[Intracranial hypertension and cerebral hypoperfusion, frequent complications in severe burns].
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to C Bouchard.
Explore the source record for details and available documents.
Obesity has a multifactorial origin. However, although environmental variables undoubtedly play a role in the development of obesity, it is now clear that genetic variation is also involved in the determination of an individual's susceptibility to body fat accumulation. In addition, it is also widely accepted that obesity is not a single homogeneous phenotype. It is also heterogeneous regarding its causes and metabolic complications. The regional distribution of body fat appears to be an important correlate of the metabolic complications that have been related to obesity. Due to their higher accumulation of abdominal fat, men are generally more at risk for the metabolic complications of obesity than women whereas some obese women, with large gluteal-femoral adipose depots may have a cosmetic problem which may not necessarily require medical intervention. Several studies have been conducted to understand the mechanisms by which abdominal obesity is related to diabetes, hypertension and cardiovascular disease. It appears that the increased risk of abdominal obesity is the result of complex hormonal and metabolic interactions. Studies in genetic epidemiology have shown that both total body fatness and the regional distribution of body fat have a significant genetic component. Standardized intervention studies using an identical twin design have shown that individuals that have the same genetic background tend to show similar changes in body fat and in plasma lipoprotein levels when exposed to standardized caloric excess or energy restriction. Finally, although abdominal obesity is a significant risk factor for cardiovascular disease, not every abdominal obese subject will experience metabolic complications, suggesting that some obese individuals may be more susceptible than others. Variation in several genes relevant to lipid and lipoprotein metabolism may alter the relation of abdominal obesity to dyslipoproteinemias. Abdominal obesity should therefore be considered as a factor that exacerbates an individual's susceptibility to cardiovascular disease.
The hypothermia induced by the serotonin (5-HT)1A receptor agonist 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) was attenuated in rats that had received a course of six electroconvulsive shocks (ECS) over a two-week period. The firing activity of dorsal raphe 5-HT neurons, as well as their responsiveness to microiontophoretic applications of 5-HT and 8-OH-DPAT, was unaltered in ECS-treated rats. The electrically evoked overflow of [3H]5-HT from preloaded slices of guinea pig hypothalamus was unchanged after the same ECS treatment. The concentration-effect curves of the 5-HT autoreceptor agonist 5-carboxyamidotryptamine (0.1-100 nM) were similar in slices prepared from control and ECS-treated guinea pigs. In addition, the reduction in the evoked [3H]5-HT overflow obtained by increasing the stimulation frequency from 1 to 5 Hz, which is due to a greater activation of terminal 5-HT autoreceptors at the higher frequency, was not altered by the ECS treatment. The enhancing effects of the 5-HT autoreceptor antagonist methiothepin (0.1-1 microM) and of the 5-HT3 agonist 2-methyl-5-HT (0.1-1 microM) on the evoked [3H]5-HT overflow were unaltered by the ECS treatment. These results thus indicate that repeated ECS attenuates the 8-OH-DPAT-induced hypothermia in rats, as previously reported, but does not affect the firing activity of 5-HT neurons and the sensitivity of their somatodendritic 5-HT1A autoreceptors in the dorsal raphe. The function of 5-HT terminals in the guinea pig hypothalamus was also unaffected by repeated ECS. In conclusion, repeated ECS does not affect the function of 5-HT neurons at the cell body and nerve terminal.
The interaction between environmental and genetic factors in the alterations of glucose-insulin homeostasis was studied in 104 non-diabetic men. Family history of diabetes mellitus was used as an index of genetic predisposition to diabetes. Body composition was measured by underwater weighing whereas subcutaneous and visceral adipose tissue areas were measured at the abdominal and femoral levels by computed tomography. The sample was first divided into two groups. The first group included subjects with "normal" glycaemic and insulinaemic responses during a 75 g oral glucose tolerance test. The second group was composed of subjects either with a high glucose response or high insulin response or both. Men included in the second group were different from the "normal" subjects for almost all body fatness variables. They also presented a prevalence of a positive family history of diabetes which was significantly higher than "normal" subjects. The second group was then divided into three distinct subgroups based on insulin and glucose responses of the subjects during the oral glucose tolerance test. Subjects with high insulin but "normal" glucose responses were characterized by significantly higher levels of total body fat and deep abdominal adipose tissue when compared to the "normal" group (p less than 0.05). Men with both high insulinaemic and glycaemic responses displayed higher body fatness values and higher deep and subcutaneous abdominal adipose tissue areas (p less than 0.05) in comparison with "normal" subjects. They also had a higher body mass index at age 20 years than control subjects and subjects with high insulin but "normal" glucose responses.(ABSTRACT TRUNCATED AT 250 WORDS)
Thirty-one obese, premenopausal women aged 35.4 +/- 5.1 (SD) years exercised for 90 minutes at approximately 55% of maximal aerobic power (VO2max) four to five times a week for a period of 6 months. The training program induced a significant increase in VO2max (P < .001) and significant improvements in carbohydrate and lipid metabolism, as reflected by decreased plasma insulin (INS) concentrations measured in the fasting state and after glucose (GLU) ingestion (INS area, P < .001), by reduced plasma cholesterol (C) and low-density lipoprotein cholesterol (LDL-C) levels (P < .001), and by increased ratios of high-density lipoprotein cholesterol (HDL-C)/LDL-C and HDL2-C/HDL3-C (P < .05 and P < .001, respectively). Changes in body fat mass were positively associated with changes in the INS area/GLU area ratio (r = .49, P < .05) and with changes in very-low-density lipoprotein triglycerides ([VLDL-TG] r = .49, P < .05). Furthermore, changes in the INS area were positively associated with changes in VLDL-TG (r = .51, P < .05). Although no significant mean change in body composition was observed, important individual variation was noted. Twenty women showed a reduction in body fat mass (mean reduction, 2.63 +/- 2.2 kg), whereas 11 women showed an increase in adipose mass (mean increase, 2.79 +/- 2.36 kg). Comparable increases in VO2max were observed between the two groups. The group that showed a decrease in body fat mass with exercise also had significant improvements in carbohydrate and lipid metabolism.(ABSTRACT TRUNCATED AT 250 WORDS)
Soluble forms of receptors for the Fc portion of IgG (sFc gamma R) were detected in biological fluids from mice and humans. In mouse bearing tumors, circulating amounts of sFc gamma R increased concurrently with tumor growth. Tumors secreting IgG2a, IgG2b or IgG3 led to a 5- to 10-fold increase in serum sFc gamma R levels whereas tumors secreting IgG1, IgGA or other types of tumors (non Ig B cell tumors, T cell lymphoma and a melanoma) increased 2- to 3-fold the levels of circulating sFc gamma R. In the human, sFc gamma R were also detected in whole unstimulated saliva. Levels of sFc gamma RII and of sFc gamma RIII were variable and did not seem to depend on the dental status of the individuals. Finally, a murine recombinant sFc gamma R (rsFc gamma R) composed of the two extracellular domains of Fc gamma RII was produced by culture of transfected L cells in bioreactors. The purified rsFc gamma R was found to inhibit antibody production in vitro in anti-SRBC responses and by cultures of small B cells stimulated by anti-IgM antibodies in the presence of IL-4 and IL-5. Moreover, the i.p. injection of this material into adult mice immunized with SRBC led to a decrease of IgG antibody production by splenocytes, as measured by a hemolytic plaque assay, and in serum, as measured by antigen-specific ELISA.
The haemodynamic time course of 16 patients with severe burn injury was investigated using a flow-directed balloon-tipped pulmonary artery catheter. The patients, aged 33.8 +/- 5.5 years, were burnt over 60 +/- 10% of body surface area, with a UBS score of 228 +/- 43. The measurements were obtained every six hours after insertion of the catheter. Fluid load was determined with Evans' formula, and modified according to the haemodynamic data. Catecholamines were introduced when this and a trial of fluid loading with 5 ml.kg-1 of macromolecules during a 20 min period had failed, starting with dobutamine or dopamine, followed by adrenaline as required. During the first hours after the injury, circulatory shock was partly linked to hypovolaemia: mean arterial pressure was 60.1 +/- 7.8 mmHg, right auricular pressure 4.5 +/- 2 mmHg, pulmonary wedge pressure 4.7 +/- 2 mmHg, cardiac index 3.5 +/- 0.8 l.min-1 x m-2. However, during the second and third days, cardiac output increased, with a cardiac index at 4.7 +/- 0.6 l.min-1 x m-2 and 5.2 +/- 0.2 l.min-1 x m-2 respectively, and arterial vascular resistances were decreased (536 +/- 125 dyn.s.cm-5). These data suggest a specific haemodynamic profile in severe burn patients which justifies invasive monitoring, and the use of catecholamines, in those patients that do not respond to fluid loading. The link between these data and the concomitant metabolic disturbances due to the burn injury has not yet been established. The increase in cardiac index could be related to the inflammatory response.(ABSTRACT TRUNCATED AT 250 WORDS)
Associations of body mass index (BMI), absolute fat mass, percent body fat, and regional fat distribution with concentrations of fasting blood glucose and blood pressure were examined cross-sectionally in 1551 men and women aged 15-79 y from two study centers. Measurements included height, weight, multiple skinfold thicknesses, body density by underwater weighing, and waist and hip girths. Three principal findings emerged: 1) Absolute overall body mass and fat mass were stronger predictors of blood pressure and blood glucose than were relative fat mass, after age, height, and current cigarette-smoking status were adjusted for; 2) when diastolic blood pressure and serum glucose were used as the external validity criteria, densitometry was not a "gold standard" for body composition associated with risk for increased blood pressure and serum glucose; and 3) BMI was as good a predictor of blood pressure and glucose as was any other measure of body fat in nearly all analyses.
This report deals with the association between the constituents of lean body mass (LBM) and resting metabolic rate (RMR) before and after a 100-d overfeeding period. Computed-tomography (CT) scan of 22 young adult males at nine different body levels were used to estimate adipose tissue mass (ATMCT), LBMCT, skeletal-muscle mass (SMMCT), and non-muscular LBMCT (NM-LBMCT). Before overfeeding, all body constituents, except ATMCT, were significantly correlated with RMR. Only body mass changes were significantly correlated with RMR changes. Comparison of these results with those of several studies in the literature reveals that the relationship between RMR and fat-free mass is highly influenced by the size of the SD for the latter variable. In stepwise-multiple-regression analysis, only SMMCT could be used to predict RMR. It was concluded that SMMCT and ATMCT, but not NM-LBMCT, increased during overfeeding and that the best correlates of RMR remain LBMCT, SMMCT, and body mass.
The effect of overfeeding on energy expenditure was investigated in 23 young men subjected to a 353-MJ energy intake surplus over 100 d. The major part of this excess (222 MJ) was stored as body energy. The increase in energy cost of weight maintenance amounted to 52 MJ and was proportional to body weight gain. When it was added to the obligatory cost of fat and fat-free mass gains, the overall increase in energy expenditure amounted to a mean of 100 MJ. Four months after overfeeding, subjects had lost 82%, 74%, and 100% of the overfeeding gain in body weight, fat mass, and fat-free mass, respectively. We conclude that 1) in response to overfeeding, two-thirds of the excess energy intake is stored as body energy; 2) overfeeding induces an increase in energy cost of weight maintenance proportional to body weight gain, and 3) preoverfeeding energy balance tends to be restored when nonobese individuals return to their normal daily-life habits.
This study was undertaken (1) to examine the relation of plasma catecholamine and insulin levels to the blood pressure response during and after submaximal exercise, (2) to verify whether the blood pressure response to an epinephrine infusion is associated with the blood pressure response to a prolonged submaximal exercise, and (3) to study some potential correlates of the hypotensive effect of prolonged aerobic exercise. Nine normotensive young men (mean age 22.0 +/- 1.4 years) were subjected to a 1-h epinephrine infusion protocol and a 1-h submaximal exercise test on a cycle ergometer. The two tests were performed 1 week apart. The physiological and hormonal responses observed during the submaximal exercise test were generally greater than those observed during the epinephrine infusion test. Blood pressure responses in both tests showed no significant association with changes in plasma insulin levels. Changes in plasma norepinephrine concentration were positively correlated with changes in systolic blood pressure during the submaximal exercise test but not during the epinephrine infusion. Results also showed that the blood pressure response to epinephrine infusion was not correlated with the blood pressure response to submaximal exercise. However, post-exercise and post-infusion systolic blood pressure responses (differences between "post-test" and "resting" values) were significantly associated (r = 0.81, p less than 0.01). In addition, a significant hypotensive effect of submaximal exercise was observed for both systolic and diastolic blood pressure.(ABSTRACT TRUNCATED AT 250 WORDS)
The relations of regional adipose tissue (AT) distribution measured by computed tomography (CT) to plasma insulin-glucose homeostasis and lipoprotein-lipid levels were studied in 58 obese and 29 lean control men. In the group of obese men, the visceral AT area measured by CT was positively correlated with fasting plasma triglyceride and insulin levels and with glucose and insulin areas under the curves measured during a 75-g oral glucose tolerance test. Visceral AT area was also negatively associated with plasma high-density lipoprotein (HDL) and HDL2 cholesterol levels. The relative accumulation of abdominal fat, estimated by the ratio of abdominal to femoral AT areas obtained by CT, was also a significant correlate of indices of carbohydrate metabolism and was the best univariate correlate of plasma lipoprotein levels. No significant associations were observed between the visceral AT area, the ratio of abdominal to femoral AT areas, and indices of carbohydrate and lipoprotein metabolism in the group of lean men. On the other hand, the subcutaneous abdominal AT area was a significant correlate of the glucose area under the curve in both groups of men, but this association was not independent from the percentage of total body fat. No relationship was observed between the femoral AT area and indices of carbohydrate metabolism in either lean or obese groups. In obese men, however, the femoral AT area was negatively correlated with plasma triglyceride concentration and positively correlated with plasma HDL and HDL2 cholesterol levels.(ABSTRACT TRUNCATED AT 250 WORDS)
Explore the source record for details and available documents.
SOS (Swedish obese subjects) is an on-going intervention trial designed to determine whether the mortality and morbidity rates among obese individuals who lose weight by surgical means (gastric banding, vertical banded gastroplasty and gastric by-pass) differ from the rates associated with conventional treatment. For this purpose, the study is recruiting a sample of obese men and women who constitute a registry of potential subjects from which the participants are drawn. Eligibility criteria for participation in the registry were: age at application 37-57 years and BMI greater than or equal to 34 kg/m2 for men and greater than or equal to 38 kg/m2 for women. Before receiving a health examination, all patients complete extensive questionnaires on current and past health status, utilization of medical care and medications, socio-economic status, psychological profiles, dietary habits, physical activity, weight history, and familial disposition to obesity. Each surgical case is matched to its optimal control in the registry, to ensure that the two groups do not differ systematically with respect to any of 18 matching variables that may affect prognosis. The first 1006 subjects included in the registry have been studied with respect to morbidity and compared with on-going population studies of men and women in Göteborg, Sweden. The relative risks of prevalent disease and symptoms associated with obesity in 50-year-old males and females respectively were 4.3 and 4.7 (dyspnoea), 14.7 and 11.8 (angina), 6.3 (myocardial infarction, males only), 2.1 and 4.5 (hypertension), 5.2 and 6.6 (diabetes), 4.6 and 26.1 (claudication) and 1.7 and 1.8 (gall bladder disease). Correspondingly, obese males and females display elevations of systolic and diastolic blood pressure, fasting glucose, insulin, triglyceride, and uric acid levels. However, total cholesterol was not increased in obese males and was in fact significantly lower in obese compared with reference women. HDL-cholesterol was lower in obese than reference men (data were not available in reference women). The rate of taking sick pensions was over twice as high in SOS obese patients than in population controls. Finally, comparison of measurements with self-reported prevalence estimates revealed a considerable amount of previously undiagnosed hypertension and diabetes in the obese subjects. These data suggest that the excess health risks associated with obesity may not be fully appreciated.
Regional fat distribution is related to higher risk of diabetes and cardiovascular morbidity and mortality, independent of excess body mass for height. In particular, the male (android) pattern of fat deposition, which is characterized by greater truncal and abdominal fat stores relative to extremity fat levels, is associated with a higher propensity to metabolic complications. Motivated by these considerations, we have initiated a systematic investigation of several measures of regional fat distribution aimed at the detection of possible single gene effects. In this paper, we assess the evidence for commingling in the distributions of these variables in a large French-Canadian study. Two measures approximating the size of subcutaneous fat stores relative to total body fat were considered: the sum of six skinfolds (SF6 = abdominal + supra-iliac + subscapular + calf + tricep + bicep), and the sum of three trunk skinfolds (TSF3 = abdominal + supra-iliac + subscapular). In addition, two measures assessing the distributional pattern of subcutaneous fat were considered: the ratio of TSF3 to the sum of the three extremity skinfolds (TER), and a relative fat pattern index [RFPI = subscapular/(subscapular + supra-iliac)]. All four measures were assessed both prior to and after adjusting for total fat mass, which was measured using underwater weighing. Significant distributional heterogeneity was observed for some of these measures, either between generations and/or between the sexes. In general, however, fat mass adjustment tended to eliminate the heterogeneity; the exception was for RFPI, for which sex differences were noted both prior to and after the adjustment. The finding of commingling of distributions for almost all phenotypes is consistent with (but not evidence for) major gene effects. However, for some of the measures the effect of a putative major locus genotype may be mediated by covariates such as age and/or sex.
The relationships between body fatness, adipose tissue distribution, plasma glucose, insulin levels, lipoprotein levels, and resting blood pressure were studied in 81 men aged 36.0 +/- 3.3 years (mean +/- s.d.) (body mass index (BMI): 27.4 +/- 3.8 kg/m2, percentage body fat: 26.4 +/- 6.6%). Systolic and diastolic blood pressures (BP) were significantly associated with the BMI (r = 0.31, r = 0.33, P < 0.01), the waist circumference (r = 0.33, r = 0.27; P < 0.01) as well as with adipose tissue areas measured by computerized tomography (CT) (0.27 < or = r < or = 0.36, P < 0.01). Furthermore, the relative accumulation of subcutaneous abdominal fat, as estimated by the ratio of abdominal to femoral adipose tissue areas measured by CT, was positively correlated with systolic and diastolic BP (P < 0.01). Fasting plasma insulin level (r = 0.30, P < 0.01) as well as the insulin area measured during an oral glucose tolerance test (0.34 < or = r < or = 0.37, P < 0.01) were significantly correlated with blood pressure. Systolic and diastolic BP were significantly associated with HDL2-cholesterol (C) as well as with the HDL2-C/HDL3-C ratio (-0.24 < or = r < or = -0.34), whereas triglycerides (r = 0.23) and the HDL-C/C ratio (r = -0.23) were significantly correlated with diastolic BP only (P < 0.05). Multivariate analysis indicated that the insulin area was the most important variable associated with blood pressure and that this association was independent of total body fatness and regional adipose tissue distribution. Plasma insulin levels explained 14% and 11% of the variance observed in the systolic and diastolic blood pressures respectively. These results suggest that most of the association between abdominal obesity and high blood pressure is mediated by the hyperinsulinemia and/or the related insulin resistant state.
Explore the source record for details and available documents.
Explore the source record for details and available documents.