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Biomedical subjects

A Tremblay

Publications and source records attributed to A Tremblay.

At least 199 records · Page 11Linked to original sources
PubMed1994

Both low sodium and high potassium intake increase the level of adrenal angiotensin-II receptor type 1, but not that of adrenocorticotropin receptor.

Angiotensin-II (AII), a component of the renin-angiotensin system, is the major factor that regulates the formation of aldosterone in the adrenal cortex zona glomerulosa (ZG). The activity of this system is increased by an increase in potassium intake or a decrease in sodium intake. Using immunoblotting analysis, we determined whether these ions affect the expression of type 1 AII receptors (AT1) and compared the results thus obtained with the AT1 receptor mRNA levels. We also studied the interrelation among AII, AT1 receptors, cytochrome P450 aldosterone synthase (P450c18), and plasma aldosterone levels in rats fed a normal diet or a low sodium or high potassium diet with or without captopril, an inhibitor of angiotensin-converting enzyme, for 7 days. The effects of ions on the level of ACTH receptor mRNA were also analyzed. We found that a low sodium intake increased plasma aldosterone levels from 5.5 to 236 ng/dl and led to 2.3- and 3.7-fold increases in the levels of adrenal ZG AT1 receptor protein and AT1 receptor mRNA, whereas a 11.8-fold increase was found in the level of P450c18 mRNA. Captopril almost completely reversed these effects. We have shown that a high potassium intake increased plasma aldosterone levels to 25.9 ng/dl and also led to 1.84- and 1.95-fold increases in the level of ZG AT1 receptor protein and AT1 receptor mRNA, whereas the ZG P450c18 mRNA level was increased 3.5-fold. The plasma aldosterone level of animals fed a high diet of potassium and captopril was still higher than that in control animals at 16.6 ng/dl, and the levels of ZG AT1 receptor and P450c18 mRNAs were only slightly less than those of the high potassium groups, indicating that captopril did not efficiently block aldosterone formation under these conditions. ACTH receptor mRNA levels remain unaffected by either low sodium or high potassium intake. Collectively, these results indicate that the increased aldosterone secretion induced by low sodium or high potassium intake involves concomitant increases in AT1 receptor and P450c18 mRNAs, which are effectively translated into their respective proteins, and that the expression of both proteins is mediated in part by AII.

Aldosterone↗
PubMed1994

Thyroid hormones and thyrotropin variations during long term overfeeding in identical twins.

The aim of this study was to evaluate variations in plasma thyroid hormones and TSH during a standardized long term overfeeding protocol (4.2 megajoules/day [corrected] during a 100-day period) in 24 lean adults (12 pairs of monozygotic twins) and to assess their relationships with body composition and resting metabolic rate (RMR) changes. Compared to preoverfeeding values, basal plasma T3 concentrations were increased on day 25, but not later; basal plasma T4 and free T4 (FT4) concentrations were unchanged; basal plasma rT3 concentrations were persistently decreased throughout the entire protocol; and the TSH response to TRH stimulation was persistently enhanced. The TSH response to TRH before overfeeding was positively correlated with the changes in RMR with overfeeding (r = -0.53; P < 0.01). No association was found between changes in basal plasma T3 concentrations and changes in RMR. However, changes in basal T3 were positively related to changes in body weight (r = 0.46; P < 0.05). A significant within-pair similarity was found for changes in T4 and FT4 with overfeeding (P < 0.05). We conclude that 1) during overfeeding, the early increase in T3 concentrations is a transitory phenomenon, whereas the decrease in rT3 concentrations and the increased TSH response to TRH are more sustained; 2) the TSH responsiveness to TRH stimulation could be a predictor of the changes in RMR during times of increased energy intake; 3) there is no evidence for a direct role of T3 in the adaptation of resting energy expenditure during a long term overfeeding protocol; and 4) the genotype could be involved in the changes in T4 and FT4 during a prolonged positive energy balance period.

Adult↗
PubMed1994

Energy expenditure measurement in male cross-country skiers: comparison of two field methods.

The purpose of this study was to compare estimations of daily energy expenditure (DEE) made with a physical activity journal (PAJ) and a heart rate monitoring method (HR-VO2) in endurance athletes. Seven male cross-country skiers (21 +/- 5 yr of age, mean +/- SD) with high aerobic power (70.4 +/- 7.2 mlO2.kg-1.min-1) and eight lean and moderately active males serving as controls (22 +/- 1 yr; 50.9 +/- 9.9 mlO2.kg-1.min-1) were tested. VO2max, resting metabolic rate (RMR), energy cost of standardized activities, PAJ, HR monitoring, and food diaries for measurement of daily energy intake (DEI) were measured in October, before the specific training period. Results indicated that the skiers had a higher RMR (P < 0.05) than the controls (8.2 +/- 1.6 vs 6.9 +/- 0.6 MJ.d-1), as measured by indirect calorimetry. DEE estimates made with the PAJ and the HR-VO2 methods were similar in the controls subjects but the HR-VO2 method yielded significantly higher results in the skiers (17.0 +/- 4.0 vs 13.1 +/- 2.1 MJ.d-1). DEI measurements were similar to HR-VO2 DEE in both groups. Thus, it appears that the PAJ, which was established with a sedentary population, underestimated DEE in trained cross-country skiers. Thus, the physical activity status of subjects has to be investigated before using a physical activity diary.

Adult↗
PubMed1993

Differential expression of corticostatins/defensins: higher levels of CS-4 (NP-2) transcripts compared with CS-6 (NP-5) in rabbit lung.

cDNA clones encoding two members of the corticostatin (CS)/defensin family of peptides have been isolated from a rabbit bone marrow cDNA library through cross-hybridization with cDNA encoding the human corticostatin HP-4. They encode the precursors of CS-4 (NP-2, MCP-2) and CS-6 (NP-5). Highly specific probes were generated for Northern blotting of RNA from various normal rabbit tissues. Both detected high levels of message in bone marrow, moderate in spleen, and low in thymus. In lung, however, while moderate levels were detected with the CS-4 probe, CS-6 message was barely detectable. This correlates with the report of CS-4, but not CS-6 peptide in lung macrophages, and implies that differential regulation of CS/defensin expression in rabbit lung is at the level of gene transcript abundance.

Amino Acid Sequence↗
PubMed1993

Transcriptional activation of adrenocortical steroidogenic genes by high potassium or low sodium intake.

We have previously shown that the long-term alterations in the intake of sodium and potassium which stimulated aldosterone production in the rat adrenal significantly increased cytochrome P450scc (P450scc) and P45011 beta (P45011 beta) mRNA's and also the mRNA of their electron donor adrenodoxin. In the present study run-on analyses showed an accumulation of nascent RNA in isolated nuclei of zona glomerulosa cells in K(+)-supplemented and Na(+)-depleted rats for P450scc (5- and 6-fold), 3 beta-HSD (3.6- and 2.0-fold) and P45011 beta (6.0- and 6.1-fold), but not for P450c21 (1.4- and 1.1-fold). In contrast, that of adrenodoxin decrease (0.6-fold) in high K+ and remained near control (1.3-fold) in low Na+ intake. Moderate variations in the rate of transcription of P450scc, P450c21, P45011 beta and adrenodoxin genes were observed in the zona fasciculata-reticularis cells of the treated rats. Our results thus demonstrated that positive modulators of aldosterone such as long-term K+ supplementation and Na+ restriction provoked an increase in transcription of the genes encoding key regulatory steroidogenic enzymes of aldosterone biosynthesis in the zona glomerulosa. The rates of transcription of the genes encoding 3 beta-HSD and P450c21, two enzymes catalyzing intermediate steps in the aldosterone pathway, were moderately affected by such treatments. However, according to the known stimulation of adrenodoxin mRNA levels following these treatments, a decreased turnover of the adrenodoxin mRNA rather than initiation of transcription of its gene might be involved in the response to K+ ions, and partially so in the response to Na+ restriction. Finally, the effects of salt-modified intake were mainly restricted to the zona glomerulosa cells, which are solely responsible for aldosterone production.

Adrenal Cortex↗
PubMed1993

Exercise and obesity.

This paper reviews succinctly the evidence for a role of regular exercise in the prevention and the treatment of obesity and of its metabolic complications. Seventeen propositions relevant to an understanding of the topic are considered. The evidence suggests that regular exercise can be an important factor in the development of sustained negative energy balance conditions provided the volume of activity is high. This implies a program of low to moderate intensity exercise performed on an almost daily basis for at least one hour per session. To induce significant weight and fat losses and to treat overweight and obese patients, compliance to the program for several years becomes a necessity. Exercise increases lipid substrate oxidation and may favor carbohydrate intake for the same amount of energy intake. The acute effects of exercise on resting metabolic rate are well documented, but the long-term influences of exercise training seem to be small and are rapidly suppressed with the cessation of training. The obese benefits also from a regular exercise regimen in terms of improved insulin sensitivity, lipid and lipoprotein profile, and blood pressure, as well as reduced risk of death. Regular exercise, such as walking, is a healthy course of action for the overweight or the obese patients.

Adipose Tissue↗
PubMed1993

Non linear weight gain with long term overfeeding in man.

This study deals with the pattern of body weight gain during an overfeeding period with a constant energy intake, in order to assess whether total daily energy expenditure (TEE) increased with body weight and thus could account for the progressive slow down in body weight gain over time. Twenty-four young adult males (12 pairs of identical twins) were overfed by 4.2 MJ per day, six days a week, for a total of 84 days during a 100-day overfeeding period. The total excess amount each man consumed was 353 MJ. It was assumed that, at a given time, the TEE increase (E) was dependent on body weight gain and energy cost (C) was proportional to the daily body weight gain. Results show an exponential increase in body weight, fat free mass, and fat mass (with half-times of 86, 57, and 84 days, respectively) that allows the calculation of E (246 +/- 37 kJ x kg(-1) x d(-1), mean +/- SE) and C (32.3 +/- 2.4 MJ x kg(-1)). Energy expenditure from other sources besides resting metabolic rate, such as physical activity and thermic effect of food, may represent as much as 65% of E. At the beginning of the overfeeding period, almost all the energy surplus was recovered as body substances but this proportion decreased to 60% after 100 days of overfeeding. It is concluded that 1) TEE changes were related to body weight change, 2) about 65% of E were accounted for by physical activity, thermic effect of food, or some other components, and 3) the fraction of the energy surplus stored as body substances decreased with the duration of overfeeding.

Adipose Tissue↗
PubMed1993

Genetic influences on energy expenditure in humans.

Variations in human energy expenditure are partly because of an influence of the genotype, even after control for the well-established concomitants of energy expenditure. Using the techniques of genetic epidemiology, we have found that about 40% of the variance in resting metabolic rate, thermic effect of food, and energy cost of low-to-moderate intensity exercise (< or = 5 times the resting metabolic rate) is explained by inherited characteristics. A significant genetic effect has also been reported for the level of habitual physical activity. The existence of a genotype-environment interaction has also been investigated. Thus, in response to chronic overfeeding, as well as negative energy balance, changes in the components of energy expenditure exhibit significant identical twin pair resemblance. Nutrient partitioning is emerging as a major determinant of the individual differences in metabolic rate responses to overfeeding or negative energy balance conditions. Taken as a whole, these observations consistently support the hypothesis that heredity plays a significant role in the various components of energy expenditure in humans.

Adult↗
PubMed1993

Sex differences in the relation of visceral adipose tissue accumulation to total body fatness.

The associations between the amount of abdominal adipose tissue (AT) measured by computed tomography (CT) or estimated with predictive equations and the amount of total body fat were compared in samples of 89 men and 75 women. After correction for total body fat mass, men had significantly higher values of visceral AT volume (P < 0.0001) and also higher abdominal visceral AT areas, measured by CT or estimated by predictive equations than women (P < 0.0001). In addition, an increase in total fat mass was associated with a significantly greater increase in visceral AT volume in men than in women (P < 0.0001). In conclusion, these results suggest that the greater health hazards associated with excess fatness in men than in women may be explained by the fact that premenopausal women can accumulate more body fat than men of the same age before reaching the amounts of visceral AT found in men.

Adipose Tissue↗
PubMed1993

Abdominal and femoral adipose tissue lipolysis and cardiovascular disease risk factors in men.

The relationships between subcutaneous abdominal and femoral fat cell lipolyses, plasma free-fatty acid (FFA) levels and metabolic variables considered as risk factors for cardiovascular disease (CVD) (plasma glucose, insulin and lipoprotein levels) were investigated in 54 men, aged 36 +/- 3 (SD) years, covering a wide range of body fatness values (body mass indices from 19 to 34 kg m-2). Although there were no consistent relationships between femoral fat cell weight and the metabolic profile, positive and significant associations were found between abdominal fat cell weight and most of the metabolic indices. However, abdominal fat cell lipolysis measured with an alpha 2-(clonidine) or a beta-agonist (isoproterenol) was unrelated to metabolic variables. In contrast, femoral fat cell lipolysis measured in the presence of clonidine was positively associated with fasting plasma insulin, cholesterol (CHOL) and apolipoprotein (apo) B levels, as well as with LDL-CHOL and LDL-apo B concentrations. No association was found between isoproterenol-stimulated lipolysis of femoral adipocytes and the metabolic profile. Comparison of two subgroups of men with either low or high femoral residual lipolysis with clonidine revealed that subjects with the lowest femoral alpha 2-adrenergic component (i.e. the highest residual lipolysis) displayed significant alterations in both plasma lipid-lipoprotein and glucose-insulin levels which could be predictive of an increased risk of CVD. Free fatty acid (FFA) levels measured in the fasting state and during an oral glucose tolerance test (OGTT) were positively associated with fasting plasma insulin and triglyceride levels as well as with both glucose and insulin areas measured during the OGTT. However, regional adipose tissue lipolysis measured in vitro was unrelated to plasma FFA levels. These results support the view that both femoral adipose tissue lipolysis and plasma FFA levels are significant correlates of plasma glucose-insulin homeostasis and lipoprotein-lipid levels, in men. However, as adipose tissue lipolysis and plasma FFA are unrelated to each other, they may be associated with risk variables through independent mechanisms.

Abdomen↗
PubMed1993

Metabolic heterogeneity associated with high plasma triglyceride or low HDL cholesterol levels in men.

To further understand the factors involved in the regulation of high plasma triglyceride (TG) or low plasma high density lipoprotein cholesterol (HDL-C) levels, three groups of male subjects (normal TG with low HDL-C levels, high TG with normal HDL-C levels, and high TG with low HDL-C levels) were compared with a sample of normolipemic men with normal TG and HDL-C plasma levels. Mean age was 34 years (range, 20-42 years), and none of the subjects had plasma TG levels > 4.0 mmol/l or familial hypercholesterolemia. Both groups of subjects with high TG levels had a higher body mass index, waist circumference, waist-to-hip circumferences ratio, and a higher ratio of abdominal to femoral adipose tissue areas as measured by computed tomography when compared with normolipemic control subjects. However, during an oral glucose tolerance test only high TG-low HDL-C men had fasting hyperinsulinemia and higher plasma insulin levels compared with normolipemic subjects. In addition, the high TG-low HDL-C group showed reduced HDL apoprotein (apo) A-I levels and a low HDL2-C/HDL3-C ratio. These changes were observed along with a nonsignificant trend for a lower plasma postheparin lipoprotein lipase activity. However, among subjects with high TG and normal HDL-C levels, no evidence of insulin resistance or of a reduction in postheparin lipoprotein lipase activity was observed, suggesting that the high plasma TG levels could be attributed to an increased production of apo B-containing lipoproteins, as high plasma apo B and low density lipoprotein (LDL)-apo B levels were observed in this group.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Apolipoprotein E polymorphism modifies relation of hyperinsulinemia to hypertriglyceridemia.

The effect of apolipoprotein E polymorphism on the established relationships between glucose tolerance, plasma insulin levels, and plasma lipoprotein concentrations were investigated in a sample of women defined on the basis of apolipoprotein E phenotypes. In women with the apolipoprotein E epsilon 2 allele (n = 22), fasting plasma insulin and glucose and insulin areas under the curve measured during an oral glucose tolerance test were positively correlated with plasma triglyceride levels (0.48 < or = r < or = 0.70; P < 0.05). In this group, very-low-density lipoprotein cholesterol and very-low-density lipoprotein triglyceride concentrations were positively correlated with fasting insulin levels, the insulin area, and with the ratio of insulin area to glucose area. In women (n = 24) homozygous for the apolipoprotein E epsilon 3 allele (the most common allele), essentially similar associations were found. In contrast, in women (n = 17) with the apolipoprotein E epsilon 4 allele, no association was found between glucose tolerance, fasting and postglucose plasma insulin levels, and plasma lipid and lipoprotein levels. These results suggest that apolipoprotein E polymorphism substantially modifies the associations between glucose tolerance, plasma insulin levels, and plasma lipoprotein concentrations. Additional analysis of the data revealed that apolipoprotein E polymorphism did not alter the relationships between body fat distribution and fasting insulin and postglucose insulin levels, but no correlation was observed between fatness indexes and glucose tolerance among apolipoprotein E epsilon 2 carriers.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue↗
PubMed1993

Evidence for a role of insulin in the regulation of abdominal adipose tissue lipoprotein lipase response to exercise training in obese women.

Abdominal and femoral adipose tissue lipoprotein lipase (AT-LPL) activities were measured in ten obese premenopausal women (mean age 35 +/- 5 years) who took part in a six month endurance exercise training programme. The programme involved four to five 90 min training sessions per week at about 50 to 55% of maximal endurance power (VO2max). Before training, the ratio of insulin to glucose area measured during an oral glucose tolerance test (OGTT) was significantly correlated with fat mass (r = 0.72, P < 0.05) as well as with abdominal AT-LPL activity (r = 0.69, P < 0.05). The training programme induced a significant increase in VO2max (P < 0.05) whereas no significant change in the mean body composition was observed. Abdominal as well as femoral AT-LPL activities were significantly reduced after the exercise training programme (P < 0.05) whereas plasma post-heparin (PH) LPL activity was significantly increased by training (P < 0.05). No significant association was observed between changes in VO2max and in body composition parameters and changes in abdominal or femoral AT-LPL activities. However, changes in insulin sensitivity, as estimated by changes in the insulin area/glucose area ratio were positively correlated with changes in abdominal AT-LPL activity expressed on a per cell (r = 0.72, P < 0.05) or per surface area (r = 0.81, P < 0.01) basis. These results suggest that the reduction in AT-LPL activity in both fat depots following endurance training in obese women can occur despite the lack of significant decrease in body weight and average fat cell size.(ABSTRACT TRUNCATED AT 250 WORDS)

Abdomen↗
PubMed1992

Genetic aspects of susceptibility to obesity and related dyslipidemias.

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.

Adipose Tissue↗