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PubMedDate not supplied

Comorbidity among the morbidly obese: a comparative study of 2002 U.S. hospital patient discharges.

BACKGROUND: Increased morbidity is associated with increasing severity of obesity. However, among morbidly obese patients, comorbid prevalence has been reported primarily in the bariatric surgical literature. This study compares demographic characteristics and selected comorbid conditions of morbidly obese patients discharged after surgical obesity procedures and morbidly obese patients discharged after all other hospital procedures. METHODS: The 2002 National Hospital Discharge Survey (a nationally representative sample of hospital discharge records) and the International Classification of Diseases, 9th Revision, Clinical Modification were used to identify and describe all morbidly obese patient discharges (n = 3,473) and to quantify the prevalence of selected obesity-related comorbid conditions. RESULTS: Compared with all other morbidly obese patients, the obesity surgery patients (n = 833) were younger (median, 42 vs 48 years; range, 17 to 67) and more female (82.3% vs. 63.7%), with higher rates of sleep apnea (24.0% vs. 11.8%), osteoarthritis (22.9% vs. 11.8%), and gastroesophageal reflux disease (27.7% vs. 11.7%) (all P < .001). The prevalence of type 2 diabetes mellitus was lower in the obesity surgery patients (16.1% vs. 24.3%; P = .003), whereas the rates of hypertension (45.9% vs. 41.0%; P = .13) and asthma (9.6% vs. 12.0%; P = .26) were similar in the two groups. CONCLUSIONS: Demographic characteristics and comorbid prevalence of morbidly obese patients discharged after obesity surgery are consistent with reports in the bariatric surgical literature. Obesity surgery patients had a higher prevalence of some comorbid conditions. Possible explanations for this include preferential diagnosis, differential diagnostic coding, or increased severity of morbid obesity. Advancing surgical and insurance guidelines for bariatric surgery will require clinical data that accurately describe and quantify the demographic distribution of obesity and the associated burden of disease.

Adolescent↗
PubMed1996

Long-term administration of acipimox potentiates growth hormone response to growth hormone-releasing hormone by decreasing serum free fatty acid in obesity.

Obesity is associated with an impairment of normal growth hormone (GH) secretion and blunted responses to all stimuli. A high plasma free fatty acid (FFA) level is frequently observed in obesity. FFA participates in the regulation of pituitary GH secretion. To determine whether the derangement of GH secretion in obesity is associated with high plasma FFA levels, tests with GH-releasing hormone (GHRH) and acipimox (ACX), an antilipolytic agent able to decrease FFA, were undertaken in six obese subjects and seven normal control subjects. In addition, the effect of prolonged suppression of FFA level on GH response to GHRH after administration of ACX for 1 month was also examined in each of the obese subjects. The GH response in obese subjects (median, 9.1 microg/L) to GHRH (1-29) (1 microg/kg intravenously [IV]) was significantly blunted as compared with normal control subjects (23.5 microg / L, P < .05). Basal FFA levels were higher in obese subjects (855.2 microEq / L than in normal control subjects (514.6 microEq / L, P < .05). One-dose ACX (500 mg) decreased FFA levels in both obese and normal subjects: the lowest FFA levels in obese subjects (158.3 microEq/L 2 to 2.5 hours after ACX were similar to those of normal control subjects (108.7 microEq/L). One-dose ACX potentiated GHRH-stimulated GH response in both obese and normal subjects. GH responses potentiated by ACX in obese subjects (27.1 microg/L) were similar to GH responses to GHRH in normal control subjects, but lower than in normal subjects treated with ACX plus GHRH (58.5 microg / L, P < .05). Thereafter, all of the obese subjects were treated with ACX for 1 month, after which the ACX plus GHRH tests were repeated. After 1 month of acipimox administration in the obese subjects, GH responses (38.8 microg/L) were significantly higher than those of obese subjects treated with GHRH and one-dose ACX plus GHRH (P < .05). They were similar to GH responses of normal control subjects receiving the one-dose ACX plus GHRH test. In conclusion, in obesity the prolonged suppression of FFA levels induced by long-term administration of ACX potentiated somatotrope responsiveness, likely acting at the pituitary level, suggesting that the duration of FFA suppression had an important relation to the magnitude of GH response.

Adult↗
PubMed1996

Islet dysfunction in obese women with impaired glucose tolerance.

Insulin sensitivity and islet function were examined in 22 obese women: 11 with normal glucose tolerance (mean +/- SD body mass index [BMI], 32.2 +/- 2.8 kg/m2) and 11 with impaired glucose tolerance (BMI, 30.1 +/- 2.2 kg/m2). Thirteen non-obese women with normal glucose tolerance (BMI, 20.9 +/- 1.3 kg/m2) served as controls. All women were 58 to 59 years of age. Insulin sensitivity was measured with the euglycemic, hyperinsulinemic clamp. Insulin secretion was studied after intravenous arginine (5 g) at fasting, and at blood glucose levels of 14 and greater than 25 mmol/L. Insulin sensitivity was higher in non-obese (99.8 +/- 11.5 nmol/kg/min/pmol insulin/L) than in obese subject (P < or = .002), but did not differ between obese subjects with normal versus impaired glucose tolerance (47.2 +/- 8.8 v 45.5 +/- 5.2 nmol/kg/min/pmol insulin/L, difference not significant [NS]). Obese subjects with normal glucose tolerance had a higher insulin response to both glucose (P < or = .004) and arginine (P < or = .02) than nonobese women, and higher glucose potentiation of insulin secretion, slopeAIR (P = .05). Compared with obese subjects with normal glucose tolerance, the obese subjects with impaired glucose tolerance had a lower insulin response to glucose (P = .03) and to arginine at blood glucose levels of 14 mmol/L (P = .03), as well as a lower slopeAIR levels ( P = .03). Fasting glucagon was higher in obese subjects with normal glucose tolerance than in non-obese subjects with normal glucose tolerance (P = .006). In obese subjects with impaired glucose tolerance, the glucose inhibition of glucagon secretion, slope AGR, was lower than in obese subjects with normal glucose tolerance (P = .04). Thus, obese subjects with impaired glucose tolerance have altered glucose modulation of islet function, mainly manifested as reduced slope AIR and slope AGR, yet insulin sensitivity is not different than in equally obese subjects with normal glucose tolerance. We therefore conclude that islet dysfunction, and not a further reduction of insulin sensitivity, determines the development of impaired glucose tolerance in obesity.

Arginine↗
PubMed1996

Antiobesity effect of diazoxide in obese Zucker rats.

Hyperinsulinism and insulin resistance are characteristic findings in obese subjects. Obesity in both humans and experimental animals is associated with a reduced number of insulin receptors and a decreased insulin-mediated glucose disposal, whereas sensitivity to insulin's antilipolytic action is unaltered. To evaluate the antiobesity effect of diazoxide (DZ), an inhibitor of glucose-stimulated insulin release, 7-week-old Zucker obese and lean rats were studied. Obese and lean rats were grouped into DZ-treated (150 mg/kg/d) and control (C) groups. DZ-treated obese rats consumed similar amounts of calories per kilogram body weight (BW) compared with C obese animals, but gained less weight (P<.01). Postabsorptive plasma free fatty acids (FFA), cholesterol, and triglycerides were significantly higher in obese versus lean animals (P<.01). DZ treatment reduced plasma triglyceride levels in obese animals (P<.001), but had no significant effect on FFA or cholesterol concentrations. Plasma glucose concentrations in the postabsorptive state and during glucose tolerance tests (GTTs) were significantly lower in DZ obese versus C obese rats (P<.01) despite a decrease in plasma insulin concentrations in DZ-treated animals (P<.01). In contrast, DZ lean rats developed glucose intolerance (P<.05). Sensitivity and responsiveness to the antilipolytic effect of insulin in isolated adipocytes were significantly decreased in DZ obese as compared with C obese rats (P<.01). Moreover, adipocyte specific insulin receptor binding was increased in both DZ lean and DZ obese animals (P<.01). This was accompanied by increased basal and insulin-stimulated glucose transport in both genotypes (P<.01). In conclusion, DZ increased insulin receptor binding and glucose transport while decreasing hyperinsulinemia and insulin sensitivity to the antilipolytic action of insulin. This combined effect resulted in improved glucose tolerance and a decrease in weight gain in obese rats, implying that pharmacologic modification of the disturbed insulin metabolism of obesity may be therapeutically beneficial.

Adipocytes↗
PubMed1992

Genetic, hypothalamic and endocrine features of clinical and experimental obesity.

Obesity occurs in both clinical and animal forms in a variety of specific models which allow study of its underlining endocrine and mechanistic features. Among the neuroendocrine varieties of obesity, polycystic ovaries are probably the most common. The importance of the gonadal feedback system for regulation of food intake and obesity is indicated by the effects of castration in experimental animals which is a widely used mechanism for producing experimental obesity. Cushing syndrome and hypothalamic obesity are rare clinical syndromes. The current evidence suggests that there are two types of hypothalamic obesity from a mechanistic point of view--one associated with hyperphagia as a necessary and sufficient cause and a disturbance of the autonomic nervous system without hyperphagia as a second mechanism. Although genetic factors underlie most types of human obesity, there are several dymorphic forms of obesity including the Prader-Willy syndrome, Cohen's syndrome, Carpenter's syndrome, Ahlstrom's syndrome and the Bardet-Biedel syndrome. The Prader-Willi syndrome is characterized by obesity hypotonia hypogonadism and mental retardation. In animals, a dominant form of inheritance of obesity is seen in the yellow mouse. Current evidence suggests that this syndrome can be explained by reduced acetylation of MSH in the pituitary and/or hypothalamus. Several recessively inherited forms of obesity exist including the obese mouse, the diabetes mouse, fatty rat, the fat mouse, tubby mouse and the corpulent rat. In addition, there are a number of polygenic types of experimental obesity. The final mechanistic classification of obesity are those due to dietary manipulation. For both human beings and animals, a highly fat diet appears to be particularly problematic for the development of obesity.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1997

Evaluation of chronic opioid receptor antagonist effects upon weight and intake measures in lean and obese Zucker rats.

Body weight and food intake are significantly reduced in rats during development of dietary obesity following chronic central administration of mu (beta-funaltrexamine, BFNA), mu1 (naloxonazine), kappa1 (nor-binaltorphamine, NBNI), delta1 ([D-Ala2,Leu5,Cys6]-enkephalin, DALCE) and delta2 (naltrindole isothiocyanate, NTII) opioid receptor subtype antagonists. In contrast, rats made obese by maintainance on a 'cafeteria' diet failed to display weight loss following chronic mu1 receptor antagonism. To test the hypothesis that chronic administration of opioid antagonists are less effective in controlling intake and weight in obese animals, the present study assessed whether chronic, central administration of either BFNA (20 micrograms), naloxonazine (50 micrograms), NBNI (20 micrograms), DALCE (40 micrograms) or NTII (20 micrograms) altered weight and intake in lean and obese Zucker rats over seven days. Body weight was reduced following chronic mu (lean: 42 g; obese: 49 g), mu1 (lean: 71 g; obese: 38 g), kappa1 (lean: 30 g; obese 14 g), delta1 (lean: 43 g; obese: 22 g) or delta2 (lean: 37.5 g; obese: 36 g) antagonism. Overall food intake was reduced following chronic mu (lean: 8.8 g; obese: 16.1 g), mu1 (lean: 12.6 g; obese: 17.0 g), kappa1 (lean: 6.5 g; obese 7.0 g), delta1 (lean: 9.7 g; obese: 11.1 g) or delta2 (lean: 9.4 g; obese: 14.3 g) antagonism. Therefore, both lean and obese Zucker rats display weight loss and reduced intake following chronic central administration of opioid receptor subtype antagonists.

Animals↗
PubMed2000

Access and use of medical care among obese persons.

The prevalence of obesity and severe obesity is growing rapidly, along with obesity-related comorbidities and mortality. Given the increased health risks associated with obesity, it is vital that obese persons have adequate access to, and make consistent use of, medical care services. Assuming obese persons have access to medical care that is comparable to non-obese persons, one would expect to observe greater use of medical services among obese persons. In this article we briefly review empirical evidence of the access to and use of medical care among obese persons. Although certain subgroups that tend to have disproportionately high prevalences of obesity (i.e., low socioeconomic status, minority groups) have reduced access to care, no studies have specifically examined whether or not obese persons have the same access to health care as do their lean counterparts. With respect to use of health care services, however, obesity has been consistently linked with greater rates of utilization and increased health care expenditures. Both the increased use and cost appear to be largely a function of treating obesity-associated comorbidities such as diabetes and hypertension. We conclude that, although it is clear that obesity is associated with both greater use and cost of medical care, the relationship between obesity and access to medical care has not been determined.

Health Services Accessibility↗
PubMed2002

Obesity affects myocardial vasoreactivity and coronary flow response to insulin.

OBJECTIVE: Obesity is associated with increased risk for cardiovascular diseases and peripheral endothelial dysfunction. We examined whether myocardial vasoreactivity and coronary-flow response to insulin stimulation are altered in obesity. RESEARCH METHODS AND PROCEDURES: Myocardial blood flow was quantitated in 10 obese men (body mass index, 33.6 +/- 1.9 kg/m(2)) and 10 healthy matched non-obese men (body mass index, 24.2 +/- 1.9 kg/m(2)), using positron emission tomography and oxygen-15-labeled water. The measurements were performed basally and during adenosine infusion (140 microg/kg per minute), with or without simultaneous physiological (1 mU/kg per minute) and supraphysiological (5 mU/kg per minute) hyperinsulinemia. RESULTS: Basal myocardial blood flow was not significantly different between obese and non-obese subjects. Adenosine-stimulated flow was blunted in obese (3.2 +/- 0.6 mL/g per minute) when compared with non-obese subjects (4.0 +/- 1.1 mL/g per minute, p < 0.05). Simultaneous physiological hyperinsulinemia increased adenosine-stimulated myocardial flow significantly in both groups (to 4.03 +/- 1.24 and 4.85 +/- 1.04 mL/g per minute in obese and non-obese men, respectively; p < 0.05 vs. adenosine). Supraphysiological hyperinsulinemia further enhanced the adenosine-stimulated flow in non-obese subjects (to 5.56 +/- 0.98 mL/g per minute; p < 0.05) but not in obese subjects. DISCUSSION: Young obese, healthy men have reduced myocardial vasoreactivity, which may represent an early precursor of future coronary artery disease. Additionally, insulin-induced enhancement of myocardial blood flow is blunted in obesity. Thus, endothelial dysfunction seems to also characterize myocardial vasculature of obese subjects.

Adenosine↗
PubMed2006

The growth of children in relation to the timing of obesity development.

OBJECTIVE: To examine whether there is an association between the timing of the development of obesity and children's growth. RESEARCH METHODS AND PROCEDURES: This study investigated 141 prepubertal obese children (76 girls) and 72 healthy non-obese children (39 girls). The target height standard deviation score (SDS), the percentage weight for height, and the height SDS (H-SDS) at presentation and at the age of 2 years were calculated. Patients were classified, according to whether obesity developed before or after the age of 3 years, as presenting with early-onset or late-onset obesity, respectively. RESULTS: Mean age (+/-SD) at presentation was 9.4 (2.1) years. At the age of 2 years, the H-SDS of the children with early-onset obesity was 1.3 (1.0) vs. 0.9 (1.3) for the late-onset obese (p > 0.5) and 0.4 (1.0) for controls (p < 0.001), and the children with late-onset obesity were also significantly taller than controls (p < 0.005). At presentation, children with early-onset obesity were significantly taller than children with late-onset obesity [1.1 (0.8) vs. 0.6 (1.0); p < 0.001] and controls [0.2 (0.8); p < 0.001]. There was no increase in H-SDS after the age of 2 years in the late-onset obese children (p > 0.05). H-SDS values were below average in 21% of the children with late-onset obesity and in only 4% of the children with early-onset obesity. DISCUSSION: These findings indicate that late development of obesity is not associated with increased stature in prepubertal children; however, it may be preceded by growth acceleration in the early years of life. Growth acceleration in early life may be a predictor for future obesity.

Body Height↗
PubMed2004

Hydralazine as antihypertensive therapy in obesity-related hypertension.

OBJECTIVE: The objectives were two-fold: (1) determine whether the use of hydralazine as antihypertensive therapy during obesity development exacerbated obesity-related cardioacceleration and hormonal abnormalities; (2) determine whether the absence of hypertension in obesity attenuated obesity-related abnormalities in hemodynamics, cardiac hypertrophy, and hormonal profile. DESIGN: Female New Zealand White rabbits were divided into lean control (n=12), lean hydralazine-treated (n=9), obese control (n=11), and obese hydralazine-treated (n=8) groups. Pretreatment mean blood pressure (BP) and heart rate (HR) were determined using telemetry. Pretreatment BP was maintained during 12 weeks of obesity development using hydralazine. MEASUREMENTS: Chronically measured BP and HR; plasma/blood volume; wet and dry ventricular weights; body fat/water; and hormonal profile (plasma renin activity, aldosterone, cortisol, atrial natriuretic peptide, adrenaline, and noradrenaline). RESULTS: Hydralazine treatment in obese animals attenuated obesity-related renin-angiotensin system (RAS) activation. In contrast, RAS was activated in lean hydralazine, as indicated by increased plasma aldosterone. The absence of hypertension in obese hydralazine did not result in attenuation of cardioacceleration, cardiac hypertrophy, or intravascular volumes. CONCLUSIONS: Hydralazine treatment in obese rabbits did not exacerbate obesity-related cardiovascular and hormonal alterations. Cardioacceleration and cardiac hypertrophy persisted in obese hydralazine despite BP control, suggesting hypertension-independent effects of obesity on these variables. Hydralazine's effects on RAS activation differed in lean and obese rabbits, suggesting that the systemic effects of hydralazine as a control therapy in evaluation of antihypertensive medications may differ depending on the underlying pathology.

Animals↗
PubMedDate not supplied

Obesity after childhood craniopharyngioma--German multicenter study on pre-operative risk factors and quality of life.

BACKGROUND: Craniopharyngiomas are tumorous embryogenic malformations. As the survival rate after craniopharyngioma is high (92 %), prognosis and quality of life (QoL) in survivors mainly depend on adverse late effects such as obesity. PATIENTS AND METHODS: We analyzed 214 children and adolescents with craniopharyngioma. The records of 185 patients (86 %) were available for retrospective analysis of weight profiles and risk factors for obesity. Quality of life (QoL) was measured in 145 patients by the Fertigkeitenskala Münster/Heidelberg score (FMH) and in 77 patients by PEDQOL questionnaire. RESULTS: Eighty-two of 185 patients (44 %) developed severe obesity (body mass index [BMI] > 3 SD). Obese patients were compared with 79 patients (43 %) who kept normal weight (BMI < 2 SD). No differences between obese and normal weight patients were found in terms of gender distribution, age at diagnosis and follow-up period. However, the BMI SDS at the time of diagnosis was higher (p < 0.0001) in patients who developed obesity than in those who did not. Furthermore, obese patients presented with bigger tumors (p < 0.05) and a higher rate of a hydrocephalus requiring a shunt (p < 0.05) and hypothalamic involvement (p < 0.05). The mothers of patients who developed severe obesity had a higher BMI (p < 0.001) at the time of diagnosis. Obese patients had a higher height-SDS at diagnosis (p < 0.05) and at the time of last follow-up (p < 0.05) when compared with normal weight patients. A prediction model for severe obesity after craniopharyngioma was calculated by logistic regression based on the risk factors: patient's BMI > 2 SD at diagnosis (p < 0.05; odds ratio: 16.4), hypothalamic involvement (p < 0.05; odds ratio: 3.4) and maternal BMI > 25 kg/m(2) (p < 0.05; odds ratio: 4.6). Significant increases in BMI (p < 0.001) occurred during the early post-operative period especially during the first three years after diagnosis. FMH percentiles correlated negatively with BMI SDS (Spearman r: - 0.37; p < 0.001). Children with craniopharyngioma rated their QoL more negative (p < 0.05) in regard to physical abilities, cognitive functioning and social functioning when compared with healthy children of the same age group. Severely obese patients with craniopharyngioma estimated their QoL lower (p < 0.05) for all domains except for autonomy, cognition and familial integration in comparison with non-obese patients. CONCLUSION: Hypothalamic tumor involvement and familial disposition for obesity are risk factors for the development of severe obesity in patients with craniopharyngioma. As weight gain starts early after diagnosis and severe obesity causes a reduction in QoL, early therapeutic efforts should be considered in patients at risk. To confirm our results the prospective multicenter study Kraniopharyngeom 2000 on children and adolescents with craniopharyngioma was initiated (www.kraniopharyngeom.com).

Adolescent↗
PubMed2006

Hemodynamic and metabolic responses to interstitial angiotensin II in normal weight and obese men.

OBJECTIVE: The expression of the AT1 receptor in adipose tissue is not decreased or even increased in obese subjects despite systemic activation of the renin-angiotensin system. Therefore, we hypothesized that peripheral tissues of obese subjects are hypersensitive to angiotensin (Ang) II. METHODS: We characterized the effect of locally applied Ang II in skeletal muscle and subcutaneous adipose tissue of healthy non-obese (n = 12) and obese (n = 11) men using the microdialysis technique. Tissues were perfused with Ringer's solution + ethanol and incremental doses of Ang II (0.01, 0.1 and 1 micromol/l). Dialysate ethanol, glycerol, glucose, lactate, and pyruvate concentrations were measured to assess changes in blood flow (ethanol dilution technique), lipolysis and glycolysis, respectively. RESULTS: In adipose tissue, basal ethanol ratio was significantly higher and dialysate metabolite concentrations were significantly lower in obese versus non-obese men. In muscle, basal dialysate glycerol was significantly higher in obese versus non-obese men. Ang II elicited small increases in ethanol ratio and decreases in dialysate glucose in adipose tissue and skeletal muscle in both non-obese and obese men. Dialysate lactate increased significantly in both tissues of obese, but not non-obese men. Dialysate glycerol increased in adipose tissue of non-obese (+ 40%) but not of obese and remained almost unchanged in muscle of both groups. CONCLUSIONS: Interstitially applied Ang II elicits subtle changes in tissue perfusion and metabolism. However, we did not find a major increase in interstitial Ang II responsiveness in obese men.

Adipose Tissue↗
PubMed2005

The impact of obesity on the outcomes of 1,153 critically injured blunt trauma patients.

BACKGROUND: Several small series have had mixed conclusions regarding the impact of obesity on outcomes of trauma patients. The purpose of the present study was to evaluate a large cohort of critically injured patients to better understand the influence of obesity on the outcomes of patients after severe blunt trauma. METHODS: Retrospective review using the trauma registry and intensive care unit (ICU) database of all blunt trauma patients admitted to the ICU at our urban, Level I trauma center over a 5-year period (1998-2003). Obese patients (body mass index [BMI] > or = 30 kg/m) were compared with non-obese patients (BMI < 30 kg/m). RESULTS: There were 1,153 blunt trauma patients admitted to the ICU during the study period, including 283 (25%) obese (mean BMI = 35 +/- 6 kg/m) and 870 (75%) non-obese (mean BMI = 25 +/- 3 kg/m) patients. There was no difference between groups regarding age, sex, Injury Severity Score, or admission vitals. Obese patients had fewer head injuries (42 versus 55%; p = 0.0001) but more chest (45 versus 38%; p = 0.05) and lower extremity (53 versus 38%; p < 0.0001) injuries. There was no difference in the need for laparotomy, thoracotomy, or craniotomy. Obese patients suffered more complications (42 versus 32%; p = 0.002). Although there was only a trend toward higher mortality in obese patients (22 versus 17%; p = 0.10), stepwise logistic regression revealed obesity as an independent risk factor for mortality (odds ratio, 1.6; 95% confidence interval, 1.0-2.3; p = 0.03). Among survivors, obese patients required longer stays in the hospital (24 +/- 21 versus 19 +/- 17 days; p = 0.01), the ICU (13 +/- 14 versus 10 +/- 10 days; p = 0.005), and 2 more days of mechanical ventilation (8 +/- 13 versus 6 +/- 9 days; p = 0.07). CONCLUSION: Obese patients incur different injuries after severe blunt trauma than their non-obese counterparts. Despite sustaining fewer head injuries, obese patients suffer more complications, require longer stays in the hospital, more days of mechanical ventilation, and obesity is independently associated with mortality.

Body Mass Index↗
PubMed2003

Effects of isolated obesity on systolic and diastolic left ventricular function.

BACKGROUND: Obesity is associated with increased cardiovascular morbidity and mortality. A direct effect of isolated obesity on cardiac function is not well established. OBJECTIVE: To determine the direct effect of different grades of isolated obesity on echocardiographic indices of systolic and diastolic left ventricular function. METHODS: 48 obese and 25 normal weight women were studied. They had no other pathological conditions. Obesity was classed as slight (n = 17; body mass index (BMI) 25-29.9 kg/m2), moderate (n = 20; BMI 30-34.9 kg/m2), or severe (n = 11; BMI > or = 35 kg/m2). Echocardiographic indices of systolic and diastolic function were obtained, and dysfunction was assumed when at least two values differed by > or = 2 SD from the normal weight group. RESULTS: Ejection fraction (p < 0.05), fractional shortening (p < 0.05), and mean velocity of circumferential shortening (p < 0.05) were increased in slight and moderate obesity. Left ventricular dimensions were increased (p < 0.001) but relative wall thickness was unchanged. No obese patients met criteria for systolic dysfunction. In obese subjects, the mitral valve pressure half time (p < 0.01) and the left atrial diameter (p < 0.001) were increased and the deceleration slope was decreased (p < 0.01); all other diastolic variables were unchanged. No differences were found between obesity subgroups. Subclinical diastolic dysfunction was more prevalent among obese subjects (p = 0.002), being present in two with slight obesity (12%), seven with moderate obesity (35%), and five with severe obesity (45%). BMI correlated significantly with indices of left ventricular function. CONCLUSIONS: Subclinical left ventricular diastolic dysfunction is present in all grades of isolated obesity, correlates with BMI, and is associated with increased systolic function in the early stages of obesity.

Adolescent↗
PubMed1990

Reduced adipsin expression in murine obesity: effect of age and treatment with the sympathomimetic-thermogenic drug mixture ephedrine and caffeine.

Adipsin gene expression is greatly diminished in certain forms of genetic and acquired obesity. In the present study we evaluate the time course for the development of adipsin deficiency in obesity and its regulation by the sympathomimetic-thermogenic drug mixture ephedrine and caffeine. Previously, it was unknown whether adipsin deficiency occurred before or after the development of massive obesity. In the first series of experiments in which mice were treated with monosodium glutamate (MSG) for the first week of life, we demonstrate that adipsin deficiency occurs early in the development of MSG-induced obesity as evidenced by decreased circulating adipsin concentrations by 1 week of age and deficient adipsin mRNA levels in white adipose tissue (WAT) by 2 weeks. In db/db mice, diminished circulating adipsin was noted at 2 weeks of age. In both models, decreased adipsin gene expression precedes the development of marked obesity. Little is known about the factors which regulate adipsin gene expression in obesity. Common to the ob/ob, db/db and MSG models is diminished thermogenesis and sympathetic nervous system activity. In a second series of experiments we sought to determine whether adipsin deficiency in obesity could be corrected by treatment with ephedrine and caffeine (E+C), a sympathomimetic-thermogenic mixture previously shown to increase thermogenesis and reverse obesity in some models. In the present study, E+C treatment of MSG obese mice reversed obesity and markedly increased serum adipsin and adipsin mRNA levels in WAT and brown adipose tissue (BAT). In ob/ob mice, however, E+C treatment produced a negligible increase in adipsin mRNA levels in WAT and BAT as well as serum adipsin concentrations and this correlated with only a very small decrease in obesity. Thus, the ability of E+C to increase adipsin gene expression correlated with its ability to reverse obesity in these two models. Finally, the effect of E+C on adipsin gene expression may not be exerted directly on the fat cell since treatment of cultured 3T3-F442A adipocytes and isolated rat adipocytes in primary culture produced no effect on adipsin mRNA or secreted protein despite a lipolytic effect as measured by increased glycerol release. In summary, decreased adipsin gene expression occurs early in the development of MSG and db/db obesity and is markedly increased in the MSG model by the sympathomimetic-thermogenic drug mixture, E+C, which also reverses obesity. Elucidation of the factors responsible for these effects may enhance our understanding of fat cell gene regulation and obesity.

Adipose Tissue, Brown↗
PubMed2002

Thiazolidinediones influence plasma steroids of male obese Zucker rats.

Insulin sensitizing thiazolidinediones (TZDs) inhibit steroidogenic enzyme activities in vitro and affect plasma steroids in women with polycystic ovary syndrome. This study was to examine TZD action on circulating steroids in male genetically obese Zucker rats (fa/fa), which were treated with troglitazone or rosiglitazone (0.3% and 0.01% food admixture, respectively) and were compared to untreated obese and lean littermates. After 36 days of TZD administration, obesity- associated derangement of carbohydrate metabolism was ameliorated (e.g., insulin-stimulated glucose oxidation by isolated soleus muscle, nmol/g/h: lean controls, 1049 +/- 100; obese controls, 518 +/- 30; troglitazone-treated obese, 672 +/- 43; rosiglitazone-treated obese, 761 +/- 77; p < 0.01 each vs. obese controls). While plasma pregnenolone and testosterone were neither affected by obesity nor by TZDs, a marked reduction of 17-hydroxyprogesterone in obese vs. lean controls (27 +/- 3 vs. 58 +/- 10 ng/dl; p < 0.01) was partially reversed by TZD treatment (46 +/- 5 and 48 +/- 9 ng/dl for troglitazone and rosiglitazone, respectively; p < 0.02 each vs. untreated obese). Plasma 5-alpha-dihydrotestosterone, in contrast, was not reduced by obesity (76 +/- 9 vs. 59 +/- 7 ng/dl in obese vs. lean controls; n.s.) but blunted by TZD treatment of obese rats (38 +/- 4 and 44 +/- 3 ng/dl for troglitazone and rosiglitazone, respectively; p < 0.05 each vs. untreated obese). We conclude that (i) oral TZD treatment influences circulating steroid concentrations of male obese Zucker rats, and (ii) these effects are at least in part mediated via mechanisms other than those underlying TZD-induced insulin sensitization.

Animals↗
PubMed2005

Androgens before and after weight loss in obese children.

CONTEXT: Little information is available on androgens in obese children, and it is unknown whether these hormones change after weight loss. OBJECTIVE: The objective of this study was to compare androgens between obese and normal-weight children and to study the effect of weight loss on androgens. DESIGN: The design was a cross-sectional comparison between obese and normal-weight children separated according to pubertal stage and longitudinal 1-yr follow-up study in obese children participating in a weight-loss intervention. SETTING: The setting of this study was a primary care facility. PATIENTS: A total of 273 obese and 79 lean children (aged 4-14 yr) were studied, including a subgroup of 155 obese children for the longitudinal study. INTERVENTION: The intervention program was an outpatient 1-yr intervention program based on exercise, behavior, and nutrition therapy (high-carbohydrate low-fat diet). MAIN OUTCOME MEASURES: The outcome measures included testosterone and dehydroepiandrosterone sulfate (DHEAS) at baseline and 1 yr later. RESULTS: The obese prepubertal children and the obese pubertal girls showed significantly (P < 0.01) higher testosterone and DHEAS levels, whereas obese pubertal boys did not significantly differ in androgens from their lean counterparts. Significant correlations with body mass index were demonstrated in multivariate regression analyses for DHEAS in all children and for testosterone in prepubertal children and in pubertal girls. The obese prepubertal children and obese girls losing substantial weight showed a significant (P < 0.05) decrease in their testosterone concentrations. CONCLUSIONS: Moderately increased testosterone and DHEAS levels were found in obese prepubertal children and in obese pubertal girls, whereas androgen concentrations did not differ between obese and normal-weight pubertal boys. Weight loss induced a decrease in testosterone in obese prepubertal children and pubertal girls pointing to a reversible increase of androgens.

Adolescent↗
PubMed1995

Acipimox potentiates growth hormone (GH) response to GH-releasing hormone with or without pyridostigmine by lowering serum free fatty acid in normal and obese subjects.

Obesity is associated with an impairment of normal GH secretion and blunted responses to all stimuli. Recent reports suggest that increased somatostatinergic activity is the basis for the GH derangement of obesity. However, the basic mechanism of this alteration is still being debated. The high plasma free fatty acid (FFA) is frequently observed in obesity. FFA participates in the regulation of pituitary GH secretion. To determine whether the derangement of GH secretion in obesity is associated with high plasma FFA levels, several tests with GHRH with or without pyridostigmine (PYR) and acipimox (ACX), antilipolytic agents able to decrease FFA, were undertaken in six obese and seven normal control subjects. In obese subjects, the GH response (mean peak +/- SEM: 8.9 +/- 1.1 ug/L) to GHRH-(1-29) (1 ug/kg, i.v.) was significantly blunted when compared with the response in normal control subjects (25.7 +/- 1.8 ug/L; P < 0.05). After PYR (120 mg), the response to GHRH was enhanced in the obese subjects (21.4 +/- 4.9 ug/L; P < 0.05) and was similar to that of the controls with GHRH only, but remained significantly reduced compared with controls treated with PYR plus GHRH (43.2 +/- 6.0 ug/L; P < 0.05). Basal FFA levels were higher than those of normal controls (P < 0.05). ACX (500 mg) decreased FFA levels in both obese and normal subjects; the lowest FFA levels of obese subjects at 15 min were similar to those of normal controls. ACX also potentiated GHRH-stimulated GH response in both obese and normal subjects. The GH responses potentiated by ACX in obesity (22.7 +/- 5.5 ug/L) were similar to those of PYR plus GHRH in obese subjects and GHRH in normal controls, but they were lower than those of control treated with ACX plus GHRH (50.8 +/- 6.7 ug/L; P < 0.05). After the combined pretreatment with ACX and PYR, GH responses in obesity (44.1 +/- 6.0 ug/L) were significantly higher than those in GHRH test, PYR plus GHRH, and ACX plus GHRH in obese subjects (P < 0.05), and they were similar to PYR plus GHRH or ACX plus GHRH in normal controls. However their enhanced GH responses were reduced compared with the control with ACX plus PYR plus GHRH (64.9 +/- 4.5 ug/L; P < 0.05). Our results are in agreement with the hypothalamic hypothesis: an increase in somatostatinergic tone is responsible for the blunted GH response to GHRH in obesity.(ABSTRACT TRUNCATED AT 250 WORDS)

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