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 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.
Alcohol Alcohol Suppl 1987
PMID:Individual and ethnic differences in ethanol elimination. 342 6

Adult male golden hamsters with continuous access to Purina chow, water and either 15, 30 or 45% ethanol (v/v) for 14 weeks derived an average of 34, 37 and 22%, respectively, of their total calories from ethanol. Animals in the 15 and 45% ethanol groups derived up to 12.0 and 9.9 kcal/day, respectively, from ethanol, but the Purina chow intakes of these animals were such that their total caloric consumption and their body weights did not significantly exceed those of a control group having access only to Purina chow and water. In contrast, the 30% ethanol group derived up to 16.4 kcal/day from ethanol, and consistently consumed 25% more total calories than the control group, despite eating significantly less Purina chow. Furthermore, hamsters in the 30% ethanol group were 27% heavier and had significantly larger epididymal and retroperitoneal fat pads than controls. Similarities are noted between ethanol-induced obesity in hamsters and the dietary obesity which has been observed in rats having continuous access to Purina chow and a 32% sucrose solution.
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PMID:Voluntary ethanol consumption and obesity in golden hamsters. 351 15

Although a number of studies have demonstrated a link between alcohol intake and blood pressure, virtually no research has examined this relationship or the relevance of psychosocial variables in this context over time. This study utilized data from 416 subjects in the Air Traffic Controller Health Change Study to track these associations across five examinations over a 3-year period. Following obesity, alcohol consumption was consistently the second-best predictor of blood pressure. Alcohol intake rose among those subjects who developed sustained elevated blood pressure during the course of the study. Further, obesity became less important in predicting blood pressure at higher levels of alcohol intake. Factors predictive of alcohol use were also studied, and the suggestion is made that psychosocial variables may be linked primarily to alcohol use, which in turn combines with obesity to influence blood pressure levels.
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PMID:A longitudinal investigation of the relationships among alcohol consumption, psychosocial factors, and blood pressure. 360 96

It is not clear why blood pressure rises with age in civilized countries. We examined the relationship between alcohol consumption, obesity, family history of hypertension and blood pressures at medical checkups in 534 male office workers, aged 20 to 40. The results in two age groups, 20-30 and 31-40, are as follows. Those who drank heavily (greater than 60 ml of ethanol) the previous night and/or habitual heavy drinkers (greater than 60 ml/day) had the highest blood pressure. Obese workers had higher blood pressure. Subjects with a family history of hypertension had higher blood pressure. The frequencies of heavy drinkers and obesity were higher in the group aged 31 to 40 than in the other group. These factors might contribute to the blood pressure elevation with age. 5) A histogram of the first readings of systolic blood pressure showed a bimodal distribution only in persons with a family history of hypertension.
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PMID:Relationship between alcohol consumption, body weight, family history of hypertension and blood pressure in young adults. 370 79

Mefenorex, N-(3-chloropropyl)-alpha-methylphenethylamine, (RONDIMEN), is included in the list of centrally acting stimulants and/or hallucinogens or related compounds to be considered by a World Health Organization (WHO) Expert Committee in 1985 for possible scheduling under the Convention on Psychotropic Substances, 1971. The therapeutic efficacy of mefenorex as an adjunctive support in the treatment of obesity for limited periods of time, as well as its ability to be well tolerated, has been amply demonstrated. There have been no reports of actual abuse. There have been no reports of illicit trafficking, falsification of packages or materials, or clandestine laboratories manufacturing the compound. Data from preclinical and clinical studies do not suggest a potential for abuse similar to that of amphetamine or related compounds. Moreover, the lack of pulmonary hypertension with mefenorex has been demonstrated in both preclinical and clinical studies. There have been no reports of any public health or social problems associated with mefenorex use. The compound is a well-tolerated anorectic agent with little central stimulant activity.
Drug Alcohol Depend 1986 Jun
PMID:Mefenorex (Rondimen). 374 6

Immunoreactive neurotensin was measured in plasma and acid-ethanol extracts of brain, intestine and pancreas of obese hyperglycaemic (ob/ob) mice of the Aston strain, C57BL/KsJ diabetes-obese (db/db) mice, and their respective lean controls. In lean mice, the intestine was the major source of neurotensin (156-194 mg/g wet weight and 169-361 ng/intestine), with smaller amounts in the brain (33-43 ng/g and 13-17 ng/brain), pancreas (0.8-1.1 ng/g and 0.28-0.32 ng/pancreas) and plasma (50-100 pg/ml). Compared with lean controls, ob/ob and db/db mice exhibited 13 and 23% decreases in brain weight, and 37 and 82% increases in intestinal weight. Concentrations of neurotensin in plasma and brain were similar in lean and obese-diabetic mutant mice, but the total content of brain neurotensin was 25% lower in ob/ob mice. Neurotensin was unchanged in the pancreas of db/db mice. However, raised concentrations and total contents of neurotensin were observed in the pancreas of ob/ob mice (72 and 57%, respectively) and the intestine of both ob/ob (56 and 118%) and db/db (35 and 144%) mice. These observations raise the possibility that increased neurotensin concentrations might exert local effects in the intestine and pancreas which contribute to the pathogenesis of obesity-diabetes syndromes in mice.
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PMID:Immunoreactive neurotensin in spontaneous syndromes of obesity and diabetes in mice. 388 30

An investigation of the staff of a car assembly plant (3,351 persons) revealed a similarity between the change in relative body weight and diastolic blood pressure with age. There is a good temporal correlation between the course of alcohol consumption during life and the change of the relative body weight. German women had significantly less blood pressure for the same relative body weight than German men, and foreign employees had lower blood pressure than Germans. In both cases the main cause is the difference in alcohol consumption. Besides obesity and hereditary factors, alcohol is the main cause of "essential" hypertension today. Epidemiological and experimental data indicate that there are two ways from alcohol to high blood pressure, a more direct one and an indirect one via obesity. Alcohol causes obesity via a change in metabolism (hyperinsulinism) rather than by higher caloric intake. In both ways alcohol is an important cause of stroke. To reduce body weight and blood pressure, a reduction of alcohol consumption should be recommended in addition to reduced caloric intake and increased physical activity as means of preventive neurology.
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PMID:Alcohol and obesity: a new look at high blood pressure and stroke. An epidemiological study in preventive neurology. 389 16

Recent data suggest that the protection against ischemic heart disease afforded by high density lipoprotein (HDL) cholesterol (C) may be concentrated in the HDL2 subfraction. To examine the behavioral correlates of the HDL subfractions, we recalled 33 men and 17 women of a random sample from the Pacific Northwest Bell Telephone Company Health Survey. Adiposity and very low density lipoprotein (VLDL) triglyceride were negatively correlated with HDL2C. Smoking was not correlated with HDL2C, but was negatively correlated with HDL3C (men, rs = -0.635, p = 0.001; women, rs = -0.534, p = 0.014); this relationship was independent of alcohol consumption, adiposity, and VLDL triglyceride. Alcohol consumption was also more strongly related to HDL3C (men, rs = 0.248, p = 0.082; women, rs = 0.586, p = 0.007). Lecithin cholesterol acyltransferase (LCAT) mass was negatively related with HDL2C, but was positively correlated with HDL3C and apolipoprotein A-II. Smoking was negatively correlated with LCAT mass. Since it is believed that HDL3C is not associated with the risk of ischemic heart disease and since both smoking and alcohol consumption may mainly affect HDL3C, the current study suggests that the increase in risk of ischemic heart disease with smoking and the possible decrease with alcohol consumption may be mediated through mechanisms other than their effects on HDLC.
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PMID:Epidemiological correlates of high density lipoprotein subfractions, apolipoproteins A-I, A-II, and D, and lecithin cholesterol acyltransferase. Effects of smoking, alcohol, and adiposity. 391 1

A multiple regression analysis was performed on statistically independent factors derived from blood pressure measurements and possible predictive variables in 618 Utah adults. Nine blood pressure factors obtained in a previous study composed the dependent variables; 35 anthropometric, questionnaire, and biochemical variables were reduced by factor analysis to 10 factors and used as independent variables. Body size and obesity had significant independent effects on different types of blood pressure: body size correlated most highly with systolic blood pressure, while obesity correlated most highly with sitting diastolic blood pressure measurements. Smoking did not correlate with sitting blood pressure but did show a significant positive correlation (after controlling for obesity) with tilt and supine diastolic pressure. Alcohol consumption correlated positively with sitting diastolic pressure when the effects of body size and obesity were controlled. No correlations were found between urinary potassium or sodium excretion and any blood pressure factors, but a significant positive correlation was seen between plasma sodium concentration and several different types of diastolic blood pressure measurements. Psychological stress showed a significant independent positive correlation with systolic blood pressure measurements that was strongest in adults over 35 years of age. The multiple correlation values for the multiple regression equations ranged from 0.19 to 0.52.
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PMID:Factor analysis suggesting contrasting determinants for different blood pressure measurements. 394 76

We report on clinical, nutritional, and hepatic histological findings in 50 non-selected obese subjects (mean overweight +74%; range +21-138%). The pathogenesis of the liver damage was assessed with the help of multidimensional analysis of a number of clinical variables. According to the severity of the hepatic lesions, the patients have been ranged in five groups: O (normal liver) 10%; I (fatty liver) 48%; II (fatty hepatitis) 26%; III (fatty fibrosis) 8%; IV (fatty cirrhosis) 8%. The more severe changes (groups III and IV) were constantly associated with excessive alcohol intake. The multidimensional analysis was unable to find a relationship between obesity and the development of fibrosis and cirrhosis whereas it showed that: (a) there was a highly significant correlation between the daily ethanol intake and the degree of overweight, (b) severe fatty metamorphosis was significantly associated with the degree of overweight, the existence of diabetes mellitus, and the amount of alcohol and fat intake, (c) nutritional factors, in particular deficient protein intake, have only an accessory effect in the development of mild inflammation and fibrosis, (d) the consumption of potentially hepatotoxic drugs, very high in the obese (about five drugs per day) could have a role in the development of cirrhosis. In conclusion in our study, there was no evidence that obesity per se could result in severe liver damage.
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PMID:Liver in obesity. 396 30


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