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PubMed2006

Risk of obesity enhanced by poor physical activity in high school students.

BACKGROUND: The aim of this study was to elucidate the interactions between a family history of obesity and poor physical activity. METHODS: A case-control study was performed based on medical check data for all first year high school students admitted to Aichi Prefectural public high schools in the 2004 academic year. Prior to the post-admission medical check up, all students received an interview sheet containing questions on family history of obesity and extent of physical activity. Experienced nurses measured body mass and height. Valid answers and measurements were obtained from 20,155 boys and 19,682 girls. RESULTS: A family history of obesity, reluctance to exercise, current and recent past sedentary lifestyles each significantly increased risk of obesity (body mass index [BMI] >or= 25) and severe obesity (BMI >or= 30) in both boys and girls. Two-way ANOVA revealed that a family history of obesity, associated with poor exercise, positively affected BMI in both boys and girls. Moreover, significant positive interaction was found between a family history of obesity and each of the unfavorable physical activity conditions. Synergistic effects (synergy indexes >1) increasing risk of obesity were noted in both boys and girls when a family history of obesity overlapped with reluctance to exercise, current physical inactivity, or recent physical inactivity. CONCLUSION: Overlapping of family history of obesity and exercise risk factors synergistically increase the BMI and risk of obesity in both boys and girls. Intervention to promote exercise in adolescents who have obese family member(s) should be encouraged.

Adolescent↗
PubMed2006

Poverty and the extent of child obesity in Canada, Norway and the United States.

The goal of this paper is to compare the extent of child obesity in Canada, Norway and the United States. As child poverty is an important correlate of child obesity, we wish to examine the potential role of international differences in child poverty in explaining international differences in the extent of child obesity. We use three representative microdata surveys containing parental reports of child height and weight collected in the mid-1990s in Canada, Norway and the US. We calculate both the prevalence and proportional severity of child obesity for 6-11-year-old children in each country, and represent the 'extent' of obesity diagrammatically. Differences in patterns of child poverty are similarly depicted. Obesity extent is also compared for poor and non-poor children in Canada and the US. Finally, child obesity in the three countries is compared using only non-poor children where we find that the extent of child obesity is much lower in Norway than in Canada or the US. The pattern apparent for obesity is remarkably similar to that found for child poverty. In Canada and especially in the US, we find a much greater extent of obesity for poor than non-poor children. However, when we compare only non-poor children in the three countries, although the magnitude of difference is smaller, it remains clear that Norwegian children are much less likely to be obese. Policy and research directed towards reducing the extent of child obesity in both Canada and the US should pay particular attention to issues of child poverty.

Body Height↗
PubMed2006

Prevalence of obesity in Kuwait and its relation to sociocultural variables.

This study ascertains the prevalence of obesity and its relationship with some sociocultural characteristics in Kuwaiti society. The sample involved 212 men and 212 women, most of whom are overweight and obese. Grades 1 (body mass index [BMI] > 25-30 kg m(-2)), 2 (BMI > 30-40) and 3 (BMI > 40) of obesity characterize 71.2% of the sample. Most individuals are in grade 2 obesity, 37.2%. Grade 1 obesity is seen in 31.4% of the sample. Obesity increases with age, especially in women. The heaviest women are aged 60 years or older (mean BMI of 33.8), about the same mean as in the 50-59-year-old age group. The highest frequency of grades 1 and 2 obesity occur in women 30-39 years old. Fifty per cent of the underweight women are 20-29 years old or are over 60 years old. Most women of normal weight are 20-29 years old. For the men, 60% of the underweight sample are 50-60 years old. Male respondents between 30 and 39 years old are the heaviest; 42.7% of the sample are within grade 1 obesity and 40.7% of the sample within grade 2 obesity. The smallest percentage of men in grades 1 and 2 obesity are those 50-59 years old. An association was found between some sociocultural variables and obesity. Data show an increasing prevalence of obesity in Kuwait compared with some previous studies.

Adult↗
PubMed2006

Characterization of obesity in Japanese monkeys (Macaca fuscata) in a pedigreed colony.

BACKGROUND: Japanese monkey, Macaca fuscata, is recognized as the monkey species inhabiting the northernmost area in the world, and thus likely to possess unique fat-depositing mechanisms to resist cold weather in winter. We report that obese females are present in the Wakasa group of Japanese monkey reared in an open enclosure of the Primate Research Institute, Kyoto University. METHODS AND RESULTS: Eight of 12 females were categorized as obese, showing percentage body fat of over 22%. The levels of serum leptin (mean +/- SD, 4.9 +/- 2.3 ng/ml) measured in these obese monkeys were significantly higher than those of non-obese peers of the same group (n = 4; 1.2 +/- 0.5 ng/ml) and another Japanese monkey group (Takahama, n = 14; 0.8 +/- 0.25 ng/ml); however, serum levels of adiponectin, insulin, glucose, hemoglobin A1c, and fructosamine did not differ between obese and non-obese monkeys. Few serum lipid parameters such as triglyceride and cholesterol showed lower levels in obese monkeys than their non-obese peers. CONCLUSIONS: These results show that these obese monkeys in the Wakasa group have not developed obesity-related diseases/disorders such as diabetes. In the Wakasa group, the frequency of obese individuals was high in some maternal lineages, suggesting that genetic factors responsible for obesity may have been inherited in these lineages.

Adiposity↗
PubMed1970

Effects of obesity, glucocorticoid, and oral contraceptive therapy on plasma glucose and blood pyruvate levels.

THE PLASMA GLUCOSE AND BLOOD PYRUVATE LEVELS WERE DETERMINED AFTER ORAL GLUCOSE TOLERANCE TEST IN SIX GROUPS OF WOMEN: non-obese and obese controls and in non-obese and obese women receiving glucocorticoid or oral contraceptive therapy. The mean fasting plasma glucose level was similar in all groups, but glucose tolerance was impaired in the obese controls, non-obese women on oral contraceptives or being treated with glucocorticoids, and appreciably impaired in the obese oral contraceptive and glucocorticoid groups compared with mean levels in non-obese subjects of the same groups. Obesity was associated with abnormally raised blood pyruvate levels in response to a glucose tolerance test in all groups. Striking similarities were observed between the responses of the plasma glucose and blood pyruvate levels to glucose tolerance tests in the obese control and non-obese oral contraceptive and non-obese glucocorticoid-treated groups. It is suggested that these abnormalities result from a common mechanism-namely, glucocorticoid excess.

Adult↗
PubMed1978

Resistance to chenodeoxycholic acid (CDCA) treatment in obese patients with gall stones.

In most patients with radiolucent gall stones who were given chenodeoxycholic acid (CDCA) in doses of 13-15 mg/kg body weight/day the bile became unsaturated in cholesterol, and their gall stones dissolved. The patients whose stones did not dissolve were significantly heavier and fatter than the responders, which suggested that obese patients might be "resistant" to the effects of CDCA. To test this hypothesis, 32 consecutive patients presenting for medical treatment of gall stones had their ideal body weight (IBW) and estimated body fat mass calculated. The eight most obese and the eight least obese patients were then selected, and their fasting bile lipid responses to CDCA 13-15 mg/kg/day were measured. The very obese patients were also given larger doses, and any changes in bile lipid composition were studied in relation to subsequent gall-stone dissolution.Before treatment the obese patients had a higher mean biliary cholesterol saturation index than the non-obese patients, and this difference was maintained during treatment with the normal dose of CDCA: the bile in the obese patients remained supersaturated while that in the non-obese became unsaturated with cholesterol. When the obese patients were given larger doses of CDCA their bile ultimately became unsaturated in cholesterol. Gall stones dissolved partially or completely in five of the eight non-obese patients after 6-18 months of 13-15 mg CDCA/kg/day, but none of the obese patients showed any response after comparable periods of treatment with this standard dose. With increased doses and unsaturated bile, however, three of the obese patients showed partial gall-stone dissolution after 3-12 months' treatment and one showed complete gall-stone dissolution after three years' treatment.These results suggest that when giving CDCA to patients with gall stones, larger than normal doses (some 18-20 mg/kg/day) should be prescribed. Alternatively the lipid composition of the patients' bile should be monitored by duodenal intubation and the CDCA dose increased until the bile becomes unsaturated in cholesterol.

Adult↗
PubMed1983

Brown adipose tissue of mice with gold thioglucose-induced obesity: effect of cold and diet.

Gold thioglucose (GTG)-obese mice have a larger than normal amount of brown adipose tissue (BAT) with ultrastructurally normal mitochondria. The tissue grows normally when the mice adapt to cafeteria feeding or to cold (8 degrees C). Acute exposure to cold causes a fairly normal thermogenic activation of BAT mitochondria of GTG-obese mice, both in dynamic and static phases of their obesity. However, chow-fed GTG-obese mice have BAT mitochondria that are in a low state of thermogenic activation, and these mice fail to respond to eating a cafeteria diet for 3 wk by a normal thermogenic activation of their BAT mitochondria. More prolonged cafeteria feeding for 11-13 wk, into the static phase of obesity, is associated with thermogenic activation of BAT mitochondria of GTG-obese mice. The capacity of GTG-obese mice to respond to noradrenaline (norepinephrine) by an increase in metabolic rate is greater than that of lean mice and is further enhanced by cold acclimation. It is concluded that BAT of the GTG-obese mouse is inherently functional, as is control of its thermogenic function and growth during cold exposure and cold acclimation. Dietary influences on BAT thermogenic function are, however, defective in the GTG-obese mouse at least during the dynamic phase of its obesity. The resulting failure of diet-induced thermogenesis would be expected to contribute to the known high metabolic efficiency of the GTG-obese mouse and, together with the hyperphagia, to the obesity induced by GTG.

Acclimatization↗
PubMed2001

Postprandial dyslipidemia in men with visceral obesity: an effect of reduced LDL receptor expression?

Postprandial lipemia after an oral fat challenge was studied in middle-aged men with visceral obesity. The two groups had similar plasma cholesterol levels, but obese subjects had higher levels of plasma triglyceride and reduced amounts of high-density cholesterol. Fasting plasma insulin was fourfold greater in obese subjects because of concomitant insulin resistance, with a calculated HOMA score of 3.1 +/- 0.6 vs. 0.8 +/- 0.2, respectively. Plasma apolipoprotein B(48) (apoB(48)) and retinyl palmitate (RP) after an oral fat challenge were used to monitor chylomicron metabolism. Compared with lean subjects, the fasting concentration of apoB(48) was more than twofold greater in obese individuals, suggestive of an accumulation of posthydrolyzed particles. After the oral lipid load, the incremental areas under the apoB(48) and RP curves (IAUC) were both significantly greater in obese subjects (apoB(48): 97 +/- 17 vs. 44 +/- 12 microg.ml(-1). h; RP: 3,120 +/- 511 vs. 1,308 +/- 177 U. ml(-1). h, respectively). A delay in the conversion of chylomicrons to remnants probably contributed to postprandial dyslipidemia in viscerally obese subjects. The triglyceride IAUC was 68% greater in obese subjects (4.7 +/- 0.6 vs. 2.8 +/- 0.8 mM. h, P < 0.06). Moreover, peak postprandial triglyceride was delayed by approximately 2 h in obese subjects. The reduction in triglyceride lipolysis in vivo did not appear to reflect changes in hydrolytic enzyme activities. Postheparin plasma lipase rates were found to be similar for lean and obese subjects. In this study, low-density lipoprotein (LDL) receptor expression on monunuclear cells was used as a surrogate marker of hepatic activity. We found that, in obese subjects, the binding of LDL was reduced by one-half compared with lean controls (70.9 +/- 15.07 vs. 38.9 +/- 4.6 ng LDL bound/microg cell protein, P = 0.02). Because the LDL receptor is involved in the removal of proatherogenic chylomicron remnants, we suggest that the hepatic clearance of these particles might be compromised in insulin-resistant obese subjects. Premature and accelerated atherogenesis in viscerally obese, insulin-resistant subjects may in part reflect delayed clearance of postprandial lipoprotein remnants.

Apolipoprotein B-48↗
PubMed2001

Cardiovascular and metabolic responses to fasting and thermoneutrality are conserved in obese Zucker rats.

The primary purpose of the study was to test the hypothesis that reduced leptin signaling is necessary to elicit the cardiovascular and metabolic responses to fasting. Lean (Fa/?; normal leptin receptor; n = 7) and obese (fa/fa; mutated leptin receptor; n = 8) Zucker rats were instrumented with telemetry transmitters and housed in metabolic chambers at 23 degrees C (12:12-h light-dark cycle) for continuous (24 h) measurement of metabolic and cardiovascular variables. Before fasting, mean arterial pressure (MAP) was higher (MAP: obese = 103 +/- 3; lean = 94 +/- 1 mmHg), whereas oxygen consumption (VO(2): obese = 16.5 +/- 0.3; lean = 18.6 +/- 0.2 ml. min(-1). kg(-0.75)) was lower in obese Zucker rats compared with their lean controls. Two days of fasting had no effect on MAP in either lean or obese Zucker rats, whereas VO(2) (obese = -3.1 +/- 0.3; lean = -2.9 +/- 0.1 ml. min(-1). kg(-0.75)) and heart rate (HR: obese = -56 +/- 4; lean = -42 +/- 4 beats/min) were decreased markedly in both groups. Fasting increased HR variability both in lean (+1.8 +/- 0.4 ms) and obese (+2.6 +/- 0.3 ms) Zucker rats. After a 6-day period of ad libitum refeeding, when all parameters had returned to near baseline levels, the cardiovascular and metabolic responses to 2 days of thermoneutrality (ambient temperature 29 degrees C) were determined. Thermoneutrality reduced VO(2) (obese = -2.4 +/- 0.2; lean = -3.3 +/- 0.2 ml. min(-1). kg(-0.75)), HR (obese = -46 +/- 5; lean = -55 +/- 4 beats/min), and MAP (obese = -13 +/- 6; lean = -10 +/- 1 mmHg) similarly in lean and obese Zucker rats. The results indicate that the cardiovascular and metabolic responses to fasting and thermoneutrality are conserved in Zucker rats and suggest that intact leptin signaling may not be requisite for the metabolic and cardiovascular responses to reduced energy intake.

Animals↗
PubMed2001

Leptin and its relation to obesity and insulin in the SHR/N-corpulent rat, a model of type II diabetes mellitus.

The spontaneously hypertensive/NIH-corpulent (SHR/N-cp) rat is a genetic animal model that exhibits obesity, metabolic features of hyperinsulinemia, hyperglycemia, and hyperlipidemia, which are characteristic of type II diabetes and mild hypertension. To determine the role of leptin, the protein product of the ob gene, in the development of obesity and diabetes in this model, we measured steady-state circulating levels of leptin in obese and lean SHR/N-cp rats and examined the relation between plasma leptin levels and metabolic variables at the stage of established obesity in these animals. Mean fasting plasma leptin concentration was 8-fold higher in obese than in lean rats (p < 0.01). This was associated with a 6-fold elevation in plasma insulin in the obese group. Fasting levels of plasma glucose, cholesterol, and triglyceride were all significantly higher in obese rats than in lean controls. Spearman correlation analysis showed a significant positive correlation between plasma leptin concentration and body weight among the animals (r = 0.73, p < 0.01). Similarly, plasma insulin concentration was significantly correlated with BW in all animals (r = 0.54, p < 0.05). There was also a significant positive correlation between plasma leptin and plasma insulin in the entire group (r = 0.70, p < 0.01). However, this relationship was significant only for lean rats but not for obese rats (r = 10.59, p < 0.05 for lean rats, and r = 0.23, p = NS, for obese rats). Plasma leptin also correlated positively with fasting plasma glucose (r = 0.75, p < 0.05), total cholesterol (r = 0.63, p < 0.05), and triglyceride (r = 0.67, p < 0.05). The marked elevation of plasma leptin in obese SHR/N-cp rats suggests that obesity in this animal model is related to up-regulation of the ob gene. Circulating leptin appears to be one of the best biological markers of obesity and that hyperleptinemia is closely associated with several metabolic risk factors related to insulin resistance in the diabesity syndrome.

Analysis of Variance↗
PubMedDate not supplied

[Analysis of gastric emptying dynamics in relationship to qualitative composition of intake. Comparison between normal-weight and obese subjects].

AIMS: To analyze whether the gastric emptying profile could define obesity and to study the impact of macronutrients diet composition on gastric emptying in obese and non obese people. MATERIAL AND METHODS: 47 subjects were selected (12 non obese and 35 obese). The study was organized in 4 visits. In each visit the subject was given isocaloric breakfast differing in macronutrient composition, (either equilibrated, or lipid, protein or carbohydrate rich) quantitative gastric emptying assay was done realized, every 15 minutes for two hours using a radionuclide technique. The week prior to the visit, the subject followed a standard 1,800 cal/day diet. RESULT: A significant interaction between time and diet composition is shown regardless of the group (obese or non-obese) the subject belongs to. The different macronutrient composition differentially affected gastric emptying only in the obese group. Post hoc analysis of the results showed significant differences after 45 min post breakfast between protein and carbohydrate rich breakfast. CONCLUSIONS: Gastric emptying in obese but not in non obese subjects, was significantly modified depending on the intake qualitative composition. These differences are clear when protein rich (significantly slower emptying) is compared versus hydrocarbon enriched diet (significantly faster emptying). A significant difference in gastric emptying between obese and non-obese subjects cannot be established.

Adult↗
PubMed2006

Obesity is a definitive risk factor of severity and mortality in acute pancreatitis: an updated meta-analysis.

BACKGROUND/AIMS: Obesity is considered a risk factor in patients with acute pancreatitis. However, the relationship between obesity and mortality in this disease has not been confirmed definitively even in a previous meta-analysis. Since the publication of our previous meta-analysis, one study has been reported about the prognostic value of obesity in acute pancreatitis. We have performed a new meta-analysis to confirm the relationship between obesity and the outcome of acute pancreatitis. DATA SOURCES: A MEDLINE search using 'pancreatitis', 'obesity' and 'body mass index' as search terms. REVIEW METHODS: Clinical studies which investigated the prognostic value of obesity in acute pancreatitis with the following criteria: (a) inclusion of mild and severe acute pancreatitis; (b) use of body mass index (BMI) as the measure of obesity; (c) definition of obesity as BMI >or=30 kg/m(2); (d) definition of severity of acute pancreatitis according to the criteria established in the Atlanta Symposium. Five studies including patients with mild and severe acute pancreatitis and obesity measured by BMI were analyzed. The end points of the meta-analysis were the severity of acute pancreatitis, local complications, systemic complications and mortality. Pooled odds ratio (OR) and confidence intervals (CI) were calculated according to the Mantel-Haenszel method, and heterogeneity was assessed by the multiplicative inverse variance method. RESULTS: Seven hundred and thirty-nine patients were included. There was no heterogeneity for the variables severity, systemic complications, local complications and mortality among the included studies. Severe acute pancreatitis was significantly more frequent in obese patients (OR 2.9, 95% CI 1.8-4.6). Furthermore, those patients developed significantly more systemic (OR 2.3, 95% CI 1.4-3.8) and especially local complications (OR 3.8, 95% CI 2.4-6.6). In this new analysis, mortality was also higher in obese patients (OR 2.1, 95% CI 1.0-4.8). CONCLUSION: Obesity is not only a risk factor for the development of local and systemic complications in acute pancreatitis: it also increases the mortality of this disease.

Acute Disease↗
PubMed1993

Growth hormone secretion is differently affected in genetically obese male and female rats.

Growth hormone (GH) secretion is markedly blunted in obesity. Reportedly, genetically obese Zucker rats show a reduced GH secretion due to an impaired function of hypothalamic neurons producing the GH-releasing hormone (GHRH). The aim of this work was: (1) to compare the in vitro GH responsiveness to GHRH in genetically obese female versus male Zucker rats and, (2) to evaluate the function of hypothalamic GHRH and somatostatin and of pituitary receptors for these neurohormones as assessed by the effectiveness of GHRH and somatostatin on adenylate cyclase (AC) activity. Baseline GH secretion of pituitaries obtained from male and female obese rats was not different and similar to that present in lean counterparts. Stimulation with 10(-7) M GHRH elicited a significantly lower GH secretion from the pituitaries of obese male rats but induced a similar GH secretion from the pituitaries of lean and obese female rats. In these pituitaries, GH concentration was similar in obese versus lean male and female rats [corrected]. A sex-related difference was also evidenced when plasma concentrations of somatomedin C (IGF-I) were evaluated. Obese male rats had lower IGF-I concentrations than lean counterparts, while this was not the case for obese versus lean female rats. Evaluation of AC activity following GHRH disclosed a lower activation in obese than in lean male rats, whereas in the females the enzyme activation was higher in obese than in lean animals. Conversely, the inhibitory effect of somatostatin on forskolin-stimulated AC was similar in pituitary membranes of obese and lean rats of both sexes.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenylyl Cyclases↗
PubMed1996

Sex-related alterations in hypothalamic growth hormone-releasing hormone mRNA-but not somatostatin mRNA-expressing cells in genetically obese Zucker rats.

The possibility that the growth hormone (GH) suppression associated with obesity is due to alterations in hypothalamic GH-releasing hormone (GHRH) and/or somatostatin (SRIH) has been considered, but the data are not consistent. In the present study, we sought to clarify the roles of GHRH and SRIH in obesity by using in situ hybridization to localize and quantify the level of expression of GHRH mRNA- and SRIH mRNA-containing neurons in the hypothalamus of male and female lean and obese Zucker rats (12 weeks of age; n = 6 per group). In lean animals, the number of GHRH mRNA-expressing cells in the arcuate nucleus and SRIH mRNA-containing neurons in the periventricular nucleus was 2- to 3-fold higher in males compared to females. The obese phenotype in the male was associated with a striking reduction in arcuate GHRH mRNA expression, both in terms of number of cells (-71%; p < 0.01) and grains/cell (-44%; p < 0.05). In contrast, in obese females, there was a marked augmentation (+ 175%; p < 0.05) in the number of GHRH mRNA-containing cells in the arcuate nucleus compared to their lean littermates. The small population of GHRH mRNA-containing neurons of the ventromedial nucleus was not modified in male obese rats, while it was considerably increased (p < 0.05) in obese females. Neither the number of labeling density of SRIH mRNA-containing neurons in the periventricular and arcuate nuclei of obese rats of either sex was changed when compared to their sex-matched lean counterparts. These results demonstrate that: (1) the obese male Zucker rat exhibits a marked diminution in hypothalamic GHRH mRNA expression, while a reverse pattern is evident in the obese female; (2) hypothalamic SRIH mRNA-containing neurons are not significantly altered in obese rats of both sexes. Our findings suggest that the impaired GH secretion of the obese Zucker rat is due, at least in part, to alterations in hypothalamic GHRH gene expression and that SRIH does not play a major role.

Analysis of Variance↗
PubMedDate not supplied

Left ventricular systolic and diastolic function in severe obesity: a radionuclide study.

To verify the impact of sever obesity (defined as body mass index > 31 kg/m2) on left ventricular (LV) function, 32 asymptomatic obese but otherwise healthy subjects (16 men; age 38 +/- 11 years) voluntarily underwent first-pass and equilibrium 99mTc radionuclide angiography at rest and, in 22 of them, during bicycle supine exercise. Data were compared to those obtained from 10 normal volunteers (age 48 +/- 13; p < 0.05, vs. obeses). End-diastolic and stroke volumes did not differ between the two groups, whereas end-systolic volume was significantly higher in obese subjects (67 +/- 20 vs. 49 +/- 20 ml; p < 0.05), and, as a consequence, LV ejection fraction at rest was decreased in obese subjects (59 +/- 7%) compared to normals (65 +/- 6%; p < 0.05). Due to the higher heart rate in obese subjects (81 +/- 13 vs. 69 +/- 10 pbm, respectively; p < 0.05) cardiac output was significantly greater compared to normals (7.1 +/- 0.8 vs. 6.2 +/- 0.2 liters/min, respectively; p < 0.01). During exercise, ejection fraction normally increased in normals (70 +/- 7%; p < 0.001, vs. baseline) but not in obese subjects (60 +/- 9%; p = nonsignificant vs. baseline). In addition, systolic blood pressure/end-systolic volume ratio was significantly decreased in obese subjects (23 +/- 1.3) compared to normals (2.8 +/- 1.6; p < 0.05). Peak filling rate, normalized to end-diastolic counts per second, was significantly lower in obese subjects (2.2 +/- 1.3) compared to normals (2.8 +/- 1.6; P < 0.05). This difference was also true when peak filling rate was computed in stroke counts per second (3.8 +/- 0.8 in obeses vs. 4.4 +/- 0.4 in normals; p < 0.05). Repeat analysis in a subgroup of 10 young obese subjects (age < or = 30 years) confirmed decreased ejection fraction at rest (60 +/- 4%; p < 0.05) and peak filling rate (2.4 +/- 0.4 end-diastolic counts/s; p < 0.05), as well as the lack of ejection fraction increase during exercise (59 +/- 9%). Thus, these data indicate a subclinical impairement of LV systolic and diastolic function at rest and during exercise in asymptomatic severely obese but otherwise healthy subjects.

Adult↗
PubMed2006

Cardiovascular function in a rat model of diet-induced obesity.

The obesity-prone/obesity-resistant rat model has been used to study mechanisms responsible for obesity-related abnormalities in renal function and blood pressure, but whether this model exhibits cardiac dysfunction has not been determined. We tested the hypothesis that obesity-prone rats would display cardiovascular abnormalities seen in other diet-induced obese models (ie, hypertension, tachycardia, left ventricular hypertrophy, increased collagen deposition, reduced cardiac contractility, and increased end diastolic pressure). Male Sprague-Dawley rats were fed a control diet or a moderate fat diet containing 32% kcal as fat while hemodynamics were continuously monitored using telemetry. After 12 weeks, obesity-prone rats were significantly heavier and had greater body fat compared with obesity-resistant rats and controls, but daily (20 hours/d) averages and diurnal rhythms of blood pressure and heart rate did not differ among groups. Echocardiographic indices of cardiac structure and function, histological evidence of cardiac collagen, and directly measured heart weights did not differ among groups. Peak left ventricular pressure, end diastolic pressure, +dP/dt, and -dP/dt were also not significantly different among groups. Plasma cholesterol and hepatic cholesterol were significantly higher in obesity-prone rats compared with obesity-resistant rats and controls; hepatic triglycerides were higher in obesity-prone rats compared with controls (P< or =0.05). Leptin was significantly higher in obesity-prone rats compared with controls and across all groups was significantly correlated with body fat (P< or =0.05). These results suggest that 12 weeks of a moderate fat diet in the obesity-prone/obesity-resistant rat model induced lipid and endocrine abnormalities typical of obesity but was not sufficient to cause significant cardiac abnormalities.

Animals↗
PubMed2006

Autonomic contribution to blood pressure and metabolism in obesity.

Obesity is associated with alterations in the autonomic nervous system that may contribute to the increase in blood pressure and resting energy expenditure present in this condition. To test this hypothesis, we induced autonomic withdrawal with the ganglionic blocker trimethaphan in 10 lean (32+/-3 years) and 10 obese (35+/-3 years) subjects. Systolic blood pressure fell more in obese compared with lean subjects (-17+/-3 versus -11+/-1 mm Hg; P=0.019) because of a greater decrease in total peripheral resistance (-310+/-41 versus 33+/-78 dynes/sec/cm(-5); P=0.002). In contrast, resting energy expenditure decreased less in obese than in lean subjects, (-26+/-21 versus -86+/-15 kcal per day adjusted by fat-free mass; P=0.035). We confirmed that the autonomic contribution to blood pressure was greater in obesity after including additional subjects with a wider range of blood pressures. Systolic blood pressure decreased -28+/-4 mm Hg (95% CI: -38 to -18.0; n=8) in obese hypertensive subjects compared with lean (-9+/-1 mm Hg; 95% CI: -11 to -6; n=22) or obese normotensive subjects (-14+/-2 mm Hg; 95% CI: -18 to -10; n=20). After removal of autonomic influences, systolic blood pressure remained higher in obese hypertensive subjects (109+/-3 versus 98+/-2 mm Hg in lean and 103+/-2 mm Hg in obese normotensive subjects; P=0.004) suggesting a role for additional factors in obesity-associated hypertension. In conclusion, sympathetic activation induced by obesity is an important determinant to the blood pressure elevation associated with this condition but is not effective in increasing resting energy expenditure. These results suggest that the sympathetic nervous system could be targeted in the treatment of obesity-associated hypertension.

Adult↗
PubMed1994

Relation of obesity and gender to left ventricular hypertrophy in normotensive and hypertensive adults.

Although it is recognized that both hypertension and obesity are associated with increased left ventricular mass, the relative impacts of obesity, arterial hypertension, and gender on the prevalence of ventricular hypertrophy remain uncertain. Accordingly, echocardiographic left ventricular mass normalized for height to the power of the allometric or growth relation between ventricular mass and height was compared in 164 normotensive subjects (85 men [24 obese] and 79 women [28 obese], aged 45 +/- 12 years) and 475 hypertensive patients (325 men [126 obese] and 150 women [85 obese], aged 54 +/- 10 years) from an adult employed population. Gender-specific upper normal limits were used to identify ventricular hypertrophy. Left ventricular mass/height 2.7 was higher in obese than normal-weight normotensive subjects (P < .004) independently of the level of blood pressure and identified a higher prevalence of hypertrophy (mainly eccentric) in obese than in normal-weight normotensive subjects (14% versus 5%, P < .04), a difference that was not detected by left ventricular mass/body surface area. Left ventricular mass/height identified hypertrophy in 52% of obese and 30% of normal-weight hypertensive patients (P < .0001) because of higher prevalences in obese than normal-weight patients of both eccentric (34% versus 20%) and concentric ventricular hypertrophy (18% versus 10%). The increase in left ventricular mass was independent of blood pressure values in obese normotensive women (but not men), and the prevalence of supranormal left ventricular mass/height 2.7 was even higher in hypertensive obese women (58%) than men (49%).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗