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PubMed1993

Does obesity influence early target organ damage in hypertensive patients?

BACKGROUND: Various prospective studies have found that lean hypertensive patients have greater cardiovascular morbidity and mortality than obese hypertensive subjects. It was therefore hypothesized that hypertension is more benign when associated with obesity. In the present study, we evaluated effects of obesity on early target organ damage in patients with essential hypertension. METHODS AND RESULTS: In a total of 207 subjects, systemic and renal hemodynamics as well as left ventricular structure and function were assessed by measuring cardiac output (indocyanine green dye dilution), renal blood flow (clearance of 131I paraimmunohippuric acid), and mean arterial pressure (invasively) and by two-dimensionally guided M-mode echocardiographic findings. Systemic and renal vascular resistance, compliance of the large arteries evaluated by the stroke volume/pulse pressure index, and left ventricular mass served as parameters for early target organ damage. All individuals were categorized into four groups: lean and obese normotensive as well as lean and obese hypertensive subjects. In obese hypertensive patients, total peripheral resistance was significantly lower and stroke volume/pulse pressure index was higher than in the lean hypertensive group, almost reaching values of normotensive control subjects. No effect of obesity on the renal circulation was noted, whereas in hypertension, renal vascular resistance was elevated. The degree of left ventricular hypertrophy was more pronounced in the hypertensive groups than in their normotensive counterparts and progressively increased with obesity. Nevertheless, in obese hypertensive patients, left ventricular function, as measured by fractional fiber shortening and velocity of circumferential fiber shortening, was maintained despite the fact that the heart had been exposed to the double burden of an increased preload (obesity) and afterload (hypertension). CONCLUSIONS: Obesity had a disparate effect on target organs in hypertension. At rest, obesity seemed to mitigate cardiovascular changes in the systemic vascular bed caused by hypertension. However, no such mitigation was observed in the renal vasculature, and left ventricular hypertrophy was even exacerbated by the presence of obesity. Our findings in part negate the concept that obesity is able to exert a protective effect on early target organ damage in hypertensive patients and, in particular, on the heart.

Adult↗
PubMed1996

Hypothalamic lesions induce obesity and sex-dependent glomerular damage and increases in blood pressure in rats.

Placement of two symmetrical lesions in the ventromedial hypothalamus of the rat causes massive overeating and obesity. We have studied male (n=8) and female (n=5) Munich-Wistar rats 7 months after induction of obesity and compared them with age-matched controls. Body weight and kidney weight were greater in control males versus females (396 +/- 7 and 1.5 +/- 0.1 g versus 229 +/- 4 and 1.0 +/- 0.1 g, respectively; both P <.001). Both obese males and females were heavier than lean counterparts (592 +/- 30 and 361 +/- 19 g, both P <.001), whereas kidney weight was similar between obese and control rats of each sex (obese males, 1.5 +/- 0.1 g; obese females, 1.1 +/- 0.1 g). Blood pressure was higher in obese versus control males; there was no differences between other groups. Single-nephron glomerular filtration rate was similar in control females and males and obese females but depressed in obese males. Glomerular blood pressure was normal in all groups. Urinary protein excretion and the percentage of sclerosed glomeruli were similar in control females and males and obese females but elevated in obese males. Plasma triglyceride levels were elevated in obesity, particularly in males. We conclude that hypothalamic lesioning induces overeating and obesity and selectively in the male causes hypertension and glomerular damage as well as declines in renal function. This injury is not hemodynamically mediated (glomerular blood pressure is normal) but may be related to the elevation in plasma triglyceride levels, which has previously been causally linked to glomerular damage in genetically obese rats.

Animals↗
PubMed2005

Obesity and risk of new-onset atrial fibrillation after cardiac surgery.

BACKGROUND: New-onset postoperative atrial fibrillation (AF) is a common complication of cardiac surgery that has substantial effects on outcomes. In the general (nonsurgical) adult population, AF has been linked to increasing obesity, which correlates with left atrial enlargement. It is not known whether postoperative AF is similarly linked to obesity. METHODS AND RESULTS: This was a retrospective analysis of the incidence of AF in terms of body mass index (BMI). A total of 8051 consecutive cardiac surgery patients (1994 to 2004; mean age 64 [SD 11] years; 5372 men [67%]) who were free of any history of preoperative AF or flutter were included in the analysis. This series included 3164 obese patients (39%; median age 62 years) and 4887 nonobese patients (61%; median age 66 years), who were further divided on the basis of BMI (kg/m2) into 6 groups: BMI <22 kg/m2, 22< or =BMI< or =25 kg/m2 (normal), 25 or =30 kg/m2 (overweight), 30 or =35 kg/m2 (obese I), 35 or =40 kg/m2 (obese II), and BMI >40 kg/m2 (obese III). Unadjusted AF incidence was similar in obese and nonobese patients (n=742 [23.5%] versus n=1068 [21.9%], respectively; P=0.099). Covariate-adjusted ORs for AF were systematically greater for larger patients than for patients in the normal group (adjusted OR [95% CI]=1.18 [1.00 to 1.40], 1.36 [1.14 to 1.63], 1.69 [1.35 to 2.11], and 2.39 [1.81 to 3.17] for overweight, obese I, obese II, and obese III, respectively). Other AF predictors included age (adjusted OR=1.52 [95% CI 1.46 to 1.58] per 10 years), mitral valve surgery (adjusted OR=2.42 [95% CI 1.92 to 3.06]), aortic valve surgery (adjusted OR=1.79 [95% CI 1.45 to 2.22]), chronic obstructive pulmonary disease (adjusted OR=1.28 [95% CI 1.12 to 1.46]), male gender (adjusted OR=1.24 [95% CI 1.10 to 1.40]), preoperative beta-blocker use (adjusted OR=1.17 [95% CI 1.05 to 1.32]), vascular disease (adjusted OR=1.18 [95% CI 1.05 to 1.32]), white race (adjusted OR=1.33 [95% CI 1.07 to 1.66]), history of arrhythmia other than AF/flutter (adjusted OR=0.80 [95% CI 0.68 to 0.96]), ejection fraction <40% (adjusted OR=1.16 [95% CI 1.03 to 1.31]), left main disease (adjusted OR=1.15 [95% CI 1.00 to 1.32]), and off-pump surgery (adjusted OR=0.61 [95% CI 0.44 to 0.83]). The obesity-AF association was confirmed in 4 1-to-1 propensity-matched obese versus nonobese comparisons and in 2 separate derivation/validation subcohort analyses. CONCLUSIONS: Obesity is an important determinant of new-onset AF after cardiac surgery. Future postoperative AF risk models should incorporate BMI or obesity levels. Studies examining the efficacy of AF-minimizing prophylactic interventions in high-BMI patients, particularly in the elderly, may be warranted.

Aged↗
PubMed1992

Independent effects of obesity and insulin resistance on postprandial thermogenesis in men.

The putative blunted thermogenesis in obesity may be related to insulin resistance, but insulin sensitivity and obesity are potentially confounding factors. To determine the independent effects of obesity and insulin resistance on the thermic effect of food, at rest and after exercise, lean and obese men were matched at two levels of insulin sensitivity determined by insulin-stimulated glucose disposal (milligrams per kilogram fat-free mass [FFM] per minute) during the euglycemic, hyperinsulinemic (40 mU/m2.min) clamp: 5.4 mg/kg FFM for the lean and obese groups with low insulin sensitivity, and 8.1 mg/kg FFM for the groups with high insulin sensitivity. The two lean groups were matched for percent fat (approximately 15 +/- 1% fat), as were the two obese groups (approximately 33 +/- 2% fat). Energy expenditure was measured for 3 h in the fasting state and for 3 h after a 720-kcal mixed meal, each at rest and immediately after 1 h of cycling at 100 W. The thermic effect of food (TEF) was calculated as the postprandial minus fasting energy expenditure (kcal/3 h) during rest and after exercise. During rest, TEF was blunted by both obesity (24 +/- 5 and 34 +/- 6 kcal/3 h for obese groups with low and high insulin sensitivity vs. 56 +/- 6 and 74 +/- 6 kcal/3 h for the lean groups with low and high insulin sensitivity; P less than 0.01 lean vs. obese) and insulin resistance (insulin-resistant less than insulin-sensitive, at both levels of obesity; P less than 0.01). After exercise, TEF was also impaired in the obese (47 +/- 6 and 44 +/- 5 kcal/3 h for the insulin-resistant and -sensitive groups) and in the lean insulin-resistant (55 +/- 5 kcal/3 h), compared with the lean insulin-sensitive men (71 +/- 3 kcal/3 h), P less than 0.01. Compared with rest, TEF after exercise was improved, but not normalized, in both obese groups (P less than 0.05), but unchanged in the lean groups. These results suggest that both insulin resistance and obesity are independently associated with impaired TEF at rest, but the responsiveness of thermogenesis to exercise before a meal is related to the obese state and not independently to insulin resistance per se.

Adult↗
PubMed2005

Childhood obesity, prevalence and prevention.

Childhood obesity has reached epidemic levels in developed countries. Twenty five percent of children in the US are overweight and 11% are obese. Overweight and obesity in childhood are known to have significant impact on both physical and psychological health. The mechanism of obesity development is not fully understood and it is believed to be a disorder with multiple causes. Environmental factors, lifestyle preferences, and cultural environment play pivotal roles in the rising prevalence of obesity worldwide. In general, overweight and obesity are assumed to be the results of an increase in caloric and fat intake. On the other hand, there are supporting evidence that excessive sugar intake by soft drink, increased portion size, and steady decline in physical activity have been playing major roles in the rising rates of obesity all around the world. Consequently, both over-consumption of calories and reduced physical activity are involved in childhood obesity. Almost all researchers agree that prevention could be the key strategy for controlling the current epidemic of obesity. Prevention may include primary prevention of overweight or obesity, secondary prevention or prevention of weight regains following weight loss, and avoidance of more weight increase in obese persons unable to lose weight. Until now, most approaches have focused on changing the behaviour of individuals in diet and exercise. It seems, however, that these strategies have had little impact on the growing increase of the obesity epidemic. While about 50% of the adults are overweight and obese in many countries, it is difficult to reduce excessive weight once it becomes established. Children should therefore be considered the priority population for intervention strategies. Prevention may be achieved through a variety of interventions targeting built environment, physical activity, and diet. Some of these potential strategies for intervention in children can be implemented by targeting preschool institutions, schools or after-school care services as natural setting for influencing the diet and physical activity. All in all, there is an urgent need to initiate prevention and treatment of obesity in children.

Child↗
PubMed1990

Abnormal regulation of the hypothalamo-pituitary-adrenal axis in the genetically obese fa/fa rat.

Adrenalectomy has been shown to reverse most facets of the syndrome of the genetically obese fa/fa rat. However, a detailed analysis of the hypothalamo-pituitary-adrenal (HPA) axis in these animals is lacking. In the present study, morning corticosteronemia was higher in obese rats of both sexes than in lean ones, whereas evening corticosteronemia was higher only in obese male rats. The HPA axis was further investigated using stressful stimuli. Immobilization, ether, and cold stresses resulted in greater corticosterone levels in obese than in lean animals. These abnormalities consisted in upward shifts of the corticosterone response in obese females and absolute increases in that of obese males, indicating that such alterations were more pronounced in obese male than obese female rats. Due to this, the putative origin of the increased corticosterone output of obese rats was studied in males. Greater levels of ACTH were reached in obese than in lean rats when submitted to a cold stress (6 C). Dexamethasone produced a complete suppression of corticosterone output in both lean and obese rats. During the recovery from such suppression, corticosterone levels rose to higher values in obese than in lean rats. This observation together with the greater cold-induced ACTH output in obese rats suggest that the increased activity of the HPA axis of these animals is of central origin. Whatever its precise etiology within the central nervous system, it is proposed that the increased HPA axis activity in obese rats and its resultant hypercorticism play a role in the establishment and maintenance of their syndrome.

Animals↗
PubMed1976

Control of prolactin and growth hormone secretion in mice by obesity.

Prolactin (PRL) and growth hormone (GH) secretions in mice rendered obese by the administration of gold thioglucose (GTG) are abnormal. The objective of the present experiments was to determine whether the effects were related to the drug or to the resultant obesity. Perphenazine-induced PRL release in normal mice and in GTG-injected non-obese mice was compared to that of GTG-injected obese mice after the initial development of obesity, after body weight reduction by diet control and after the resumption of obesity by ad lib. feeding. The GTG-injected mice which did not become obese had greater (50%) than normal levels of serum PRL following perphenazine stimulation in 2 of 3 experiments. This suggested that the injection of GTG directly affected the control mechanism for PRL secretion, but that the abnormal PRL secretion was probably not the cause of obesity that develops after GTG treatment. Perphenazine-induced PRL levels in mice rendered obese with GTG were much greater (2-3 times higher than normal). However, the unusually high levels of PRL were totally abolished when the body weights of these mice were brought down to normal by dietary restriction. Conversely, when obesity was permitted to recur by giving the mice free access to food, PRL levels reverted back to the original obese pattern. The concentrations of GH were usually lower than normal in GTG-obese mice, and these levels were also more often associated with the development of obesity than with the injection of GTG. The data show a marked influence of obesity on the control of PRL and GH secretions in the mouse.

Animals↗
PubMed1984

Insulin responsiveness of adipose tissue lipoprotein lipase is delayed but preserved in obesity.

Because increases in adipose tissue lipoprotein lipase (ATLPL) may be important in the pathogenesis of obesity, the response of ATLPL to insulin during maintenance of euglycemia was examined in 22 obese and 8 normal weight subjects. Basal levels of ATLPL per g fat tissue for the obese and control groups were 18.7 +/- 2.0 (+/- SEM) and 9.6 +/- 2.7 neq/g X min, respectively. Insulin and glucose infusion rapidly produced antilipolysis in both groups, as evidenced by large falls in FFA by 20 min. When the responses of ATLPL in absolute change from basal were compared between the obese and control groups, no significant differences were found. However, because of the higher baseline ATLPL values in the obese subjects, the percent change in ATLPL from basal was significantly blunted at the 80 (P = 0.02), 180 (P less than 0.05), and 360 (P = 0.005) min timepoints compared to those in the normal subjects. By 3 h into the infusion, the control group had a significant rise in ATLPL above the basal level (4.2 +/- 1.3 ngq/g X min; P = 0.01), whereas the obese group did not (2.3 +/- 1.9 neq/g X min; P = NS). However, by 6 h, the ATLPL per g response above baseline was significantly increased in both normal (19.2 +/- 6.5 neq/g X min; P = 0.01) and obese subjects (9.8 +/- 2.3; P less than 0.001). Because adipose cell size was greater in obese subjects, data were also expressed per 10(6) cells. Basal ATLPL per 10(6) cells [11.8 +/- 1.7 neq/10(6) cells X min (obese); 3.4 +/- 0.9 neq/10(6) cells X min (normal)] was a function of cell size (rs = 0.713; P less than 0.001), body mass index (rs = 0.565; P less than 0.005), and basal insulin levels (rs = 0.434; P less than 0.05). As with the ATLPL per g response, the increases in ATLPL per 10(6) cells above basal were significant at both the 3 and 6 h marks for the normal subjects, but only at the 6 h timepoint for the obese group. Both steady state insulin levels [342 +/- 24 microU/ml (obese); 251 +/- 27 microU/ml (normal)] and the glucose infusion rates needed to maintain euglycemia [319 +/- 23 mg/m2 X min (obese); 312 +/- 33 mg/m2 X min (normal)] did not correlate with changes in ATLPL. Thus, insulin responsiveness of ATLPL in obese subjects was delayed but preserved. This phenomenon may be important in maintenance of the obese state.

Adipose Tissue↗
PubMed2000

A preponderance of circulating basic isoforms is associated with decreased plasma half-life and biological to immunological ratio of gonadotropin-releasing hormone-releasable luteinizing hormone in obese men.

Hormonal abnormalities of the reproductive axis have been described in obesity. In men, extreme obesity is associated with low serum testosterone (T) and high estrogen [estrone and estradiol (E(2))] levels. As changes in the sex steroid milieu may profoundly affect the carbohydrate heterogeneity and thus some of the biological and physicochemical properties of the LH molecule, we analyzed the relative distribution of LH isoforms circulating under baseline conditions (endogenous GnRH drive) as well as the forms discharged by exogenous GnRH stimulation from putative acutely releasable and reserve pituitary pools in overweight men. Secondarily, we determined the impact of the changes in LH terminal glycosylation on the in vitro bioactivity and endogenous half-life of the gonadotropin. Seven obese subjects with body mass indexes ranging from 35.7-45.5 kg/m(2) and seven normal men with body mass indexes from 22.5-24.2 kg/m(2) underwent blood sampling at 10-min intervals for a total of 10 h before and after the iv administration of 10 and 90 microg GnRH. Basally released and exogenous GnRH-stimulated serum LH isoforms were separated by preparative chromatofocusing and identified by RIA of eluent fractions. Serum pools of successive samples collected across 2-h intervals (five serum pools per subject) containing LH released under baseline and exogenous GnRH-stimulated conditions were tested for bioactivity employing a homologous in vitro bioassay. Mean serum T and E(2) levels were significantly lower and higher, respectively, in the obese men than in the control group [serum T, 13.5 +/- 2.4 vs. 19.4 +/- 1.4 nmol/L (mean +/- SEM; P: = 0.01); serum E(2), 0.184 +/- 0.01 vs. 0.153 +/- 0.01 nmol/L (P: < 0.05)]. Mean baseline serum LH levels were similar in obese subjects and normal controls (13.3 +/- 1.3 and 12.2 +/- 1.2 IU/L). Although multiple parameter deconvolution of the exogenous GnRH-induced LH pulses revealed that the magnitude of the pituitary response in terms of secretory burst mass, secretory amplitude, and half-duration of the LH pulses was similar in obese and control subjects, the apparent endogenous half-life of LH was significantly (P: < 0.05) shorter in the obese group (98 +/- 11 min) than in the normal controls (132 +/- 10 min). Under all conditions studied, the relative abundance of basic isoforms (those with pH >/=7.0) was significantly (P: < 0.05) increased in the obese subjects compared with the controls (percentages of LH immunoactivity recovered at pH >/=7.0: obese subjects, 34-57%; normal controls, 22-46%). The biological to immunological ratio of LH released in baseline and low dose (10 microg) GnRH-stimulated conditions were similar in obese subjects and normal controls, whereas LH released by obese subjects in response to the high (90 microg) GnRH dose exhibited significantly lower ratios than those detected in normal individuals (0.62 +/- 0.07 and 0.45 +/- 0.09 vs. 1.01 +/- 0.10 and 0.81 +/- 0.09 for LH released within 10-120 min and 130-240 min after GnRH administration in obese and controls, respectively; P: < 0.05). Collectively, these results indicate that the altered sex steroid hormone milieu characteristic of extreme obesity provokes a selective increase in the release of less acidic LH isoforms, which may potentially modify the intensity and duration of the blood LH signal delivered to the gonad. Altered glycosylation of LH may therefore represent an additional mechanism modulating the hypogonadal state prevailing in morbid obesity.

Adult↗
PubMed2003

Difficult tracheal intubation is more common in obese than in lean patients.

UNLABELLED: Whether tracheal intubation is more difficult in obese patients is debatable. We compared the incidence of difficult tracheal intubation in obese and lean patients by using a recently validated objective scale, the intubation difficulty scale (IDS). We studied 134 lean (body mass index, <30 kg/m2) and 129 obese (body mass index, >or=35 kg/m2) consecutive patients. The IDS scores, categorized as difficult intubation (IDS >or=>5) or not (IDS <5), and the patient data, including oxygen saturation (SpO2) while breathing oxygen, were compared between lean and obese patients. In addition, risk factors for difficult intubation were determined in obese patients. The IDS score was >or=5 in 3 lean and 20 obese patients (P = 0.0001). A Mallampati score of III-IV was the only independent risk factor for difficult intubation in obese patients (odds ratio, 12.51; 95% confidence interval, 2.01-77.81), but its specificity and positive predictive value were 62% and 29%, respectively. SpO2 values noted during intubation were (mean +/- SD) 99% +/- 1% (range, 91%-100%) and 95% +/- 8% (range, 50%-100%) in lean and obese patients, respectively (P < 0.0001). We conclude that difficult intubation is more common among obese than nonobese patients. None of the classic risk factors for difficult intubation was satisfactory in obese patients. The high risk of desaturation warrants studies to identify new predictors of difficult intubation in the obese. IMPLICATIONS: We report a difficult intubation rate of 15.5% in obese patients and 2.2% in lean patients. None of the risk factors for difficult intubation described in the lean population was satisfactory in the obese patients. We also report a high risk of desaturation in obese patients with difficult intubation.

Adolescent↗
PubMed2003

Clinical significance of central obesity in laparoscopic bariatric surgery.

BACKGROUND: Laparoscopic surgery had increased the interest and growth of bariatric surgery. Whether central obesity has any adverse effect in laparoscopic bariatric surgery is not clear. METHODS: 612 morbidly obese patients received laparoscopic bariatric surgery,in a prospectively controlled clinical trial of the outcome of the bariatric surgery. For comparison, subjects were dichotomized into either a central obesity group or peripheral obesity group, based on waist/hip ratio (WHR). Various biochemistry and blood count variables, and perioperative and postoperative results were measured. RESULTS: There were more female (458) than male patients (154). Male patients had higher BMI, and female patients were younger. 56 of 154 male patients (36.4%) belonged to the central obesity (WHR >1.0), and 321 of 458 female patients (70.1%) had central obesity (WHR >0.85). Central obesity was associated with age but not with BMI in males. In females, central obesity was associated with increased BMI. Central obesity predicted increased hyperglycemia and triglyceride levels in both male and female patients. Male patients with central obesity had higher WBC counts than the other patients. Although central obesity was associated with more intra-operative blood loss and prolonged recovery in female patients, there was no increase in complication rate or difference in postoperative weight loss. CONCLUSION: Central obesity is associated with a higher degree of hyperglycemia, hyperlipidemia and leukocytosis in morbidly obese patients who undergo bariatric surgery. Although there is increased technical difficulty in patients with severe central obesity, laparoscopic bariatric surgery is safe and effective in producing weight loss.

Adipose Tissue↗
PubMed2005

Metabolic syndrome in childhood: association with birth weight, maternal obesity, and gestational diabetes mellitus.

OBJECTIVE: Childhood obesity has contributed to an increased incidence of type 2 diabetes mellitus and metabolic syndrome (MS) among children. Intrauterine exposure to diabetes and size at birth are risk factors for type 2 diabetes mellitus, but their association with MS in childhood has not been demonstrated. We examined the development of MS among large-for-gestational-age (LGA) and appropriate-for-gestational age (AGA) children. STUDY DESIGN: The major components of MS (obesity, hypertension, dyslipidemia, and glucose intolerance) were evaluated in a longitudinal cohort study of children at age 6, 7, 9, and 11 years who were LGA (n = 84) or AGA (n = 95) offspring of mothers with or without gestational diabetes mellitus (GDM). The cohort consisted of 4 groups, ie, LGA offspring of control mothers, LGA offspring of mothers with GDM, AGA offspring of control mothers, and AGA offspring of mothers with GDM. Biometric and anthropometric measurements were obtained at 6, 7, 9, and 11 years. Biochemical testing included measurements of postprandial glucose and insulin levels and high-density lipoprotein (HDL) cholesterol levels at 6 and 7 years and of fasting glucose, insulin, triglyceride, and HDL cholesterol levels at 9 and 11 years. We defined the components of MS as (1) obesity (BMI >85th percentile for age), (2) diastolic or systolic blood pressure >95th percentile for age, (3) postprandial glucose level >140 mg/dL or fasting glucose level >110 mg/dL, (4) triglyceride level >95th percentile for age, and (5) HDL level <5th percentile for age. RESULTS: There were no differences in baseline characteristics (gender, race, socioeconomic status, and maternal weight gain during pregnancy) for the 4 groups except for birth weight, but there was a trend toward a higher prevalence of maternal obesity before pregnancy in the LGA/GDM group. Obesity (BMI >85th percentile) at 11 years was present in 25% to 35% of the children, but rates were not different between LGA and AGA offspring. There was a trend toward a higher incidence of insulin resistance, defined as a fasting glucose/insulin ratio of <7, in the LGA/GDM group at 11 years. Analysis of insulin resistance at 11 years in a multivariate logistic regression revealed that childhood obesity and the combination of LGA status and maternal GDM were associated with insulin resistance, with odds ratios of 4.3 (95% confidence interval [CI]: 1.5-11.9) and 10.4 (95% CI: 1.5-74.4), respectively. The prevalence at any time of > or =2 components of MS was 50% for the LGA/GDM group, which was significantly higher than values for the LGA/control group (29%), AGA/GDM group (21%), and AGA/control group (18%). The prevalence of > or =3 components of MS at age 11 was 15% for the LGA/GDM group, compared with 3.0% to 5.3% for the other groups. Cox regression analysis was performed to determine the independent hazard (risk) of developing MS attributable to birth weight, gender, maternal prepregnancy obesity, and GDM. For Cox analyses, we defined MS as > or =2 of the following 4 components: obesity, hypertension (systolic or diastolic), glucose intolerance, and dyslipidemia (elevated triglyceride levels or low HDL levels). LGA status and maternal obesity increased the risk of MS approximately twofold, with hazard ratios of 2.19 (95% CI: 1.25-3.82) and 1.81 (95% CI: 1.03-3.19), respectively. GDM and gender were not independently significant. To determine the cumulative hazard of developing MS with time, we plotted the risk according to LGA or AGA category for the control and GDM groups from 6 years to 11 years, with Cox regression analyses. The risk of developing MS with time was not significantly different between LGA and AGA offspring in the control group but was significantly different between LGA and AGA offspring in the GDM group, with a 3.6-fold greater risk among LGA children by 11 years. CONCLUSIONS: We showed that LGA offspring of diabetic mothers were at significant risk of developing MS in childhood. The prevalence of MS in the other groups was similar to the prevalence (4.8%) among white adolescents in the 1988-1994 National Health and Nutrition Examination Survey. This effect of LGA with maternal GDM on childhood MS was previously demonstrated for Pima Indian children but not the general population. We also found that children exposed to maternal obesity were at increased risk of developing MS, which suggests that obese mothers who do not fulfill the clinical criteria for GDM may still have metabolic factors that affect fetal growth and postnatal outcomes. Children who are LGA at birth and exposed to an intrauterine environment of either diabetes or maternal obesity are at increased risk of developing MS. Given the increased obesity prevalence, these findings have implications for perpetuating the cycle of obesity, insulin resistance, and their consequences in subsequent generations.

Birth Weight↗
PubMed2006

Obesity and cardiovascular risk factors among men and women aged 40 years and older in a rural area of Japan.

Obesity is one of the most common health problems, and is recognized worldwide as an "escalating epidemic." For the establishment of an obesity-prevention strategy in Japan, it is important to assess the association between obesity and cardiovascular risk factors. Therefore, we conducted anthropometric measures of obesity and investigated the association of obesity with cardiovascular risk factors such as hypertension, diabetes, and dyslipidemia among community-dwelling men (N=85) and women (N=173) aged 40 years and older. Height, weight, and waist circumference (WC) were measured, and body mass index (BMI) was calculated. Subjects with a BMI> or =25 kg/m(2) were considered obese (BMI obesity), while men with a WC> or =85 cm and women with a WC> or =90 cm were classified as obese (WC obesity). In the present study, we defined 'obesity' as a BMI> or =25 kg/m(2) or a WC> or =85 cm for men, and a BMI> or =25 kg/m(2) or a WC> or =90 cm for women. The results of an age- and sex-adjusted logistic regression analysis indicated that BMI obesity was associated with dyslipidemia (p=0.04), WC obesity was associated with dyslipidemia (p=0.07), and 'obesity' was associated with diabetes (p=0.06) and dyslipidemia (p=0.01). These results emphasize the importance of preventing obesity in Japan. Therefore, healthcare professionals should measure BMI and WC in order to enhance their assessment of cardiovascular risk.

Adult↗
PubMedDate not supplied

Drug disposition in obese humans. An update.

Drug disposition for many drugs has now been studied in obese individuals and some general conclusions can be drawn. Absorption of drugs evaluated to date is unchanged due to obesity. Apparent volume of distribution is greatly increased for some drugs including most benzodiazepines, thiopentone, phenytoin, verapamil and lignocaine (lidocaine). Modest increases in volume of distribution have been noted for methylxanthines, aminoglycosides, vancomycin, ibuprofen, prednisolone and heparin. Distribution of digoxin, cimetidine and procainamide is unchanged in obesity. The mechanism for the increased distribution of some drugs and unchanged distribution of others in obesity is unclear at present. It may be in part due to the lipophilic character of the drug molecule; however, other complex and as yet poorly understood factors contribute to the variability in drug distribution in obese patients. Protein binding of drugs bound to albumin is not dramatically changed in obesity. In contrast, some studies report that drugs bound to alpha 1-acid glycoprotein (AAG) may have increased binding that is related to increased serum AAG concentration; however, this is not a consistent finding. Oxidative drug biotransformation is minimally changed in obesity with the exceptions of ibuprofen and prednisolone, for which clearance increases as a highly correlated function of total bodyweight. Drug conjugation uniformly increases as a function of bodyweight in obesity, with paracetamol (acetaminophen), lorazepam and oxazepam having been studied. Drug acetylation may be unchanged in obesity, with only procainamide evaluated at this time. High clearance drugs, including lignocaine, verapamil and midazolam, have no change in clearance in obese individuals compared to normal bodyweight controls. Renal clearance of drugs is little changed for some drugs evaluated (digoxin, cimetidine), and increased for others (aminoglycosides, unmetabolised procainamide). Characterisation of appropriate animal models of obesity is underway to clarify the mechanisms for these in vivo pharmacokinetic observations in obese man. Two models, the Zucker obese and the obese cafeteria-fed male Sprague-Dawley rat, have provided preliminary physiological pharmacokinetic data with evaluations of theophylline, phenobarbitone and verapamil.(ABSTRACT TRUNCATED AT 400 WORDS)

Aminoglycosides↗
PubMed2004

Psychotropic drugs in the treatment of obesity: what promise?

Obesity is a chronic and highly prevalent medical condition associated with increased risk for the development of numerous and sometimes fatal diseases. Despite its severity, there are few anti-obesity agents available on the market. Although psychotropic agents are not approved for the treatment of obesity, they have been used by clinicians as a therapeutic tool in daily clinical practice. The purpose of this article is to review the rationale, as well as the evidence, for the potential use of these agents in obesity treatment. Evidence for the efficacy of psychotropic agents in obesity treatment comes from different sources. The first type of evidence is weight loss observed with treatment in clinical trials of patients with neuropsychiatric syndromes (e.g. mood disorders, epilepsy). A recent example of such findings is the weight reduction reported in clinical trials involving obese patients with binge eating disorder. While randomised, controlled trials specifically designed to investigate the weight loss properties of psychotropic agents in obese patients are the most appropriate source of evidence of anti-obesity action, such trials remain scarce. The most studied psychotropic agents in obesity trials are drugs used in the treatment of mood disorders, i.e. mainly antidepressants and antiepileptics. SSRIs (e.g. fluoxetine, sertraline and fluvoxamine) were amongst the first psychotropic agents investigated in the treatment of obesity. Additional data have also been published for other antidepressants (e.g. venlafaxine, citalopram and bupropion) and antiepileptics (e.g. topiramate and zonisamide). Based on the available data for the efficacy of psychotropic agents in obesity and other related conditions, SSRIs may be considered for the management of certain subgroups of obese individuals with comorbid conditions such as depression, binge eating disorder and type 2 diabetes mellitus. In addition, some newer agents, such as bupropion, topiramate and zonisamide, appear to be promising candidates for selective use in the treatment of obesity. However, further studies are needed to define their possible role as new pharmacological options in the treatment of obesity.

Animals↗
PubMed2003

Soluble tumor necrosis factor-alpha receptors in young obese subjects with normal and impaired glucose tolerance.

OBJECTIVE: Tumor necrosis factor-alpha (TNF-alpha) is a possible link between obesity and impaired glucose tolerance (IGT) and type 2 diabetes. Data about TNF-alpha and soluble forms of its receptors (sTNFR1 and sTNFR2) in IGT are controversial. The aim of the present study was to assess plasma TNF-alpha, sTNFR1, and sTNFR2 levels and to evaluate the relationships with insulin resistance in obese subjects with IGT. RESEARCH DESIGN AND METHODS: A total of 104 subjects participated in the present study: 30 obese subjects with IGT (obese-IGT), 32 obese subjects with normal glucose tolerance (obese-NGT), and 42 lean healthy control subjects (control-NGT). Anthropometry and blood biochemical parameters were measured and euglycemic-hyperinsulinemic clamp was performed. RESULTS: Obese-IGT subjects were more insulin resistant in comparison with obese-NGT and control-NGT groups; obese-NGT subjects were more insulin resistant than control-NGT. Plasma sTNFR1 and sTNFR2 were markedly higher in both groups of obese subjects in comparison with control-NGT and in the obese-IGT versus obese-NGT group. Plasma sTNFR1 and sTNFR2 were inversely related to insulin sensitivity. Both relationships remained significant after adjustment for age, BMI, waist girth, percent body fat, plasma glucose, insulin, nonesterified fatty acids, cholesterol, and triglycerides. Correlation between sTNFR2 and insulin sensitivity was also present in all the groups analyzed separately, but the correlation between sTNFR1 and insulin sensitivity was present only in the obese-NGT group. CONCLUSIONS: Our data suggest that TNF-alpha receptors are increased in obese-IGT subjects and are related to insulin resistance. These findings indicate that the TNF-alpha system might contribute to the development of insulin resistance in glucose-intolerant subjects.

Adult↗
PubMed1992

[The significance of obesity in UOEH medical students--multiple regression analysis of the annual physical checkup data in 1991].

For the purpose of evaluating the significance of obesity in a young population as a risk factor toward various chronic diseases, a multiple regression analysis was performed on the data from the annual physical checkup of medical students of UOEH in 1991. The following results were obtained. (1) The average obesity index of the students showed a progressive and significant increase in the past 13 years from 1979 to 1991. (2) A close correlation between the obesity index and serum GPT was recognized by elevation of the standard partial regression coefficient of serum GPT to obesity index and that of obesity index to serum GPT when the data from all 617 students was analysed in one group. This finding was intensified in 142 obese students with an obesity index of over 10%, but it was not seen in the remaining non-obese students. (3) The correlation between the obesity index and serum GPT was found solely in the group of students with constant obesity; i.e., whose obesity index was always more than 10% during a maximum of 9 years in the past. (4) Systolic blood pressure was related to the red blood cell count rather than to the obesity index in this young population. (5) No particularly close correlation to serum cholesterol was found with any of 10 representative items examined in this physical checkup, including the obesity index, indicating that the other factors should be related to serum cholesterol levels. From the above findings, it can be concluded that constant obesity in students is related to liver dysfunction, probably due to fatty liver frequently seen in the precise examination of these individuals.

Adolescent↗
PubMed1999

[QT interval dispersion and the type of obesity in women].

UNLABELLED: The risk of sudden cardiac death is higher in patients with obesity, particularly in the upper body obesity. The most common cause of cardiac events are serious ventricular arrhythmias. Delayed cardiac repolarization leading to the prolongation of the QT interval is a well characterised precursor of arrhythmias. The QT interval dispersion reflects inhomogeneity of repolarization. The aim of this study was to assess QT interval dispersion (QTd) in obese women and to establish the relationship between obesity and QTd. 62 patients with obesity (group 1) and 15 apparently healthy women (group 2) were included in our study. Obese subjects were distinguished in accordance to the waist to hip ratio (WHR) into three subgroups: 1a--obese women with upper body obesity; 1b--obese women with WHR: 0.75-0.85; 1c--obese women with lower body obesity. A standard 12-lead ECG was performed in each subjects and QTd, QTdc (QT correlated interval dispersion), QTdR (QTd ratio) were calculated. The left ventricular mass (LVM) and left ventricular mass index (LVMI) were obtained from echocardiograms. We found QTd, QTdc, QTdR and LVM, LVMI to be significantly higher in obese women as well as positive correlation between BMI and both LVM, LVMI. QTdR was significantly higher in subgroup 1a compared with subgroup 1c. CONCLUSIONS: 1) QT interval dispersion was increased in obese women compared with healthy subjects, 2) supposedly increased QTd was associated with the type of obesity.

Adipose Tissue↗