin in a human population, and demonstrate the utility of using interspecies syntenic relationships to find relevant disease loci in humans.
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PMID:Identification of an obesity quantitative trait locus on mouse chromosome 2 and evidence of linkage to body fat and insulin on the human homologous region 20q. 927 42

Metformin often promotes weight loss in patients with obesity with non-insulin-dependent diabetes mellitus (NIDDM). The mechanism may be attributed to decreased food intake. This study has tested the effect of metformin on satiety and its efficacy in inducing weight loss. Twelve diet-treated NIDDM women with obesity were randomly given two dose levels (850 mg or 1700 mg) of metformin or placebo at 0800 for three consecutive days followed by a meal test on the third day on three occasions using a 3x3 Latin square design. The number of sandwich canapes eaten in three consecutive 10-minute periods beginning at 1400 hours was used to quantitate food intake, and the level of subjective hunger was rated just before the sandwich meal with a linear analogue hunger rating scale at 1400 after a 6-hour fast. The prior administration of metformin produced a reduction in calorie intake after each of the two doses of metformin treatment. The 1700-mg metformin dose had the most marked appetite suppressant action. Similarly, hunger ratings were significantly lowered after metformin, and the effect was most pronounced after the administration of 1700 mg of metformin. To assess the efficacy of metformin in reducing bodyweight, 48 diet-treated NIDDM women with obesity who had failed to lose weight by diet therapy were first placed on a 1200-kcal ADA (American Diabetes Association) diet before being randomized to receive either metformin (850 mg) or placebo twice daily in a double-blind fashion for 24 weeks. A 4-week single-blind placebo lead-in period preceded and a 6-week single-blind placebo period followed the 24-week double-blind treatment period. Subjects treated with metformin continued to lose weight throughout 24 weeks of treatment; their mean maximum weight loss was 8 kg greater than that of the placebo group, with corresponding lower HbA1C and fasting blood glucose levels at the end of the active treatment period. These results indicate that metformin decreases calorie intake in a dose-dependent manner and leads to a reduction in bodyweight in NIDDM patients with obesity.
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PMID:Metformin decreases food consumption and induces weight loss in subjects with obesity with type II non-insulin-dependent diabetes. 952 70

A highly prevalent, atypical genotype in low Km aldehyde dehydrogenase (ALDH2) may influence alcohol-induced liver injury because of higher production of acetaldehyde in the liver. In the present study, we examined relationships between the ALDH2 genotype, alcohol intake, and liver-function biomarkers among Japanese male workers. Study subjects were 385 male workers in a metal plant in Japan, who were free from hepatic viruses and did not have higher aminotransferase activities (<100). The subjects completed a questionnaire on alcohol drinking habits and other lifestyles. The ALDH2 genotype was determined by the PCR method followed by restriction-enzyme digestion. In the moderately and heavily drinking groups, those with ALDH2*1/*2 exhibited significantly lower levels than those with ALDH2*1/*1 for all three parameters of liver function, whereas no such differences were observed in the least-drinking group. Multiple linear-regression analysis, adjusting for age, obesity, and smoking habits, revealed that aspartate aminotransferase activity was positively associated with alcohol intake only in those with ALDH2*1/*1. On the other hand, alanine transferase activity was negatively associated with alcohol intake only in those with ALDH2*1/*2. The present study indicates that effects of alcohol intake on liver-function biomarkers are likely to be modified by the ALDH2 genotype in adult males.
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PMID:The ALDH2 genotype, alcohol intake, and liver-function biomarkers among Japanese male workers. 1094 5

To assess the usefulness of random capillary plasma glucose (RCPG) measurement in screening for diabetes mellitus in high-risk subjects, a RCPG measurement and a 75-g oral glucose tolerance test (OGTT) were performed in 684 women and 164 men, aged 16-76 years (mean+/-SD: 41.9+/-11.3 years). Risk factors included family history of diabetes in first degree relatives (53.8%), obesity (BMI > or =27 kg/m(2)) in 37.9%, dyslipidemia (78.4%), hypertension, i.e. BP > or =140/90 mmHg (28.5%), and history of gestational diabetes mellitus (16.6%). According to the 1997 ADA/1998 WHO Consultation criteria for a full OGTT, 118 cases (13.9%) were found to have diabetes. Each of 19 cases with RCPG > or =13.3 mmol/l had diabetes according to OGTT, 4.7% of 427 cases with RCPG<6.1 mmol/l had diabetes. Among 402 subjects with RCPG between 6.1 and <13.3 mmol/l, 19.7% were found to have diabetes. Thus, 446 (52.6%) of 848 subjects would have been saved from OGTT if RCPG was used as a screening test, in comparison to 33.1% if the cutpoints for RCPG (12.2 and 5.5 mmol/l) recommended by WHO Study Group (1985)/WHO Consultation (1998) were applied. Therefore, RCPG measurement is a useful screening test for the screening of diabetes mellitus in high-risk subjects.
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PMID:Random capillary plasma glucose measurement in the screening of diabetes mellitus in high-risk subjects in Thailand. 1116 92

In order to demonstrate the effect of family history (FH) coexisting with obesity in insulin resistance (IR) and secretion in subjects at risk for type 2 diabetes, fasting and 2 h post-glucose load serum glucose and insulin concentrations were measured in 143 individuals, 66 men and 77 women, ages ranging from 18 to 68 years, who were considered at risk but were normoglycemic following ADA criteria. Insulin resistance was estimated using HOMA(IR), basal hyperinsulinemia and I(0)/G(0) ratio. Insulin secretion was estimated by means of HOMA(beta-cell), DeltaI(30-0)/DeltaG(30-0) ratio and the insulin concentration at 30 min post-glucose load (I(30)). Disposition index (DI) was calculated to verify if insulin secretion compensate IR. Obesity in males produced an increase in all the parameters indicative of IR in both groups of individuals, with (FH(+)) or without (FH(-)) family history of diabetes, increase that was more pronounced in those FH(-). This effect was not observed in women. The parameters indicative of insulin secretion showed that only in males the presence of FH(+) was responsible for a significant decrease in insulin secretion, mainly expressed as lower values of HOMA(beta-cell) in obese as well as in non-obese. The I(30) and the ratio DeltaI(30-0)/DeltaG(30-0), although lower, did not reach statistical significance. The DI showed that only when obesity and FH were associated the decrease in insulin secretion was not a compensatory response to the IR present in those individuals. In conclusion, normoglycemic obese and non-obese male subjects of Hispanic (Latinos) origin with a family history of type 2 diabetes present not only IR but impaired insulin secretion, having the obese FH(+) and additional risk like low DI.
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PMID:Presence of impaired insulin secretion and insulin resistance in normoglycemic male subjects with family history of type 2 diabetes. 1270 17

Recent studies indicate that some patients with nonalcoholic fatty liver have ongoing liver injury that may progress from steatosis to steatohepatitis or fibrosis. The present study was designed to clarify the clinical features of liver dysfunction observed in the course of workplace physical check-ups in relation to multiple risk factor syndrome including obesity, hyperlipidemia, hypertension, and impaired glucose tolerance, and to clarify the involvement of aldehyde dehydrogenase 2 (ALDH2) and beta(3)-adrenergic receptor (beta3-AR) gene polymorphisms in elevation of liver enzymes. One hundred forty-eight male workers 35 years of age were enrolled. They were requested to answer questionnaires about drinking and smoking habits, and underwent urinalysis, physical and peripheral blood examinations, blood chemistry, electrocardiogram and chest x-rays. The genotypes of ALDH2 and beta3-AR were analyzed by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). The subjects were divided into active ALDH2 or inactive ALDH2 groups. They were also divided into 2 groups according to the beta3-AR genotype. The relationships between ALDH2 and beta3-AR gene polymorphism and the results of the physical examination including liver function tests were analyzed. The subjects were also divided according to the number of components of metabolic syndrome. The prevalence of elevated alanine aminotransferase (ALT) level increased with the accumulation of components of metabolic syndrome. Active ALDH2 was associated with elevated ALT level to a greater degree than beta3-AR polymorphism. Among those with normal body mass index (BMI), the genotypes of ALDH2 and beta3-AR were strongly associated with elevated ALT level. Logistic regression analysis revealed that BMI, triglyceride level, and ALDH2 genotype were associated with ALT elevation. In conclusion, evaluating the genotype of ALDH2 and beta3-AR may assist in predicting and preventing the development of fatty liver which may be related to multiple risk factor syndrome.
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PMID:Aldehyde dehydrogenase 2 and beta3-adrenergic receptor gene polymorphisms: their association with elevated liver enzymes and metabolic syndrome. 1450 13

Mice with a fat-specific insulin receptor knock-out (FIRKO) have reduced adipose tissue mass, are protected against obesity, and have an extended life span. White adipose tissue of FIRKO mice is also characterized by a polarization into two major populations of adipocytes, one small (<50 microm) and one large (>100 microm), which differ with regard to basal triglyceride synthesis and lipolysis, as well as in the expression of fatty acid synthase, sterol regulatory element-binding protein 1c, and CCAAT/enhancer-binding protein alpha (C/EBP-alpha). Gene expression analysis using RNA isolated from large and small adipocytes of FIRKO and control (IR lox/lox) mice was performed on oligonucleotide microarrays. Of the 12,488 genes/expressed sequence tags represented, 111 genes were expressed differentially in the four populations of adipocytes at the p < 0.001 level. These alterations exhibited 10 defined patterns and occurred in response to two distinct regulatory effects. 63 genes were identified as changed in expression depending primarily upon adipocyte size, including C/EBP-alpha, C/EBP-delta, superoxide dismutase 3, and the platelet-derived growth factor receptor. 48 genes were regulated primarily by impairment of insulin signaling, including transforming growth factor beta, interferon gamma, insulin-like growth factor I receptor, activating transcription factor 3, aldehyde dehydrogenase 2, and protein kinase Cdelta. These data suggest an intrinsic heterogeneity of adipocytes with differences in gene expression related to adipocyte size and insulin signaling.
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PMID:Intrinsic heterogeneity in adipose tissue of fat-specific insulin receptor knock-out mice is associated with differences in patterns of gene expression. 1513 Nov 19

The aim of this cross-sectional study was to describe the prevalence of total, known and unknown diabetes mellitus and impaired fasting glucose (IFG) in the population of Murcia (SE Spain), a Mediterranean area with a high prevalence of obesity. Therefore, 2562 subjects (>or=20 years) were selected by stratified random sampling and a survey was carried out by telephone, together with a physical examination and biochemical determinations. The ADA-1997 diagnostic criteria were used. The crude prevalence of total diabetes was 11% (9.5-12.6%), known diabetes 7.8% (6.5-9.2%), unknown diabetes 3.2% (2.4-4.2%) and IFG 4.9% (3.9-6.1%). Both total diabetes and IFG were higher in men than in women, with prevalence rates increasing with age. People with diabetes and IFG had higher BMI, blood pressure, total cholesterol, LDL-cholesterol and triglyceride values than the rest of the population. No difference in the prevalence of diabetes was observed between the rural and urban populations. The prevalence of diabetes in Murcia is high compared to the rest of Spain and the world, suggesting that the possible benefits attributed to some characteristics of the diet of this Mediterranean population are not sufficient to counteract the risk factors associated with the disease.
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PMID:Prevalence of diabetes in Murcia (Spain): a Mediterranean area characterised by obesity. 1610 90


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