Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “OBESITY”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

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

At least 1,747 records · Page 97Linked to original sources
PubMed1989

Energy metabolism in human obesity.

Obesity results from a chronic imbalance between energy intake and expenditure. Accurate measurements of total energy expenditure of lean and obese individuals with a respiration chamber have clearly shown that obese individuals expand more energy than lean sedentary subjects. Studies on the body composition of obese individuals reveal that not only the fat mass is enlarged, but the fat-free mass is also increased as compared with that of lean subjects. Since basal metabolic rate is proportional to the fat-free mass, obese subjects have a greater basal metabolic rate than lean controls. The energy cost of weight bearing activities such as walking and standing is related to body weight, and is therefore increased in obese individuals. The thermogenic response to food ingestion, the diet-induced thermogenesis, has been found to be reduced in some groups of obese people, but not in all obese individuals. The thermic effect of glucose or to meal ingestion is blunted in obese subjects with insulin resistance. Any alteration in thermogenic responses to a caloric excess can be important to store or to oxidize part of the excessive energy intake. After weight reduction in obese subjects due to a hypocaloric diet, the total 24-hour energy expenditure decreases by 20 to 25 kcal/day for each kilogram of weight loss. Failure to adapt the every day energy intake accordingly will result in body weight gain and relapse of obesity.

Basal Metabolism↗
PubMed1999

Assessment of GH/IGF-I axis in obesity by evaluation of IGF-I levels and the GH response to GHRH+arginine test.

The GH response to provocative stimuli in obese is often as low as in panhypopituitaric patients with severe GHD; however, IGF-I levels are normal or slightly reduced. In 53 patients with simple obesity (11 M and 42 F, age: 40.3+/-1.6 yr, BMI: 39.1+/-1.0 Kg/m2), we evaluated the GH response to GHRH (1 microg/kg iv)+arginine (ARG, 0.5 g/kg iv), and total IGF-I levels. The mean (+/-SE) GH peak after GHRH+ARG was markedly lower (74% reduction, p<0.0001) in obese (16.8+/-2.0 microg/l) than in normal subjects (62.7+/-4.3 microg/l). IGF-I levels in obese patients (134.0+/-7.6 microg/l) were lower (33% reduction, p<0.001) than in normal subjects (200.8+/-5.7 microg/l). Taking into account the 3rd centile limit of normal response, the GH response to GHRH+ARG was reduced in 62.3% (33/53) of the obese patients, and 21.2% (7/33) of them had low IGF-I levels. Assuming the 1st centile limit, it was reduced in 33.9% (18/53) obese subjects, and 22% (4/18) of them had low IGF-I levels. Considering 3.0 microg/L as arbitrary cut-off, the GH response was reduced in 5.7% (3/53) of the obese patients, and still one of them had low IGF-I levels. Our findings: a) confirm that the secretory capacity of somatotroph cells is often deeply impaired in obesity; b) demonstrate that IGF-I assay generally rules out severe impairment of GH/IGF-I axis in obese patients with marked reduction of the GH secretion; c) indicate that the percentage of obese patients with concomitant reduction of GH secretion and IGF-I levels is not negligible. Thus, IGF-I assay should be routinely performed in obese patients; those presenting with low IGF-I levels should undergo further evaluation of their hypothalamo-pituitary function and morphology, particularly in the presence of empty sella.

Adult↗
PubMed2002

Comparison of circulating and local adipose tissue renin-angiotensin system in normotensive and hypertensive obese subjects.

The renin-angiotensin-aldosterone system (RAAS) plays a well-recognized role in the regulation of BP and in salt and water balance. Since hypertension affects a considerable proportion of obese patients, circulating RAAS has been studied in obese subjects with and without hypertension, albeit with conflicting results. Furthermore, attention has recently focused on the expression of the components of the Renin-angiotensin system (RAS) in some organs, including adipose tissue where it seems to be involved in the regulation of growth and differentiation. The aim of our study was to investigate circulating RAAS and adipose tissue RAS in obese patients with and without hypertension and in matched controls. PRA, and plasma and urinary aldosterone levels were measured in 35 obese, 30 hypertensive obese patients and in 20 controls. In addition, the expression of angiotensinogen (AGT) and angiotensin II type 1 receptor (AT1) genes was studied in sc adipose tissue from 8 obese, 6 hypertensive obese and 6 healthy subjects. As previously demonstrated in other studies, there were no significant differences in the levels of circulating RAAS components in the 3 groups. As regards local RAS, interestingly, we found that AT1 gene was significantly more expressed in sc adipose tissue from obese patients with hypertension than in those without hypertension and controls. By contrast, AGT levels were similar in the 3 groups. Our data do not support the hypothesis of an involvement of circulating RAAS in the development of obesity-related hypertension. On the other hand, local RAS seems to be differently regulated in sc adipose tissue from obese patients with hypertension with respect to normotensive obese patients and controls.

Adipose Tissue↗
PubMed2006

Growth hormone status in morbidly obese subjects and correlation with body composition.

Morbidly obese subjects are characterized by multiple endocrine abnormalities and these are paralleled by unfavorable changes in body composition. In obese individuals, either 24-h spontaneous or stimulated GH secretion is impaired without an organic pituitary disease and the severity of the secretory defect is proportional to the degree of obesity. The GHRH+arginine (GHRH+ARG) test is likely to be the overall test of choice in clinical practice to differentiate GH deficiency (GHD) patients. Similarly to other provocative tests, GHRH+ARG is influenced by obesity per se. Therefore, a new cut-off limit of peak GH response of 4.2 microg/l in obese subjects has been recently assumed. The aim of the present study was to investigate the reciprocal influence between decreased GH secretion and body composition in a group of 110 morbidly obese subjects, using the new cut-off limit of peak GH response to GHRH+ARG test for these subjects. In our study, GHD was identified in 27.3% of the obese subjects, without gender difference. In GDH obese subjects body mass index (BMI), waist circumference, waist-to-hip ratio (WHR), fat mass (FM), and resistance (R) were higher while reactance (Xc), phase angle, body cell mass (BCM), IGF-I, or IGF-I z-scores were lower than in normal responders (p<0.001). In all obese subjects, GH peak levels showed a negative correlation with age, BMI, waist circumference and FM, and a positive correlation with IGF-I. In the stepwise multiple linear regression, waist circumference and FM were the major determinants of GH peak levels and IGF-I. In conclusion, using the new cut-off limit of peak GH response to GHRH+ARG test for obese subjects, about 1/3 morbidly obese subjects were GHD. GHD subjects showed a significantly different body composition compared with normal responders, and the secretory defect was correlated to different anthropometric variables with waist circumference and FM as the major determinants.

Adipose Tissue↗
PubMed1997

Incidence of NIDDM and the effects of gender, obesity and hyperinsulinaemia in Taiwan.

Our aim is to determine non-insulin-dependent diabetes mellitus (NIDDM) incidence in Taiwan and examine its relation to obesity and hyperinsulinaemia in Chinese men and women. A total of 995 men and 1195 women aged 35-74 years free from diabetes in two townships in Taiwan were followed up with a second examination. At baseline general and metabolic data were recorded, and detailed anthropometric parameters and plasma glucose and insulin were assessed. World Health Organisation (WHO) criteria of fasting glucose 7.8 mmol/l or greater was utilized for defining diabetes. The age-standardized incidence rate based on the United States population in 1970 was 9.3/1000 (CI 5.8-12.8) in men and 9.3/1000 (CI 6.2-12.4) in women and the based on the WHO population in 1976 was 8.9/1000 (CI .5-12.3) in men and 8.9/1000 (CI 5.9-11.9) in women for the Chinese who had a mean BMI slightly greater than 24 (kg/m2). The predictability of the plasma glucose level was greater than that of the insulin level and the obesity indices. NIDDM incidence increased approximately threefold with each 0.67 mmol/l increase in plasma glucose level in men and women. The present study demonstrated the essential relationship of not only BMI but also central obesity indices (such as subscapular and waist circumference) to the incidence of NIDDM among men and women and a stronger relationship between NIDDM incidence and obesity in women than in men. The predictive effects of obesity indices and fasting plasma insulin values on NIDDM risk were independent of each other in men. Obesity and hyperinsulinaemia each without the presence of the other can lead to an increased risk of NIDDM. In women the NIDDM incidence increased more than additively in those with both obesity and hyperinsulinaemia compared to those with single obesity or hyperinsulinaemia. A slightly higher incidence of NIDDM in Taiwan than in western countries was found. The importance of obesity is indicated for predicting NIDDM in the community. Hyperinsulinaemia was found to play a significant role in predicting NIDDM incidence independent of obesity in men and synergistically with obesity in women.

Adult↗
PubMed2000

Enhanced escape of non-esterified fatty acids from tissue uptake: its role in impaired insulin-induced lowering of total rate of appearance in obesity and Type II diabetes mellitus.

AIMS/HYPOTHESIS: To estimate non-esterified fatty acids kinetics in patients with Type II (non-insulin-dependent) diabetes mellitus and obese subjects in the postabsorptive state and during hyperinsulinaemia using non-equilibrium tracer conditions. METHODS: We evaluated the effect of hyperinsulinaemia [euglycaemic clamp with insulin infused at 30 mU x kg(-1) x h(-1) (3-4 h) and 150 mU x kg(-1) x h(-1) (3 h)] on non-esterified fatty acid kinetics, traced with [14C]-palmitate using non-equilibrium tracer conditions in non-obese and obese healthy subjects and Type II diabetic patients (10 per group). Michaelis-Menten kinetics were applied for total non-esterified fatty acid disposal, which was assumed to be composed of total arterial plasma non-esterified fatty acid rate of appearance (equalling the rate of disappearance) and tissue uptake of non-esterified fatty acids derived from intravascular triglyceride hydrolysis. A model was developed to calculate the rate of escape of non-esterified fatty acids from tissue uptake and the net rate of tissue lipolysis. RESULTS: Total arterial plasma non-esterified fatty acid rate of appearance was lower in non-obese healthy subjects than in the other groups at low insulin infusion (p < 0.05) and in obese Type II diabetic patients at high insulin infusion (p < 0.05). Plasma triglycerides were also lowest in non-obese healthy subjects during hyperinsulinaemia (p <0.05 from other groups). The rate of escape from tissue uptake decreased during hyperinsulinaemia (p < 0.05 for each group) but remained higher in obese Type II diabetic patients (p < 0.05 from non-obese healthy subjects). In contrast, net rate of tissue lipolysis was not different between the groups at baseline and its decline during hyperinsulinaemia (p < 0.05 for each group) was similar in all groups. CONCLUSION/INTERPRETATION: This study challenges the view that the antilipolytic effect of insulin is impaired in Type II diabetes and obesity. We suggest that a high plasma triglyceride concentration causes a higher escape of non-esterified fatty acids from tissue uptake, leading to an impaired suppression of total arterial plasma rate of appearance during a low degree of hyperinsulinaemia in obese subjects and Type II diabetic patients and during a high degree of hyperinsulinaemia in obese Type II diabetic patients.

Adult↗
PubMed1998

Final reflections: wellness after obesity surgery.

The articles presented in this symposium on treatment of clinically severe obesity cover most of the topics related to obesity surgery, from basic research about genetic causes of obesity to surgical techniques and clinical results on the severely obese patient. The most striking feature of those results observed after bariatric surgery for the clinically severe obese is not the remarkable weight loss and normalization of the body mass index but the amelioration of some of the metabolic and physiologic abnormalities related to obesity. In fact, carbohydrate and lipid metabolism show improvement, as do cardiac and pulmonary function. These observations justify all efforts devoted to the design and improvement of sound bariatric surgical techniques. Moreover, surgeons seek the well-being of the ex-obese patient, and in doing so they face special discriminatory attitudes from colleges, patients' families, and the society, mainly because of negative stereotypes related to the obese individuals and the lack of information on the real benefits of bariatric procedures. Bariatric surgeons will reach their goal only when an informed society, educated physicians, and properly oriented obese patients together give to bariatric surgery its real dimension. The objective of any surgeon is the wellness of his or her patient. This is important in bariatric surgery as well; beyond excess weight loss and normalization of biochemical parameters, the ex-obese patient should be able to live a normal, productive, happy life. Approaching this goal is a task that takes months or even years. Bariatric surgeons are committed to support and help their patients until they reach wellness after obesity surgery.

Health Status↗
PubMed2006

Genotype-by-nutrient interactions assessed in European obese women. A case-only study.

BACKGROUND: The development of obesity is influenced by both genetic and environmental risk factors. Whereas changes in the environment appear to be responsible for the increasing prevalence of obesity, genetic factors interacting with environmental factors would contribute to explain obesity onset and severity. AIM: To explore epidemiologic genotype-by-nutrient interactions in obesity. METHODS: A total of 42 polymorphisms of 26 candidate genes for obesity were genotyped in 549 adult obese women recruited from eight European centres in a case-only study. The nutritional variables assessed in this study were the dietary fibre intake (grams per day), the ratio of dietary polyunsaturated fat to saturated fat (P:S ratio) and the percentage of energy derived from fat in the diet as calculated from a weighed three-day food record (%E). Under the assumption of genotype-nutrient independence in the population, the odds ratio calculated in a sample of obese women would indicate the existence of genotype-by-nutrient interactions, measured as deviations from the multiplicative effects of the genetic and the nutrient factors separately. RESULTS: No new but confirmaty evidences for genotype-by-nutrient interactions in obesity were detected in this case-only study. The test of interaction between fibre intake and the -514 C > T polymorphism of the hepatic lipase gene (LIPC) yielded P-values of 0.01 across different statistical models. Likewise, the -11377G > C polymorphism of the adiponectin gene (ADIPOQ) and the -681 C > G polymorphism of the PPARG3 gene might interact with the percentage of energy derived from fat in the diet for the development of obesity (P-values in the range of 0.01-0.05 across different statistical models). The P-values were not adjusted for multiple testing, so these results should be considered with caution. CONCLUSIONS: Although the use of obese-only samples is theoretically a useful approach to detect interactions, few genotype-by-nutrient interactions have been suggested in obese European women after the analysis of candidate polymorphisms and the selected nutrient variables. The most remarkable multiplicative interaction found in this study refers to the combination of the hepatic lipase gene polymorphism -514 C > T and fibre intake.

Adiponectin↗
PubMed1997

Markers for the gene ob and serum leptin levels in human morbid obesity.

Leptin, the product of the ob gene, reduces body fat in genetically obese animals and circulates in elevated concentrations in the blood of obese patients. Polymorphic markers situated in the proximity of the human ob gene have recently been suggested to be linked to morbid obesity. We have studied the possible association between the microsatellite markers near the ob gene and morbid obesity in 252 morbidly obese patients with a mean body mass index (BMI) of 43 +/- 7 kg/m2, and 151 lean controls with a mean BMI of 22 +/- 2 kg/m2, and searched for linkage of these gene markers to obesity in 76 affected sib-pairs (BMI > or = 32). No significant association was observed between any of the eight microsatellite markers and morbid obesity, and affected-sib-pair analysis failed to show linkage of three selected ob gene markers to obesity in the sibships. There was a strong positive correlation between serum leptin levels and BMI in morbidly obese patients; a carrier status for either of the two most prevalent alleles of the microsatellite marker D7S530 in the vicinity of the ob gene was associated with serum leptin levels in the obese subjects. Two of the markers (D7S2519, D7S649) showed a significant relation to the weight-losing response to a 16-week very-low-calorie dietary intervention. We have thus been able to confirm a tight relationship between serum leptin and body mass but have found no evidence for genetic linkage of the ob gene markers to morbid obesity in a population considered to represent a genetic isolate and to be an ideal model for studies of complex disorders.

Adult↗
PubMed2006

Effect of genetic variation in the leptin gene promoter and the leptin receptor gene on obesity risk in a population-based case-control study in Spain.

There are no good genetic markers for incorporating the study of genetic susceptibility to obesity in epidemiological studies. In animal models, the leptin (LEP) and the leptin receptor (LEPR) genes have been shown to be very important in obesity because leptin functions as a negative feedback signal in regulating body-weight through reducing food intake and stimulating energy expenditure. In humans, several polymorphisms in these genes have been described. However, their association with obesity is still very controversial because there are no good case-control studies designed to specifically test this association. Our objective has been to conduct a population-based case-control study to estimate the risk of obesity arising from the -2548G > A and Q223R polymorphisms in the LEP and LEPR genes, respectively. 303 obese cases (101 men and 202 women) and 606 controls (202 men and 404 women) were selected from a Spanish Mediterranean population. Genetic, clinical and life-style characteristics were analyzed. No association was found between the -2548G > A polymorphism and obesity. However, the Q223R variant was significantly associated with obesity in a recessive model, the RR genotype being more prevalent in controls than in obese subjects. The inverse association between the Q223R polymorphism and obesity (OR = 0.62; 95% CI: 0.39-0.99) remained significant even after additional adjustment for education, tobacco smoking, alcohol, physical activity, origin of the obese patient, and the -2548G > A polymorphism in the LEP gene (OR = 0.54; 95% CI: 0.32-0.89). In conclusion, the -2548G > A polymorphism is not a relevant obesity marker in this Mediterranean population, although Q223R does seen to be so.

Adolescent↗
PubMed1987

Medical evaluation and treatment of the obese patient with cardiovascular disease.

The incidence of coronary artery disease only weakly correlates with the percent of excess body weight; however, obesity in humans is not a homogeneous condition. Classification of obesity based on anatomic distribution of body fat allows for identification of a group of patients at increased risk for cardiovascular disease. Abdominal (upper body) obesity, measured as the waist/hip ratio, is a strong independent risk factor of cardiovascular disease and should be used to assess a subgroup in need of medical weight loss treatment. A focus on dietary fat intake and the magnitude of overeating "caloric intake" are central to the pathogenesis of cardiovascular disease observed in the obese person. Identification of the process of overeating (magnitude of recent weight gain, episodes of weight cycling) is important in the design of successful medical nutrition treatment programs. A nutrition/medical history that includes age of obesity onset and duration of obesity provides additional criteria for assessment of risk of disease. Childhood-onset obesity and prolonged obesity (greater than 15 years) has been associated with increased cardiovascular disease risk. Recently, grades of obesity based on body mass index have provided a valuable marker for treatment. Each reduction in obesity grade (equal to delta 5 body mass index or delta 11.6 kg) is associated with a decrease in risk of medical illness. The new focus of obesity treatment should be to decrease body weight in 10% to 15% increments (equal to 1 grade) with emphasis on reducing the risk of medical illness and treatment intensity (e.g., number of existing medical visits, hospitalization).(ABSTRACT TRUNCATED AT 250 WORDS)

Body Weight↗
PubMed1990

Increased volume and decreased emptying of the gallbladder in large (morbidly obese, tall normal, and muscular normal) people.

Impaired gallbladder emptying has been suggested as a possible factor in the pathogenesis of gallstones. Obese people have an increased incidence of gallstones, but there is no evidence of this in nonobese large people. This study was undertaken to determine if abnormal gallbladder motility is present in obese people. Fasting gallbladder volumes were determined using real-time ultrasound in 18 morbidly obese subjects whose weights were in a steady state [45 kg (100 lb) over ideal weight or twice expected weight for age and height; 9 males, 9 females], 18 age- and sex-matched volunteers of average size, and 18 nonobese large normal males (9 tall, 9 muscular). Gallbladder emptying studies with 99mtechnetium-diisopropyliminodiacetic acid were performed using 200 ml of 10% cream as a stimulus. The small-volume liquid fatty meal contained 113indium-diethylenetriaminepentaacetic acid to control for differences in gastric emptying in obesity. The gallbladder emptying rate in large people, both obese and nonobese, was less than that in normals of average size (p = 0.05). Fasting gallbladder volumes in large people were: obese, 41 ml (37-66 ml) (median; 95% confidence limits); nonobese large normal, 40 ml (27-43 ml). These values were greater than in normals of average size [17 ml (14-21 ml) (p = 0.03)]. Postprandial gallbladder volumes were also greater in large people: obese, 15 ml (8-23 ml); nonobese large normal, 20 ml (13-23 ml) compared with 2 ml (1-5 ml) in normals of average size (p less than 0.05). There were no differences between obese and nonobese large people. There were no differences in gastric emptying rates or in cholecystokinin, gastrin, motilin, and secretin release between obese and normal subjects. Gallbladder volume is crudely proportional to body size. Although fasting and postprandial volumes are greater in obesity, this is also present in nonobese, relatively size-matched controls. These data do not support a role for impaired gallbladder emptying in gallstone formation in obese patients whose weights are in a steady state.

Adult↗
PubMed1986

Effect of diet on energy expenditure and plasma norepinephrine in lean and obese Pima Indians.

To assess whether thermogenesis or sympathetic nervous system (SNS) function might differ between lean and obese human subjects, studies of thermic and sympathetic responses to standard stimuli were undertaken in Pima Indians, an ethnic group with a high prevalence of obesity. Plasma levels of norepinephrine (NE) and energy expenditure at rest and in response to feeding, exercise, and graded infusions of NE were compared in five lean and five obese Indians during a period of weight maintenance (WM), after 3 weeks of overfeeding (OF) and, in the obese, also after 6 weeks of underfeeding (UF). Basal energy expenditure, when adjusted for fat free mass, was equivalent during WM and increased 3% with OF (P less than 0.01) in both groups. Thermic responses to exercise or a test meal did not differ in lean and obese and did not change with OF, while thermic responses to NE infusion fell during OF to a greater degree in obese than lean (P less than 0.05). A similar pattern (decreased effect in obese with OF) was also noted in the glycemic response to infused NE (P less than 0.05). Although not quantitatively different in lean and obese, the plasma NE concentration appeared to vary more in response to feeding or dietary alteration in the obese than lean, a finding that may reflect lower plasma clearance of NE in the obese. These studies, therefore, raise the possibility that overfeeding in obese Pima Indians may limit the contribution of sympathetically mediated thermogenesis to energy expenditure, though the implications of this for body weight regulation are speculative.

Adolescent↗
PubMed1993

Antihypertensive effects of CS-045 treatment in obese Zucker rats.

The association of hypertension with obesity has been well recognized, but the etiology remains poorly understood. Obesity is characterized by hyperinsulinemia, which reflects peripheral insulin resistance. Insulin resistance may participate in the development of hypertension with obesity. CS-045 [(I)-5-[4-(5-hydroxy-2,5,7,8-tetramethylchroman-2-yl-methoxy)be nzy l]-2,4- thiazolidiendion] is a new orally effective antidiabetic agent that potentiates insulin action and reduces insulin resistance in obese Zucker rats and other obese diabetic animals. In this study, we examined the antihypertensive effect of CS-045 in obese male and female Zucker rats as a model of hypertension associated with obesity. CS-045 was administered as a food admixture (approximately 16 and approximately 70 mg/kg/d) for 4 weeks (female) and (approximately 15 and approximately 67 mg/kg/d) 8 weeks (male) in obese Zucker rats at 5 to 7 months of age. CS-045 slightly but significantly decreased plasma glucose levels. Plasma insulin levels were significantly decreased in obese male rats, but were not significantly decreased in obese female rats. Drug administration led to significant decreases in plasma triglyceride and cholesterol levels and systolic blood pressure (SBP) in a dose-dependent manner from 1 week after administration in obese Zucker rats. CS-045 increased urinary sodium excretion, sodium/potassium ratio, and creatine clearance in a dose-dependent manner, and also led to a remarkable decrease in urinary protein excretion. However, CS-045 did not reduce urinary catecholamine excretion. These data indicate that CS-045 may promote renal sodium excretion and improve decreased glomerular filtration rates, which may reflect the amelioration of insulin resistance.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Effect of pyridostigmine on the growth hormone response to growth hormone-releasing hormone in lean and obese type II Diabetic patients.

A suppressed growth hormone (GH) response to GH-releasing hormone (GHRH) in both lean and overweight type II diabetics has been reported. Pyridostigmine (PD), an acetylcholinesterase inhibitor, elicits GH secretion when administered alone and enhances the GH response to GHRH in normal subjects. The aim of our study was to evaluate the effect of PD on GHRH-stimulated GH secretion in both lean and obese type II diabetic patients. We studied 16 patients with type II diabetes mellitus (seven lean and nine obese). Eleven nondiabetic subjects (six lean and five obese) served as controls. Each subjects underwent treatment with (1) 120 mg PD orally or (2) 2 tablets of placebo orally, 60 minutes before intravenous (IV) injection of 100 micrograms GHRH-(1-29)NH2. We have found no significant differences in GH responses to GHRH between obese diabetics and obese controls. On the other hand, the absolute GH levels were significantly suppressed in lean type II diabetics compared with lean controls at 15 and 30 minutes after GHRH injection. Obese diabetic subjects had slightly but not significantly decreased GH responses to GHRH+PD compared with obese nondiabetic subjects (8.36 +/- 1.62 v 14.4 +/- 7.62 micrograms/L). Lean type II diabetics showed a blunted GH release after GHRH+PD compared with normal-weight healthy subjects (GH peaks, 15.77 +/- 2.17 v 40.88 +/- 6.17 micrograms/L, P < .05). PD enhanced significantly the GH response to GHRH in obese diabetics, obese controls, and non-obese controls (P < .05), but not in non-obese type II diabetics.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Glucose↗
PubMed1990

Prevalence of vascular complications in untreated diabetics with obesity during an 18 year period.

Prevalence of vascular complications in newly diagnosed untreated diabetic patients with obesity was studied over a period of 18 years. A total of 742 patients including 241 subjects with obesity (BMI greater than 25) were analyzed. Obese patients showed higher serum cholesterol and triglyceride and lower HDL-cholesterol levels than non-obese patients. Average prevalence of obesity is shown to be 32.5% with higher prevalence in women (37.8%) than in men (28.3%, P less than 0.01). No definite change is found in yearly prevalence throughout the observation period. Ischemic ECG findings and hypertension were observed more frequently in obese (35.8% and 34.9%, respectively) than in non-obese (25.2%, P less than 0.02; 24.5%, P less than 0.01, respectively) subjects, while diabetic retinopathy was less in obese patients (P less than 0.05). The prevalence of proteinuria was almost the same in obese and non-obese groups. These results coincide with the general concept that obesity may be responsible for the development of macroangiopathy in diabetes mellitus.

Adult↗
PubMed2004

Hypertension in overweight and obese primary care patients is highly prevalent and poorly controlled.

BACKGROUND: Although the relationship between body weight and blood pressure (BP) is well established, there is a lack of data regarding the impact of obesity on the prevalence of hypertension in primary care practice. The objective of this study was to assess the prevalence of hypertension and the diagnosis, treatment status, and control rates of hypertension in obese patients as compared to patients with normal weight. METHODS: A cross-sectional point prevalence study of 45,125 unselected consecutive primary care attendees was conducted in a representative nationwide sample of 1912 primary care physicians in Germany (HYDRA). RESULTS: Blood pressure levels were consistently higher in obese patients. Overall prevalence of hypertension (blood pressure >/=140/90 mm Hg or on antihypertensive medication) in normal weight patients was 34.3%, in overweight participants 60.6%, in grade 1 obesity 72.9%, in grade 2 obesity 77.1%, and in grade 3 obesity 74.1%. The odds ratio (OR) for good BP control (<140/90 mm Hg) in diagnosed and treated patients was 0.8 (95% confidence interval [CI] 0.7-0.9) in overweight patients, 0.6 (95% CI 0.6-0.7) in grade 1, 0.5 (95% CI 0.4-0.6) in grade 2, and 0.7 (95% CI 0.5-0.9) in grade 3 obese patients. CONCLUSIONS: The increasing prevalence of hypertension in obese patients and the low control rates in overweight and obese patients document the challenge that hypertension control in obese patients imposes on the primary care physician. These results highlight the need for specific evidence-based guidelines for the pharmacologic management of obesity-related hypertension in primary practice.

Adolescent↗
PubMed2004

Morbid obesity is not a contraindication to kidney transplantation.

BACKGROUND: Concern that morbidly obese (body mass index [BMI] 35) kidney transplant recipients have worse outcomes than non-morbidly obese recipients leads many transplant centers to deny them the benefit of kidney transplantation. These concerns are supported by guidelines recently published by the American Society of Transplantation. However, successfully transplanted morbidly obese persons have a survival advantage over those that remain on dialysis. It is our practice to evaluate morbidly obese transplant candidates for transplantation under the same criteria used for nonobese candidates. This report reviews our experience with morbidly obese kidney transplant recipients having a three year follow-up. METHODS: Outcomes for 23 morbidly obese (BMI 35, range 37 to 56) kidney transplant recipients transplanted between January 1995 and February 2000 were compared with 224 nonobese (BMI 25) kidney recipients transplanted during the same period. RESULTS: Patient and graft survivals were similar between both groups. Although 3-year graft survival for morbidly obese recipients of cadaver organs was 75% compared with 90% for the nonobese group, this finding was not statistically significant, and 3-year graft survival was 100% for morbidly obese recipients of living donor organs compared with 91% for nonobese recipients. Morbidly obese recipients had significantly longer hospital stays, higher readmission rates, and a higher wound infection rate than nonobese recipients. CONCLUSIONS: We found that morbidly obese persons have 3-year graft and patient survivals similar to nonobese persons. Although they also have greater complications and greater numbers of days in the hospital, we believe these reasons are not sufficient to deny morbidly obese persons the survival and quality-of-life advantages of kidney transplantation.

Actuarial Analysis↗