PubMed HealthSearch

SEARCH · PubMed Health

Results for “Obesity”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources

Rheological determinants and red cell lipidic pattern in essential obesity, in obese subjects with non-insulin-dependent diabetes mellitus (NIDDM) and in obese subjects with impaired glucose tolerance (IGT).

In a group of subjects with essential obesity, in a group of obese subjects with non-insulin dependent diabetes mellitus (NIDDM), and in a group of obese subjects with impaired glucose tolerance (IGT), we evaluated whole-blood filtration, mean erythrocyte aggregation, erythrocyte membrane fluidity and red cell lipid pattern. From these data, it is evident that the macro- and microrheological determinants are able to discriminate normals from each group of obese subjects. Regarding the red cell lipids, few are the variations between each group of obese subjects and normal controls.

Adult

Stepwise increase in plasma insulin and C-peptide concentrations in obese, in obese hypertensive, and in obese hypertensive diabetic subjects.

Several clinical and epidemiological evidences support the increased risk of cardiovascular disease (CVD) in pathological conditions as obesity, hypertension, non-insulin-dependent diabetes mellitus, which have hyperinsulinemia as a common feature. In this study, we assessed basal plasma insulin (IRI) and C-peptide (CPR) concentrations in 297 volunteers who participated in a survey concerning risk factors of CVD. We found a stepwise increase in fasting insulin and C-peptide levels in normal subjects (IRI 9.10 +/- 0.41 microU/ml; CPR 1.79 +/- 0.08 ng/ml), in obese subjects (IRI 11.31 +/- 0.38 microU/ml; CPR 2.54 +/- 0.07 ng/ml) in obese hypertensive subjects (IRI 14.17 +/- 0.72 microU/ml; CPR 2.64 +/- 0.09 ng/ml), in obese hypertensive diabetic subjects (IRI 22.57 +/- 2.62 microU/ml; CPR 3.33 +/- 0.27 ng/ml). Thus, we found increasing levels of IRI and CPR as normal conditions changed towards progressively more severe pathological conditions. Although several other factors contribute to determine CVD, we conclude that increasing levels of insulin and C-peptide could play an important role in causing CVD.

Adult

Left ventricular function response to exercise in normotensive obese subjects: influence of degree and duration of obesity.

This study has been designed to evaluate whether duration and severity of obesity can influence left ventricular function response to exercise in obese subjects without other known cardiovascular risk factors such as hypertension, diabetes or hyperlipoproteinemia. A total of 29 obese subjects were included and they were divided, according to their body mass index and to Garrow's criteria as follows: Overweight or mildly obese subjects: body mass index from 25 to 30 kg/m2; moderately obese subjects: body mass index > 30 and < 40 kg/m2. Both obese groups were further subdivided according to their duration of obesity evaluated by accurate anamnesis in subgroup A (duration of obesity less than 120 months) and subgroup B (duration of obesity more than 120 months). Left ventricular ejection fraction was detected by blood pool gated radionuclide angiocardiography both at rest and after symptom-limited bicycle ergometer procedure. At peak exercise left ventricular ejection fraction increased significantly (p < 0.05) only in overweight subjects. Exercise produced an increase of left ventricular ejection fraction in 14 overweight and in 5 moderately obese subjects and a decrease in 2 moderately obese subjects. At peak exercise mean heart rate and mean blood pressure increased significantly (p < 0.001) in both groups. When obese subjects were subgrouped according to duration of obesity, left ventricular ejection fraction increased significantly (p < 0.05) only in overweight subjects with duration of obesity less than 120 months. Duration of obesity correlated inversely with percent change in left ventricular ejection fraction (EF) at peak exercise (delta EF) (r = -0.59; p < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult

Brown adipose tissue: contributions of nature and nurture to the obesity of an obese mutant mouse (ob/ob).

The aim of this investigation was to compare the contributions of the genotype of the brown adipose tissue (BAT) and of its environment to the obesity of the mutant mouse C57 BL/6J ob/ob. Pieces of interscapular BAT from lean or obese mice were transplanted to a site underneath the kidney capsule of recipient lean or obese mice. The grafts were left in place for 6 to 12 weeks and then examined by histological methods by electron microscopy to examine the ultrastructure of the mitochondria and by fluorescence histochemistry to examine the catecholaminergic innervation of the grafts. When lean BAT was grafted into obese mice, or when obese BAT was grafted into lean mice, kept at ambient temperatures, the characteristics of the donor BAT (i.e. lipid droplet size, mitochondrial ultrastructure and catecholaminergic innervation) transformed partially, but not completely, towards those of BAT in the host mouse. However, if lean mice containing obese BAT grafts were cold-acclimated at 4 degrees C or obese mice containing lean BAT grafts were warm-acclimated at 33 degrees C, the characteristics of the donor BAT transformed completely towards those of the BAT in the host mouse. This complete transformation occurred even if the host mice were returned to 23 degrees C after the period of temperature acclimation. Fluorescent histochemical observations indicated that the sympathetic innervation of BAT grafts was only indistinguishable from that of the lean or obese host BAT when the mice received a period of temperature acclimation (cold for lean mice; warm for obese mice). We conclude that BAT grafts from lean mice can assume the typical characteristics of BAT in obese hosts and that BAT grafts from obese mice can assume the typical characteristics of BAT in lean hosts provided that both the sympathetic innervation and the vascularization of the grafts is the same as in the host. Intrinsic properties of BAT in genetically obese mice are therefore unlikely to be of paramount importance in determining the obesity of the ob/ob mouse. Our results support the conclusions of other workers in implicating the low activity of the sympathetic innervation of BAT as being crucially important in causing the reduction of thermogenic activity.

Acclimatization

Bile lipid secretion in obese and non-obese individuals with and without gallstones.

Biliary lipid secretion rates were measured in non-obese and obese individuals with and without cholesterol gallstones, using a steady-state, amino acid duodenal perfusion method. In addition, biliary lipid secretion rates were measured in five obese gallstone patients receiving high-dose chenodeoxycholic acid therapy (16-22 mg day-1 kg-1). Bile acid secretion rates in the non-obese patients with cholesterol gallstones (563 +/- SEM 70 mumol/h, n = 6) were significantly lower than in the non-obese controls (1078 +/- 210 mumol/h, n = 10, P less than 0.05), whereas cholesterol secretion rates were similar in the non-obese individuals with and without gallstones (51 +/- 7 and 42 +/- 4 mumol/h respectively). In the obese, both with and without gallstones, the major abnormality was hypersecretion of cholesterol (107 +/- 7 mumol/h, n = 7, and 81 +/- 15 mumol/h, n = 7, respectively). Both these values were significantly greater than those in the non-obese controls (P less than 0.01-0.02). Biliary cholesterol secretion rates correlated significantly with bile acid secretion rates but, for every mole of bile acid secreted, the obese secreted more cholesterol than the non-obese. Chenodeoxycholic acid treatment lowered biliary cholesterol saturation in obese gallstone patients by reducing biliary cholesterol secretion. These results suggest that there are two major types of defect in biliary lipid secretion in gallstone patients: reduced biliary bile acid secretion in non-obese gallstone patients and excessive biliary cholesterol secretion in the obese.

Adult

Defects in insulin-receptor internalization and processing in monocytes of obese subjects and obese NIDDM patients.

We investigated intracellular processing of the insulin-receptor complex in monocytes from 12 healthy control subjects, 11 obese nondiabetic subjects, and 13 obese patients with non-insulin-dependent diabetes mellitus (NIDDM) by measuring receptor internalization, recovery of cell-surface insulin binding after receptor internalization, and the release of intracellular intact insulin (insulin retroendocytosis). When monocytes from the three groups of subjects were exposed to 100 nM unlabeled insulin for 30 min at 37 degrees C, the subsequent cell-surface 125I-labeled insulin binding was reduced, but the total number of insulin receptors, measured by radioimmunoassay, was not changed. These findings indicate a redistribution of insulin receptors from the surface to the cell interior. Insulin-receptor internalization was significantly lower in monocytes of obese NIDDM patients (mean +/- SE 17.8 +/- 4.7%) than in obese subjects and healthy control subjects (33.5 +/- 4.5%, P less than .05, and 34.4 +/- 3.7%, P less than .02, respectively). Moreover, in downregulated cells, a complete recovery of the initial insulin binding was observed in control subjects but not in obese NIDDM patients or obese nondiabetic subjects. The release of internalized insulin was also reduced in obese NIDDM patients and obese subjects (t 1/2 = 49.0 +/- 2.4 min, P less than .02; 47.4 +/- 5.7 min, P less than .05; and 32.9 +/- 3.8 in NIDDM patients, obese subjects, and control subjects, respectively). In the radioactivity released from monocytes of obese subjects and obese NIDDM patients, the percentage of intact insulin was higher (P less than .05) than in control subjects, suggesting reduced intracellular insulin degradation in obese subjects and obese NIDDM patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Diabetes Mellitus

Association of obesity and distribution of obesity with glucose tolerance and cardiovascular risk factors in the elderly.

The association of obesity and fat distribution with glucose tolerance and cardiovascular risk factor levels were investigated in a population-based study in East Finland including 396 non-diabetic men and 673 women aged from 65 to 74 years. Obese men and women (BMI greater than 27 kg/m2) had higher levels (P less than 0.001) of fasting and 2 h plasma glucose and insulin as well as total triglycerides and diastolic blood pressure, and lower levels of HDL cholesterol than normal weight men and women. Central fat distribution (the highest vs. the lowest tertile of waist-hip ratio) was associated independently of obesity with high fasting glucose (5.7 vs. 5.5 mmol/l in non-obese subjects, 5.9 vs. 5.7 mmol/l in obese subjects, P less than 0.05) and insulin levels (13.7 vs. 10.6 mU/l in non-obese subjects, 18.4 vs. 15.6 mU/l in obese subjects, P less than 0.01) and with adverse changes (P less than 0.05) in lipid and lipoprotein levels (triglycerides: 1.59 vs. 1.41 mmol/l in non-obese subjects, 1.92 vs. 1.69 mmol/l in obese subjects; HDL cholesterol: 1.33 vs. 1.43 mmol/l in non-obese subjects, 1.20 vs. 1.32 mmol/l in obese subjects). There were no marked differences in metabolic aberrations related to obesity between men and women. However, the association between waist-hip ratio and risk factors was non-linear in men whereas it was linear in women. In conclusion, obesity per se rather than its distribution was a more significant determinant of glucose and insulin as well as total triglyceride and HDL cholesterol levels in elderly subjects.

Aged

Body weight regulation in obese and obese-reduced rats.

We previously developed a model of dietary obesity in adult male rats where duration of feeding a high fat diet (HFD; 60 percent of calories from fat) influences reversibility of the obesity following a reduction in dietary fat. In the model, rats fed the HFD for 4 months show an apparent complete reversal of obesity when switched to a low fat diet (LFD; 14 percent of calories from fat), but rats fed the HFD for 7 months show persistent obesity even when switched to the LFD. This model of dietary obesity is useful for studies of energy balance and energy requirements during obesity development and reversal. In the present study, rats fed the HFD for 4 or 7 months were switched to the LFD and, after weights stabilized, were subjected to food restriction followed by ad libitum refeeding. Food restriction (15 g/day of the LFD, or about 60 percent of usual control food intake) continued until body weights of the groups stabilized at new, reduced levels (about 2-2.5 months). This was followed by ad libitum refeeding of the LFD for 3--4.5 months. Rats fed the HFD for 4 months showed complete obesity reversal after 2 months of eating the LFD. They showed a similar response to food restriction to LFD controls, but surprisingly regained significantly more body weight, body fat and total body energy during refeeding than LFD controls. Rats fed the HFD for 7 months remained heavier and fatter than LFD controls after 2 months of eating the LFD. Despite losing more carcass energy than controls during food restriction, their body weights and body energy content stabilized at higher levels than LFD controls. During refeeding, they regained their obese state relative to controls. These results demonstrate that: (1) the duration of HFD feeding is an important factor in the reversibility of the obese state; (2) sustained HFD feeding produces an obese state that is defended more by a greater restoration of carcass energy during refeeding than by a preservation of carcass energy during food restriction; (3) sustained obesity appears to produce some reductions in energy requirements; (4) even a brief period of obesity may leave the rats prone to reattain an obese state when body weight is challenged.

Animals

[Regional hemodynamics of the forearm. Comparison between obese and non-obese hypertensive patients].

Forearm hemodynamics using pulsed Doppler flowmetry were studied in 83 men: 15 non-obese and 8 obese normotensive subjects; and 30 non-obese and 30 obese hypertensive patients. Mean ages were similar in the four subgroups. The blood pressure of normotensives and hypertensives was identical in obese and non-obese subjects. Blood flow expressed in ml/mn was significantly higher in obese subjects whether normotensive or hypertensive. However, when blood flow was expressed per unit liter of forearm volume, it was similar in the four subgroups. Forearm vascular resistance, whether expressed as absolute of normalized values, was significantly higher (p less than 0.001) in non-obese hypertensives. When obese and non-obese hypertensives were compared, the former were characterized by higher values of blood velocity and blood flow, and lower values of vascular resistance, whether absolute or normalized values were used. The present study shows that: (i) forearm vascular resistance in hypertensives is increased exclusively in non-obese subjects, and (ii) obese hypertensives, when compared with non-obese hypertensives, are characterized by a hyperkinetic forearm circulation.

Adult

Metabolic profiles and lipoprotein lipid concentrations in non-obese and obese patients with polycystic ovarian disease.

Clinical parameters, androgen status and lipoprotein lipid profiles were assessed in 10 non-obese and 10 obese patients with polycystic ovarian disease (PCOD) and reference subjects matched for age, height and weight. Both obese and non-obese women with PCOD had significantly higher androgen levels when compared to the reference groups. When comparison of lipoprotein lipid profiles were made between groups, non-obese women with PCOD had significantly higher total cholesterol, triglycerides and LDL-cholesterol levels than non-obese reference subjects. Obese PCOD women manifested significantly higher total cholesterol, LDL-cholesterol, cholesterol/HDL, and LDL/HDL values than did obese reference subjects. Correlations between serum androgens and lipoprotein lipid concentrations in PCOD and normal women were unhelpful. Both non-obese and obese patients with PCOD had significantly higher systolic and diastolic blood pressures (BPs) than the reference groups. Thus, both non-obese and obese women with PCOD manifest hyperandrogenaemia which may result in a male pattern of lipoprotein lipid concentrations.

Adolescent

Personality characteristics in obesity: relation of MMPI profile and age of onset of obesity to success in weight reduction.

A group of 142 obese subjects was seen in an obesity clinic over a 2-year period. Of these, 116 had assessment of personality factors by the Minnesota Multiphasic Personality Inventory (MMPI), and 71 were followed for periods of 4 to 28 months in order to determine success at weight reduction by means of a conventional dietary regimen. The MMPI profiles of the obese subjects were compared to those of a general medical population of 50,000 patients seen in the Department of Internal Medicine at the Mayo Clinic. Obese male subjects had significantly higher scores on the F and MA scales. Obese female subjects had significantly higher scores on the F, PD, PA, SC, and MA scales, and a significantly lower score on the Q scale than the reference population. Even though these findings show that certain personality traits as measured by the MMPI may occur more frequently in obese persons, the individual MMPI profile codes point out the presence of diverse behavior patterns among obese persons rather than a single personality pattern characteristic of obesity. There were no apparent differences in the success in achieving a loss of 10% or more of initial weight among the male and female obese subjects having normal or abnormal MMPI profiles. Obese subjects having onset of obesity before age 12 years were slightly more successful in weight reduction than those whose obesity began later than this, but the differences were not statistically significant for either the male or female subjects.

Adolescent

Swedish obese subjects (SOS). Recruitment for an intervention study and a selected description of the obese state.

SOS (Swedish obese subjects) is an on-going intervention trial designed to determine whether the mortality and morbidity rates among obese individuals who lose weight by surgical means (gastric banding, vertical banded gastroplasty and gastric by-pass) differ from the rates associated with conventional treatment. For this purpose, the study is recruiting a sample of obese men and women who constitute a registry of potential subjects from which the participants are drawn. Eligibility criteria for participation in the registry were: age at application 37-57 years and BMI greater than or equal to 34 kg/m2 for men and greater than or equal to 38 kg/m2 for women. Before receiving a health examination, all patients complete extensive questionnaires on current and past health status, utilization of medical care and medications, socio-economic status, psychological profiles, dietary habits, physical activity, weight history, and familial disposition to obesity. Each surgical case is matched to its optimal control in the registry, to ensure that the two groups do not differ systematically with respect to any of 18 matching variables that may affect prognosis. The first 1006 subjects included in the registry have been studied with respect to morbidity and compared with on-going population studies of men and women in Göteborg, Sweden. The relative risks of prevalent disease and symptoms associated with obesity in 50-year-old males and females respectively were 4.3 and 4.7 (dyspnoea), 14.7 and 11.8 (angina), 6.3 (myocardial infarction, males only), 2.1 and 4.5 (hypertension), 5.2 and 6.6 (diabetes), 4.6 and 26.1 (claudication) and 1.7 and 1.8 (gall bladder disease). Correspondingly, obese males and females display elevations of systolic and diastolic blood pressure, fasting glucose, insulin, triglyceride, and uric acid levels. However, total cholesterol was not increased in obese males and was in fact significantly lower in obese compared with reference women. HDL-cholesterol was lower in obese than reference men (data were not available in reference women). The rate of taking sick pensions was over twice as high in SOS obese patients than in population controls. Finally, comparison of measurements with self-reported prevalence estimates revealed a considerable amount of previously undiagnosed hypertension and diabetes in the obese subjects. These data suggest that the excess health risks associated with obesity may not be fully appreciated.

Adipose Tissue

Onset of obesity and puberty in genetically obese SHHF/Mcc-cp rats.

SHHF/Mcc-cp rats, as a model of obesity and diabetes, were followed through breeding and throughout development to determine timing of obesity and sexual development. The obesity or corpulency gene (cp) follows recessive transmission characteristics with no segregation between sexes. Although the frequency of litter sizes was different, the mean litter size of heterozygous mating (8.9 +/- 0.3 pups/litter) was not different from homozygous lean matings (7.9 +/- 0.3 pups/litter). Body weights of the population of female obese rats statistically deviated from lean females at day 35 and obese males deviated from lean males at day 37. Vaginal opening of obese and lean females did not differ in time of occurrence (day 34.6 +/- 0.2 for lean and 33.6 +/- 0.4 for obese). To further evaluate development and examine onset of diabetes, animals were killed at six, eight and ten weeks of age and development of reproductive organs and plasma levels of insulin, glucose, and testosterone or oestradiol determined. Testes development was slightly retarded in the obese male with smaller testes at six weeks of age, however testes size increased at eight and ten weeks of age and was not significantly less than lean males. In contrast, testes function was impaired with smaller seminal vesicles and lower testosterone levels in the obese male rats. Both ovarian and uterine weights were significantly less in obese females. However, oestradiol levels were not significantly different at any of the time points examined. Development of elevated insulin levels were first noted in the obese female at six weeks of age, however marked hyperinsulinemia developed only in the obese males at ten weeks of age.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance

Anti-obesity effect of two different levels of dehydroepiandrosterone in lean and obese middle-aged female Zucker rats.

Dehydroepiandrosterone has previously been shown to prevent weight gain in growing lean and obese mice and rats. In the present study, lean and obese female Zucker rats were treated with either 0.6 or 1.0 percent DHEA in the diet from 8 until 14 months of age. In lean rats, 0.6 percent DHEA prevented weight gain and 1.0 percent DHEA resulted in significant weight loss compared to initial body weight. Control lean rats had a significant weight gain. Both 0.6 and 1.0 percent DHEA obese rats lost weight over the experimental period while control obese rats gained weight. Food intake of DHEA-treated obese rats was lowered compared to control obese rats but was similar to that of all lean groups. DHEA lowered serum insulin levels in both lean and obese rats relative to control groups. Both 0.6 and 1.0 percent DHEA lean rats had elevated hepatic G6PD activity compared to control lean rats. DHEA obese rats had lowered G6PD activity compared to the control obese rats. Hepatic malic enzyme was elevated by DHEA treatment in both lean and obese Zucker rats. Adipose tissue weights were lowered substantially in DHEA treated lean and obese rats versus their control groups. These data indicate that DHEA treatment in adult rats has an anti-obesity effect.

Adipose Tissue

Differences in clinical and endocrine features between obese and non-obese subjects with polycystic ovary syndrome: an analysis of 263 consecutive cases.

Two hundred and sixty-three women with ultrasound-diagnosed polycystic ovary syndrome were studied of whom 91 (35%) were obese (BMI greater than 25 kg/m2). Obese women with PCOS had a greater prevalence of hirsutism (73% compared with 56%) and menstrual disorders than non-obese subjects. Total testosterone and androstenedione concentrations in serum were similar in the two subgroups but SHBG concentrations were significantly lower, and free testosterone levels higher, in obese compared with lean subjects. In addition, concentrations of androsterone glucuronide, a marker of peripheral 5 alpha-reductase activity, were higher in obese than in non-obese women with PCOS. There were no significant correlations of either SHBG or free testosterone with androsterone glucuronide suggesting that obesity has independent effects on transport and on metabolism of androgen. There were no significant differences between the subgroups in either baseline gonadotrophin concentrations or the pulsatile pattern of LH and FSH secretion studied over an 8-h period. There was, however, an inverse correlation of FSH with BMI, but only in the obese subgroup. In conclusion, the increased frequency of hirsutism in obese compared with lean women with PCOS is associated with increased bio-availability of androgens to peripheral tissues and enhanced activity of 5 alpha-reductase in obese subjects. The mechanism underlying the higher prevalence of anovulation in obese women remains unexplained.

Androgens

[The personality of obese persons in psychological tests with special consideration on latent obesity].

The results of psychological tests of the obese are inconsistent and no characteristic personality structure of the obese can be deduced from them. Investigations in childhood obesity failed to establish a general psychogenetic model of obesity. Yet overweight and ideal weight-subjects differ in spontaneous eating behaviour. Appetite and satiety of obese subjects are controlled by external stimuli to a far greater extent than in nonobese. From a behavioural scientific viewpoint it is proposed that learning experiences during childhood socialisation generate the disposition for obesity which can manifest itself later, after interaction with a special environment. At this stage, however, individual reactions to starting overweight are insolved; this process is strongly influenced by individual personality structures: an inadequate conflict management favours obesity; by cognitive control normal weight can be preserved in spite of the acquired disposition for obesity. Taking these "latently obese" as an example the role of personality structure and wrong eating habits is discussed and related to possible therapeutic strategies. A model of the psychogenetic basis of obesity is proposed. In this model eating-related learning experience is attributed a primary role and individual personality structure a secondary role in the psychogenesis of obesity.

Age Factors

[Correlation between changes in obesity from adolescence to young adulthood and family obesity--the results of cross sectional and longitudinal studies].

We conducted a survey of 356 married couples and their 552 children living in Hisayama in Fukuoka prefecture in order to investigate the correlation between changes in obesity from adolescence to young adulthood. 1. A positive correlation between couples in weight and height could be found, but its coefficient was weak (r = 0.12, 0.10). There was no correlation between couples in BMI. 2. The correlation between parents and their children in height, weight and BMI was significantly positive (r = 0.18, 0.45), having a coefficient greater than that of the correlation between married couples. 3. The correlation coefficient between mother and child was greater than that of the correlation coefficient between father and child. 4. The BMI of a child with either parent obese was significantly greater than that of a child with neither parent obese. Obesity appeared more frequently in children whose BMI of parent was higher. 5. A positive correlation between the BMI of young adults and that of adolescents could be found, and the average BMI of the obesity group was higher than that of the non-obesity group even in the adolescent subjects. 6. Even after considering BMI during adolescence, the familial factor had a significant relationship to the BMI of young adulthood. These results suggest that obesity in adolescence will influence obesity in young adulthood, and that the appearance of obesity strongly correlates with the familial obesity factor. In conclusion, it is very important to take preventative measures, in cooperation with the family, early in a child's adolescent years in order to avoid obesity in adulthood.

Adolescent

Alterations in adipocyte adenylate cyclase activity in morbidly obese and formerly morbidly obese humans.

Studies examining animal models of genetic obesity have identified defects in adipocyte hormone-stimulated lipolysis that involve the adenylate cyclase transmembrane signaling system, specifically those components that decrease adenylate cyclase activity. To determine whether obese people demonstrate alterations in adenylate cyclase activity that could contribute to the maintenance of obesity by inhibiting lipolysis, we examined human adipocytes from patients who were lean, obese, or formerly obese. Fat samples were obtained from the lower abdomen of 14 women who were morbidly obese (obese group), from 10 women who were formerly morbidly obese and had lost weight after gastric stapling (postobese group), and from 10 similarly aged women of normal weight (controls). Adipocyte adenylate cyclase activity was determined under ligand-free (no stimulatory or inhibitory influences present), hormone-stimulated (isoproterenol, 10(-6) mmol/L), and maximal (cells stimulated with 10 mumol/L forskolin) conditions by measuring cyclic adenosine monophosphate (cAMP) levels by radioimmunoassay. The activity of adenylate cyclase was significantly different (p less than 0.01) in the three groups. Adipocytes from obese women had lower levels of cyclase activity under both ligand-free (5% vs 16% of maximal) and hormone-stimulated conditions (76% vs 100% of maximal) than adipocytes from normal women. Postobese women had levels of hormone-stimulated cAMP identical to those of normal women but still had abnormal ligand-free levels (under 5%). These results suggest the presence of an alteration in adipocyte adenylate cyclase regulation in morbidly obese women that is not entirely corrected when weight is lost after food intake is reduced by gastric stapling. This alteration in ligand-free cAMP activity may contribute to the development and maintenance of obesity.

Adenylyl Cyclases