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At least 541 records · Page 30Linked to original sources
PubMedDate not supplied

Obesity-related non-alcoholic steatohepatitis and TGF-beta1 serum levels in relation to morbid obesity.

Non-alcoholic steatohepatitis (NASH) can vary from mild hepatic inflammation and steatosis to cirrhosis, and is most frequently associated with obesity, Type 2 diabetes mellitus, hypertension, and the female gender. The prevalence of fatty liver and NASH in the general population is 20% and 3%, respectively. In Western countries, 15-20% of the population is obese and 74-90% of them exhibit fatty changes in liver biopsies. We assessed the prevalence of NASH in morbidly obese patients and evaluated serum TGF-beta1 concentrations in different stages of liver fibrosis. Thirty-five obese patients were evaluated, nine male and 26 female. Their mean body mass index (BMI) was 43.62 +/- 7.92 kg/m2. Liver biopsies were evaluated by light microscopy; graded and staged according to Brunt's system. Serum obtained from patients was used to detect TGF-beta1 concentrations by an ELISA method. Serum alanine transaminase (ALT) levels were elevated in four of the patients and the mean level was 49.98 +/- 94.7 (8-65 IU/L). NASH was diagnosed in 32 (91%) of the biopsies, and the most common pattern seen was mixed, predominantly macrovesicular steatosis. Some degree of fibrosis was seen in 34 (97%) of the biopsies and 22 (63%) were at stage 2 (range 1-3). Serum concentrations of TGF-beta1 had no relationship with the stages of fibrosis. In conclusion, NASH and fibrosis are common in our obese patients, as observed in other studies. TGF-beta1 may play a key role in liver fibrogenesis.

Adult↗
PubMed2004

Do obese children become obese adults: childhood predictors of adult disease.

Obesity is a multifactorial disorder influenced by genetic, behavioral, environmental and cultural factors. The prevalence of overweight and obesity in young people is increasing rapidly in both the developed and developing world and are considered today as a global epidemic. Recent studies show that obesity in adult life is heralded at birth and factors such as birth weight, adiposity rebound, socioeconomic status, early maturation and genetic predisposition may have a significant effect on the propensity to develop obesity in adulthood. Avoidance of accelerated weight gain in children should be investigated as a toll of adult obesity prevention.

Adult↗
PubMed2006

[Association of gene polymorphism at cholesterol ester transfer protein locus with obesity and response to dietary intervention in obesity].

OBJECTIVE: To study the association of gene polymorphism at cholesterol ester transfer protein (CETP) locus with obesity and response to dietary intervention in obesity. METHODS: The PCR-PFLP method was used to detect the polymorphism of CETP gene of 340 adults in Shanghai. The levels of serum lipid profile, including TG, TC, HDL and LDL were analyzed. Obesity was selected to dietary intervention. RESULTS: (1)The genotype frequencies of CETP-TaqIB B1 B1, B1 B2 and B2 B2 were 35.6%, 47.9% and 16.5% respectively, which were in agreement with Hardy-Weinberg equilibrium. There was no significant difference in the distribution of genotypes between the obesity group and control group. The result was same after several influence factors controlled. (2) The levels of HDL were significantly different among genotype groups. Subjects for the B2 B2 genotype had the highest HDL levels. The relationship was steady after adjusting several influence factors. (3)Subjects for the B1 B2 genotype had higher HDL level after intervention, which was significantly different to other genotype groups. After adjusting baseline HDL level and gender, genotype didn't effect the change in HDL. CONCLUSION: CETP-TaqIB gene polymorphism influenced serum HDL level. But this gene polymorphism at CETP locus wasn't especial in adult obesity. Baseline HDL level influenced the change in HDL response to dietary intervention in three genotype groups.

Aged↗
PubMed1991

Plasma catecholamine levels and lipid mobilization induced by yohimbine in obese and non-obese women.

Oral yohimbine administration (0.2 mg/kg) induced lipid mobilization (increase in plasma non-esterified fatty acids, NEFA) in fasting non-obese women (body mass index BMI = 20.2 +/- 0.5, age 35.5 +/- 2.7 years) without significant action on plasma glucose, insulin levels, heart rate or blood pressure during the time-course of the experiment (240 min). Plasma norpinephrine (but not epinephrine) concentrations were increased (100 percent) after oral yohimbine administration. Oral administration of propranolol (40 mg, 60 min before yohimbine) reduced the lipid-mobilizing action of yohimbine (70 percent) during the 60 min following its administration and then totally suppressed its effect until the end of the experimental period (180 min). In fasting obese women (BMI = 36.4 +/- 2.1, age 37 +/- 3.6 years), yohimbine provoked an increase in plasma NEFA levels which was not markedly different from that observed in non-obese subjects. It had no significant effect on plasma glucose, insulin levels, heart rate or blood pressure. Plasma norepinephrine increased in the same proportions. The lipid-mobilizing effect of yohimbine in women is mainly attributable to the increase in synaptic norepinephrine with a resultant increment in lipolysis by beta-adrenergic agonism. In the standard fasting conditions (12 hours) the blockade of the antilipolytic fat cell alpha 2-adrenoceptors seems to be a minor component of the lipomobilizing effect of yohimbine. Morever, when compared with non-obese women, the lipomobilizing effect of yohimbine is not enhanced in obese women.

Administration, Oral↗
PubMedDate not supplied

[Clinical and hemodynamic effects of medium-term treatment with ketanserin of 2 comparative groups of obese and non-obese hypertensive patients].

We evaluated systemic and central hemodynamics in 10 lean hypertensives and in 10 obese hypertensives (WHO stage I-II) after 8 weeks treatment regimen with a serotoninergic antagonist such as ketanserin. At the beginning and the end of the study, body weight, BMI, blood pressure and heart rate were measured and a first pass radionuclide angiocardiography was performed to determine cardiac output, cardiac index and ejection fraction of left ventricle. Total peripheral resistances were also calculated. In both hypertensive groups ketanserin significantly reduced diastolic (p less than 0,05) and mean (p less than 0.005) blood pressure. No significant change in systolic blood pressure, cardiac output, cardiac index and ejection fraction was observed in lean or obese hypertensives. Total peripheral resistance values significantly (p less than 0,05) decreased in lean hypertensives; in obese hypertensives total peripheral resistance was moderately reduced. Our results indicate that monotherapy with ketanserin is effective in treating mild to moderate hypertension in both lean and obese hypertensives and does not interfere with left ventricular performance. In conclusion the effectiveness of ketanserin treatment appears moderately higher in lean than in obese hypertensives.

Adult↗
PubMed1990

Long-term changes of body weight in adult obese and non-obese men.

In this study the long-term changes of body weight during adulthood in men obese as young adults are compared to those occurring in a random sample from the underlying population. Among 362,200 Danish draftees from 1943 to 1977, 1940 were obese (body mass index greater than or equal to 31 kg/m2). A random sample, comprising 0.5 per cent (1801), was drawn from the remaining population. In 1981-83, 4-40 years later, those living in the same region were invited to a health examination, which was attended by 964 (58 per cent) obese and 1134 (75 per cent) control subjects. In the obese group median change of body weight was 1.3 kg, and in the control group 8.3 kg. Weight change was positively correlated to duration of observation in both groups. Those with lowest body mass index at first examination tended to increase most, and those with highest body mass index tended to lose weight. However, the 5th to 95th percentiles of changes in body weight extended in the obese group from -24 to 29 kg, and in the control group from -2 to 25 kg. The range in weight change increased strikingly with increasing first body mass index exceeding 27 kg/m2. The study indicates that the greater the body mass index among young adult men, the less is the median change in body weight, but the greater is the variation of the body weight changes. These results suggest that the size of the fat mass is subject to intra-individual environmental influences that change over time.

Adult↗
PubMed1989

[Clinical and hemodynamic effects of medium-term ketanserin treatment in 2 compared groups of obese and non-obese hypertensive patients].

We evaluated systemic and central hemodynamics in 10 lean hypertensives and in 10 obese hypertensives (WHO stage I-II) after 8 weeks treatment regimen with a serotoninergic antagonist such as ketanserin. At the beginning and at the end of the study, body weight, BMI, blood pressure and heart rate were measured and a first pass radionuclide angiocardiography was performed to determine cardiac output, cardiac index and ejection fraction of left ventricle. Total peripheral resistances were also calculated. In both hypertensive groups ketanserin significantly reduced diastolic (p less than 0.05) and mean (p less than 0.005) blood pressure. No significant change in systolic blood pressure, cardiac output, cardiac index and ejection fraction of left ventricle has been observed in lean and obese hypertensives. Total peripheral resistance values significantly (p less than 0.05) decreased in lean hypertensives; in obese hypertensives total peripheral resistance moderately reduced. Our results indicated that monotherapy with ketanserin is effective in treating mild to moderate hypertension both in lean and in obese hypertensives and did not interfere with left ventricular performance. At last the effectiveness of ketanserin treatment appears moderately higher in lean than in obese hypertensives.

Adult↗
PubMed1987

Obesity and cancer. A review of epidemiological studies on the relationship of obesity to cancer of the colon, rectum, prostate, breast, ovaries, and endometrium.

Cancer of the colon, rectum, prostate, breast, ovaries and endometrium may be associated with obesity. The present paper reviews both prospective and retrospective studies of the potential associations between obesity and these cancers. This research is especially difficult because of the complex interrelations between weight and diet, physical activity, cigarette smoking, and other conditions. Epidemiological studies of body weight are subject not only to biases of sampling, selection, and confounding but also to marked difficulties in definition and measurement. Bearing in mind the methodological shortcomings, there is a distinct and reproducible association between obesity and cancer of the endometrium and postmenopausal breast cancer. The studies of cancer of the colon, rectum, prostate, and ovaries are too inconclusive to elucidate whether obesity implies an increased risk. It is recommended that future studies in this field include a standardised assessment of the distribution of fat tissue, the onset and duration of the condition, and the associated confounding factors. It is concluded that obesity, especially in females, should be avoided as a part of the general cancer preventive effort.

Breast Neoplasms↗
PubMedDate not supplied

Hypertension in obese and non-obese non-insulin dependent diabetics a matter of regional adiposity?

There is growing evidence that differences in fat distribution can be predictive for differences in the prevalence of metabolic disturbances, cardio-vascular disease, stroke and death, independent of commonly used indices of obesity. This study evaluates regional body fat distribution as a possible main reason for hypertension in obese and non-obese type II diabetics. 42% of normal weight diabetics with abdominal obesity are hypertensive versus 47% of obese diabetics; only 5% hypertension could be found when a lower body segment fat distribution is present. A significant (p less than 0.001) correlation exists between fat mass topography and both systolic (r = 0.49) and diastolic (r = 0.49) blood pressure. This correlation remains true after correction for body mass index and percent glycosylated hemoglobin. These results suggest that localization of fat in the upper body segment should be considered as a additive risk for hypertension.

Adipose Tissue↗
PubMed1986

Energy expenditure of young men from obese and non-obese families.

Sixteen young non-obese men, seven of whom had an obese parent, were studied under standardized conditions in a respiration chamber to assess their metabolic rate during sleep, at rest, in response to food and during a variety of exercises. The men from obese families were already fatter than the 'normal' group from non-obese families but reported equivalent intakes of energy, had a normal pattern of energy expenditure and could not be distinguished as a group from the men of normal-weight parents. Only the three men of lighter weight of obese parents had a lower energy expenditure per kg fat-free mass and a lower thermic response to food than the normal group; those who were already overweight did not differ from the normal group in their energy expenditure.

Adolescent↗
PubMed1982

[Effects of 3,5,3'-triiodothyroacetic acid (TRIAC) on protein metabolism of genetically obese or non-obese Zucker rats].

Genetically obese female rats (fa/fa) and their lean littermates (Fa/-) were given oral administration of 3,5,3-triiodothyroacetic acid (TRIAC) (20 micrograms/ 100 g of body weight/ day) during 4 weeks. Metabolism of proteins was evaluated in several organs and in skeletal muscle after intraperitoneal injection of 14C and 3H-leucine 6 days and 16 hrs respectively before the sacrifice of animals. We have determined radioactivity of 14C and 3H and the 3H/14C ratio. No significant differences were found in lean and obese rats except in skeletal muscle. The relative protein turnover in skeletal muscle is significantly higher in the obese rats than in the lean rats. Treatment by TRIAC decreases the body weight gain in obese rats compared with controls but it has no statistically significant effect on the relative protein turnover in either obese or lean rats.

Animals↗
PubMed1981

[Obesity in children. III. Feeding pattern in relation to the possible development of obesity].

It appears from literature that obesity among breastfed infants is less prevalent than among over bottle fed infants. There is conflicting understanding as to a significant contribution of infant food habits to lasting obesity. Attention for prudent food intake seems to be particularly indicated when one of the parents or both are obese. Too early introduction of solids in addition to milk formula does probably not contribute too much to infants overfeeding, but enlarges the risk for early manifestation of allergies or coeliac disease and for restricted iron absorption. The food pattern of toddlers and schoolchildren in the Netherlands is characterized by an over validation of the health promoting significance of animal protein rich products. This may contribute to the consumption of excess saturated fatty acids and relatively little dietary fibre. Both relatively fatty food and little dietary fibre as well as over consumption of milky products and sugar in soft drinks or lemonade can easily enhance the development of obesity in young children. Protein consumption of 2.5 grams per kg BW, two thirds of which is from animal source, is repeatedly noted, whereas 1 à 1.5 grams of mixed protein per kg BW can be considered adequate for healthy toddlers and young school age children to guarantee normal growth and development. In addition to the traditional three main meals, it appears that 8 year olds in the Netherlands consume 20 pct of the total amount of energy intake in the form of in-between-meal snacks, which may also contribute to the possible development of obesity.

Bottle Feeding↗
PubMed1980

Pathophysiological differences between obese and non-obese spontaneously hypertensive rats.

A genetic variant of the spontaneously hypertensive rat (SHR) has been produced which becomes markedly obese as well as hypertensive, i.e. Obese/SHR weigh 800 g as against 300 g for non-obese cohorts. Serum enzymes (CPK, SGOT, SGPT and LDH) are frequently abnormally elevated, concomitantly with a high incidence of myocardial necrosis. Obese/SHR are hyperlipidaemic with severe fatty infiltration of the liver; they are hyperglycaemic with enormous islets of Langerhans and extensive beta-cell degranulation; despite elevated blood urea nitrogen (BUN) levels, they manifest little or no renal damage. Measurement of corticosterone, deoxycorticosterone (DOC) and aldosterone in Obese/SHR demonstrate marked hyper-responsiveness to moderate stress. Circulating prolactin levels are lower in Obese and non-obese/SHR compared to SHR, but Obese/SHR manifest unusually high increases incirculating prolactin levels in response to stress. Obese/SHR are hyperinsulinaemic and have subnormal growth-hormone levels. Desite mild hypertension, hyperglycaemia and hyperlipidaemia, Obese/SHR show no evidence of atheromatous change but do develop early polyarteritis nodosa. It is believed that the genetically programmed hypertension and hyperglycaemia is mediated by increased DOC, aldosterone and corticosterone production respectively, and that the obesity, hypertension, and diabetes in Obese/SHR may be likened to human Cushing's disease.

Aging↗
PubMedDate not supplied

Genetic approach of family obesity: study of HLA antigens in 10 families and 86 unrelated obese subjects.

HLA A and B typing was performed in 86 unrelated obese subjects and in 10 families including at least one parent and one obese sibling. The results in the series of unrelated subjects show no significant difference in antigen frequencies as compared to the control series. However in the 10 families studied, a group of 5 families is characterized by a high penetrance of obesity. In this group, inheritance of obesity seems to be transmitted through a dominant mode, and antigen B 18 appeared 4 times out of 5. The possible existence of a genetic form of obesity is considered in the discussion.

Female↗
PubMed1994

Obesity in Pima Indians: genetic segregation analyses of body mass index complicated by temporal increases in obesity.

During the past half-century the prevalence of obesity in developed countries has increased greatly. Such short-term changes in prevalence must be environmentally determined, but genes can mediate response to environmental change, for example, through variable gene penetrance and expression. Obesity differences between bith cohorts complicate the interpretation of phenotypic comparisons between generations that span periods of change. Genetic segregation analyses of the body mass index in 618 Pima Indian nuclear families (2 generations) identified recessive major gene inheritance, which is the same pattern of transmission that has been found in several other populations. However, within-birth-cohort analyses of siblings (one generation) uniformly supported codominant major gene inheritance with no polygenic heritability. For untransformed data transmission probabilities were Mendelian in the later-born cohort and in the combined sample of siblings. After transformation to remove skewness, transmission probabilities were Mendelian only in the earlier-born cohort (i.e., those siblings born before a period of marked temporal increase following World War II). A higher penetrance of codominant obesity susceptibility genes in the younger generation would result in some genetically obese individuals who have no affected parents, thus simulating recessive inheritance. Taken together, the results of these analyses suggest that the recessive pattern we identified in the Pima Indian nuclear families could be accounted for by temporal changes in penetrance of codominant obesity-predisposing genes. By implication, more modest temporal increases in white and black populations could in part account for the recessive pattern of inheritance described by several investigators.

Adolescent↗
PubMed1999

Obesity Hypertension in the Atherosclerosis Risk in Communities Cohort: Implications of Obesity Guidelines.

An estimated 55% of the U.S. adults are overweight or obese (body mass index [BMI] equals 25 kg/m2). Overweight individuals have a threefold increased risk for the development of hypertension compared to lean individuals. The National Institutes of Health, National Heart, Lung, and Blood Institute (NHLBI) guidelines for treatment of overweight and obese adults recommend weight reduction strategies including pharmacologic treatment with antiobesity agents approved by the FDA. Treatment is recommended for obese individuals and for overweight persons with other risk factors for cardiovascular disease (CVD) including hypertension. This analysis of the Atherosclerosis Risk In Communities (ARIC) cohort for overweight/ obese hypertensive participants indicate that 64% of the hypertensive participants in ARIC deserve consideration for treatment with antiobesity agents according to the current NHLBI guidelines. Thus far there are no long term morbidity and mortality clinical trials to determine the safety of antiobesity agents currently approved by the FDA. The authors caution health care providers in the use of these agents in the obese patient with hypertension. (c)1999 by Le Jacq Communications, Inc.

Journal Article↗
PubMed1999

Rodent mutant models of obesity and their correlations to human obesity.

Obesity is a heath problem affecting a significant fraction of adult Americans and is on the rise globally. It is of importance to find treatments that achieve medically significant weight loss and successful long-term maintenance of a desired weight. Recent transgenic mouse studies and genetic characterization of spontaneous rodent obesity mutants, together with gene linkage analysis in humans, have led to an increased understanding of the physiologic and molecular mechanisms underlying obesity. However, much remains to be studied in this complex field of research. In this review, we discuss the physiology and genetics underlying obesity and how studies in rodents and humans are converging, producing a greater understanding of the mechanisms underlying this health problem.

Adult↗
PubMed1995

Overexpression of the obese gene in the genetically obese JCR:LA-corpulent rat.

Expression of the obese (ob) gene in JCR:LA-cp rats was examined. A 360 bp fragment of the conserved region of the gene was obtained by RT-PCR using total RNA isolated from adipose tissues of Sprague-Dawley (SD), JCR:LA-cp obese and lean rats. The three gene fragments were sequenced and shown to be identical. They were over 90% identical to the mouse ob gene sequence. The amplified fragments encode for 120 amino acids and have a glutamine residue at position +49. The gene was shown to be expressed only in adipose tissues, both white and brown. A ten-fold increase in ob mRNA was detected in white adipose tissues of obese animals compared to the lean ones of the JCR-LA:cp strain of rat. Ob gene was expressed in adipocytes and preadipocytes from the obese rat whereas in the lean and SD rats, ob gene expression was found in adipocytes only. No ob mRNA was detected in preadipocytes from the lean or SD rats, indicating a differentiation or maturation-dependent expression in normal rats.

Adipocytes↗