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Biomedical subjects

A Tremblay

Publications and source records attributed to A Tremblay.

At least 145 records · Page 8Linked to original sources
PubMed1997

Acute effects of exercise on energy intake and feeding behaviour.

The main objective of the present study was to evaluate the short-term effects of exercise of different intensities on energy intake. Eleven young men were submitted to three randomly assigned sessions (one control and two exercise sessions) in which they ate, ad libitum, foods from a buffet-type meal. The energy cost of exercise was the same in the two exercise sessions. Results showed that there was no significant change in post-exercise subjective levels of hunger and fullness as well as total energy and macronutrient intakes in comparison with the control session. However, when energy intake relative to expenditure was considered by subtracting the surplus of energy expended during exercise from total energy intake, high-intensity exercise exerted a greater reducing effect on this variable compared with the control and low-intensity exercise sessions. These results suggest that for a given level of energy expenditure, high-intensity exercise favours negative energy balance to a greater extent than low-intensity exercise.

Adult↗
PubMed1997

Genetic influences on the response of body fat and fat distribution to positive and negative energy balances in human identical twins.

This article summarizes a series of intervention studies conducted with pairs of young adult male identical twins and designed to determine whether there is any evidence for genotype x overfeeding or genotype x negative energy balance interaction effects in the changes in body weight, body composition, fat distribution, computerized tomography-assessed abdominal visceral fat, resting metabolic rate and thermic response to a standardized meal of mixed composition brought about by chronic exposure to appropriate experimental treatments. These studies demonstrated that individual differences in response to chronic alterations in energy balance are common. The comparison of the heterogeneity in response between the pairs of twins in contrast to the variance within pairs revealed that members of the same twin pair are significantly more alike than individuals who are not genetically related by descent. The intrapair resemblance in response was particularly strong for the changes in body mass, body composition, subcutaneous fat distribution and abdominal visceral fat. In contrast, the results of two long-term intervention studies showed that variations in resting metabolic rate following exposure to chronic overfeeding or negative energy balance induced by exercise were accounted for primarily by the changes in body mass. Finally, the thermic response to food was not modified by any of the experimental treatments. On the basis of these observations, we conclude that there are individuals at risk of gaining weight and body fat or who are resistant to weight loss. These differences in susceptibility to chronic overfeeding or in sensitivity to negative energy balance seem to be largely explained by genetic factors whose exact nature remains to be determined.

Adipose Tissue↗
PubMed1997

Effects of exercise on appetite control: implications for energy balance.

At a time of increased obesity, decreased physical activity, and high food consumption, the relationship between physical activity and appetite control needs to be examined. Many people believe that the energy expended as a result of physical activity generates a drive to eat. However, a counterintuitive conclusion arises since there is no compelling evidence that increased physical activity increases energy intake. A suppression of hunger occurs following intense exercise; however, this effect is brief and has no influence on energy intake. Indeed, there does not appear to be any within-day effect of exercise on energy intake. Day-to-day effects of exercise on energy intake could occur, but only a few provocative data exist showing a delayed effect of exercise on energy intake 2 d later. Therefore, there appears to be only a weak short-term coupling between energy expenditure and energy intake. What about the effects of increased physical activity on food selection? The natural hypothesis would be that the energy reserves used during exercise would estimate a drive for a particular nutrient. There is no clear consistent evidence to indicate that in the short-term, exercise induces changes in food or nutrient preferences. In the long-term there is some evidence that physical activity is associated with an increase in carbohydrate intake, but it is uncertain whether these changes are biologically driven for a result of changes of a psychological nature. Contrary to a popularly held view, food selection and nutrient intake constitute patterns of behavior held in place by environmental contingencies and short-acting post-ingestive physiological responses; these patterns of behavior are relatively immune to modulation by the metabolic effects of exercise.

Appetite Regulation↗
PubMed1997

Clusters of S1 nuclease-hypersensitive sites induced in vivo by DNA damage.

DNA end-labeling procedures were used to analyze both the frequency and distribution of DNA strand breaks in mammalian cells exposed or not to different types of DNA-damaging agents. The 3' ends were labeled by T4 DNA polymerase-catalyzed nucleotide exchange carried out in the absence or presence of Escherichia coli endonuclease IV to cleave abasic sites and remove 3' blocking groups. Using this sensitive assay, we show that DNA isolated from human cells or mouse tissues contains variable basal levels of DNA strand interruptions which are associated with normal bioprocesses, including DNA replication and repair. On the other hand, distinct dose-dependent patterns of DNA damage were assessed quantitatively in cultured human cells exposed briefly to menadione, methylmethane sulfonate, topoisomerase II inhibitors, or gamma rays. In vivo induction of single-strand breaks and abasic sites by methylmethane sulfonate was also measured in several mouse tissues. The genomic distribution of these lesions was investigated by DNA cleavage with the single-strand-specific S1 nuclease. Strikingly similar cleavage patterns were obtained with all DNA-damaging agents tested, indicating that the majority of S1-hypersensitive sites detected were not randomly distributed over the genome but apparently were clustered in damage-sensitive regions. The parallel disappearance of 3' ends and loss of S1-hypersensitive sites during post-gamma-irradiation repair periods indicates that these sites were rapidly repaired single-strand breaks or gaps (2- to 3-min half-life). Comparison of S1 cleavage patterns obtained with gamma-irradiated DNA and gamma-irradiated cells shows that chromatin structure was the primary determinant of the distribution of the DNA damage detected.

Animals↗
PubMed1997

Negative energy balance with exercise in identical twins: plasma glucose and insulin responses.

The effects of long-term (93 days) negative energy balance on plasma glucose and insulin were investigated by means of exercise with constant energy intake in seven pairs of young sedentary male identical twins. Results showed a significant decrease in fasting (-24%, P < 0.02) and postprandial insulin (-16%, P < 0.05). Fasting and postprandial plasma glucose and glucagon were not modified. Mean glucose disposal rate measured during a euglycemic-hyperinsulinemic clamp performed in five twin pairs was increased by 34% (P = 0.13). No significant intrapair similarity was found for the responses of fasting and postprandial insulin levels and of glucose disposal rate. Changes in glucose disposal rate were significantly greater in high compared with low losers for computerized tomography-measured abdominal visceral fat (3.0 +/- 1.1 vs. 0.3 +/- 0.5 mg x kg(-1) x min(-1), P < 0.05) despite similar losses in total body fat. We conclude that 1) a long-term negative energy balance generated by exercise training significantly reduces plasma insulin levels, whereas insulin sensitivity tends to be improved; 2) training-induced changes in insulin sensitivity are associated with changes in abdominal visceral fat; and 3) data from this experiment conducted with a small number of twin pairs suggest that the genotype does not seem to be a major determinant of the changes in insulin levels and sensitivity brought about by negative energy balance with exercise.

Abdomen↗
PubMed1997

Regional differences in adipose tissue metabolism between sedentary and endurance-trained women.

Subcutaneous (subc) abdominal and femoral adipose tissue metabolism was studied in sedentary and endurance-trained premenopausal women. Both fat cell weight and lipoprotein lipase (LPL) activity were lower in the subc abdominal depot of trained women compared with controls. Epinephrine- and isoproterenol-stimulated lipolytic responses, as well as the beta-adrenergic sensitivity of subc abdominal adipocytes, were higher in trained than in sedentary women, whereas both the antilipolytic effect of brimonidine (UK-14304) and the alpha 2-adrenoceptor sensitivity were lower in endurance-trained than in sedentary subjects. Maximal lipolysis in the presence of postadrenoceptor agents was also enhanced in subc abdominal adipose cells of trained women compared with sedentary controls. Negative relationships were found between maximal lipolytic responses of subc abdominal fat cells to catecholamines or to postreceptor agents and body fatness as well as abdominal fat distribution indexes. It is concluded that 1) endurance-trained women are characterized by a preferential lipid mobilization from the subc abdominal fat depot, and 2) differences in the metabolic characteristics of subc abdominal adipocytes between trained and sedentary women may involve changes in both LPL activity and the lipolytic cascade that include modifications at receptor and postreceptor levels. However, these alterations appear to be largely resulting from the reduced adipose cell size rather than from exercise training per se.

Abdomen↗
PubMed1997

Androstane-3alpha,17beta-diol glucuronide as a steroid correlate of visceral obesity in men.

Plasma levels of androstane-3alpha,17beta-diol glucuronide (3alpha-DIOL-G) and androsterone glucuronide (ADT-G) as well as testosterone and adrenal C19 steroid concentrations were measured in a sample of 80 men in whom visceral adipose tissue (AT) accumulation was also determined by computed tomography. Plasma 3alpha-DIOL-G concentrations showed significant positive correlations with total body fat mass (r = 0.31; P < 0.05) and percent body fat (r = 0.28; P < 0.05). Furthermore, plasma 3alpha-DIOL-G levels were significantly associated with visceral adipose tissue accumulation (r = 0.41; P < 0.0005) as well as fasting plasma insulin (r = 0.35; P < 0.005) and glycemic and insulinemic responses to an oral glucose load (r = 0.39; P < 0.0005 and r = 0.32; P < 0.005, respectively). However, associations between 3alpha-DIOL-G and plasma glucose-insulin homeostasis indexes were no longer significant after adjustment for visceral AT area. ADT-G levels were not significantly associated with any of the adiposity variables. Subjects matched for abdominal sc AT area but with either low or high levels of visceral AT area showed significant differences in 3alpha-DIOL-G concentrations (P < 0.05), whereas subjects with low or high levels of abdominal sc AT but similar levels of visceral AT had similar 3alpha-DIOL-G concentrations. Among men with high testosterone levels, subjects with reduced 3alpha-DIOL-G concentrations had lower visceral adipose tissue accumulation than subjects with increased 3alpha-DIOL-G levels. The present results indicate that plasma 3alpha-DIOL-G, but not ADT-G, is a steroid correlate of visceral obesity. Excess visceral adipose tissue and/or concomitant alterations in insulin levels or in vivo insulin action could be responsible for the increased 3alpha-DIOL-G formation observed in this condition.

Adipose Tissue↗
PubMed1997

Cloning, chromosomal localization, and functional analysis of the murine estrogen receptor beta.

Estrogen receptor beta (ER beta) is a novel steroid receptor that is expressed in rat prostate and ovary. We have cloned the mouse homolog of ER beta and mapped the gene, designated Estrb, to the central region of chromosome 12. The cDNA encodes a protein of 485 amino acids that shares, respectively, 97% and 60% identity with the DNA- and ligand-binding domains of mouse (m) ER alpha. Mouse ER beta bind to an inverted repeat spaced by three nucleotides in a gel mobility shift assay and transactivates promoters containing synthetic or natural estrogen response elements in an estradiol (E2)-dependent manner. Scatchard analysis indicates that mER beta has slightly lower affinity for E2 [dissociation constant (Kd) = 0.5 nM] when compared with mER alpha (Kd = 0.2 nM). Antiestrogens, including 4-hydroxytamoxifen (OHT), ICI 182,780, and a novel compound, EM-800, inhibit E2-dependent transactivation efficiently. However, while OHT displays partial agonistic activity with ER alpha on a basal promoter linked to estrogen response elements in Cos-1 cells, this effect is not observed with mER beta. Cotransfection of mER beta and H-RasV12 causes enhanced activation in the presence of E2. Mutagenesis of a serine residue (position 60), located within a mitogen-activated protein kinase consensus phosphorylation site abolishes the stimulatory effect of Ras, suggesting that the activity of mER beta is also regulated by the mitogen-activated protein kinase pathway. Surprisingly, the coactivator SRC-1 up-regulates mER beta transactivation both in the absence and presence of E2, and in vitro interaction between SRC-1 and the ER beta ligand-binding domain is enhanced by E2. Moreover, the ligand-independent stimulatory effect of SRC-1 on ER beta transcriptional activity is abolished by ICI 182,780, but not by OHT. Our results demonstrate that while ER beta shares many of the functional characteristics of ER alpha, the molecular mechanisms regulating the transcriptional activity of mER beta may be distinct from those of ER alpha.

Amino Acid Sequence↗
PubMed1997

Preferential localization of DNA damage induced by depurination and bleomycin in a plasmid containing a scaffold-associated region.

Recent evidence suggests that DNA damage of various origins is not randomly distributed in the genome but appears to be clustered in unidentified hypersensitive regions of the chromatin. A model was proposed that stipulates that unpaired DNA stretches, such as those found in scaffold- (or matrix)-associated regions (SARs) under torsional strain, are candidate regions of hypersensitivity to DNA damage in vivo. In this study, we assessed in vitro the relative susceptibility of supercoiled plasmids containing a SAR or chromatin loop DNA segment to DNA damage induced by acid-catalyzed depurination or FeIII-bleomycin. Single-strand specific S1 nuclease was used in combination with 3'-end-labeling to detect single-strand breaks or gaps, after cleavage of abasic sites or removal of 3'-phosphoglycolates by Escherichia coli endonuclease IV. The optimal conditions of DNA cleavage specificity by S1 nuclease were determined. Using these conditions, the DNA cleavage patterns obtained showed (i) a preferential localization of S1 hypersensitive sites in the SAR DNA as compared with plasmid or chromatin loop DNA and (ii) a strikingly similar localization of DNA damage with the two clastogenic treatments.

Base Composition↗
PubMed1996

Autoantigenic epitopes on hY5 Ro RNA are distinct from regions bound by the 60-kDa Ro and La proteins.

We recently reported the identification in human anti-Ro serum of Abs specifically immunoprecipitating deproteinized hY5 RNA. In the present report, we characterized the epitopes recognized by anti-hY5 RNA Abs. Using deletion and site-directed mutagenesis of hY5 cDNA and in vitro transcribed RNAs with intact and 3'-shortened ends, we have defined two conformational antigenic determinants distinct from the regions known to bind Ro and La proteins. One of these epitopes (epitope A) is present in the middle portion of hY5 RNA and is dependent on the presence of a four-nucleotide sequence (AACC at position 58-61) that may form a single-stranded loop. Deleting these four nucleotides or modifying the stem structures proximal or distal to this loop abolishes recognition of the mutated RNAs by Abs. The second epitope (epitope B) requires the presence of another four-nucleotide sequence (CUUG at position 74-77) in between the Ro and La binding sites. Deleting this CUUG sequence or modifying nucleotides on the 5' side of the stem structure below the Ro60 binding site severely compromises the interaction with Abs. Since Abs to deproteinized hY RNAs are restricted to anti-hY5 RNA and target determinants not involved in interactions with known hY5 RNA-binding proteins, human RohY5 particles may play a direct role in the immunization process, leading to the production of anti-hY5 RNA autoantibodies.

Antibody Specificity↗
PubMed1996

A major gene for resting metabolic rate unassociated with body composition: results from the Québec Family Study.

A major gene hypothesis for resting metabolic rate (RMR) was investigated using segregation analysis (POINTER) of data on families participating in Phase 2 of the Québec Family Study. Complete analyses were conducted on RMR adjusted for age, and also on RMR adjusted for age and other covariates, primarily fat mass (FM) and fat-free mass (FFM). Prior to adjustment for covariates, support for a major gene hypothesis was equivocal-i.e., there was evidence for either a major gene or a multifactorial component (i.e., polygenic and/or familial environment). The multifactorial model was preferred over the major gene model, although the latter did segregate according to Mendelian expectations. However, after the effects of FM and FFM were accounted for, a major gene effect was unambiguous and compelling. The putative locus accounted for 57% of the variance, affected 7% of the sample, and led to high values of RMR. The lack of a significant multifactorial effect suggested that the familial etiology of RMR adjusted for FM and FFM was likely to be entirely a function of the major locus. Comparing the RMR results from pre- and post-adjustment for FM and FFM suggests a plausible hypothesis. We know from earlier studies in this sample that there is a putative major gene for FM and a major non-Mendelian effect for FFM. The current study leads us to speculate that: (1) the gene(s) affecting body size and body composition also may have an effect on RMR, and further (2) removal of the effect of the major gene(s) for body size and composition allowed for detection of an additional major gene affecting only the RMR. Thus, RMR appears to be an oligogenic trait.

Adipose Tissue↗
PubMed1996

Genetic pleiotropy for resting metabolic rate with fat-free mass and fat mass: the Québec Family Study.

Shared genetic and familial environmental causes for the associations among resting metabolic rate (RMR), fat-free mass (FFM), and fat mass (FM) were investigated in families participating in phase 2 of the Québec Family Study. A multivariate familial correlation model assessing the pattern of significant cross-trait correlations between family members (e.g., RMR in parents with FFM in offspring) was used to infer the etiology of the associations. For each of FM and FFM with RMR, significant sibling, parent-offspring, and intraindividual cross-trait correlations suggests the associations are familial. Furthermore, the lack of significant spouse cross-trait correlations suggests that the familial aggregation is primarily genetic. Bivariate heritability estimates suggest that as much as 45% to 50% of the shared variance between FFM and RMR may be genetic, and as much as 28% to 34% for FM and RMR. This study supports the notion that the gene(s) affecting each of FFM and FM also influence the RMR. Moreover, the lack of any familial associations between FFM and FM suggests that the effects of each body size component on RMR are independent, i.e., more than one genetic source on the RMR-body size association. The possibility that RMR is an oligogenic trait (i.e., more than one underlying genetic etiology) should be further investigated using more complex multivariate segregation methods until specific genes can be tested.

Adipose Tissue↗
PubMed1996

Role of body fat loss in the exercise-induced improvement of the plasma lipid profile in non-insulin-dependent diabetes mellitus.

The study was designed to examine the impact of exercise training on the plasma lipid profile in non-insulin-dependent diabetes mellitus (NIDDM) and, more particularly, to determine the relationship between changes in body fat mass and changes in the lipid profile. Eleven men with NIDDM exercised for 1 hour thrice per week on an ergocycle over a 6-month period at 60% maximal oxygen uptake (Vo2max). Diet and hypoglycemic agents were kept constant throughout this period. Vo2max, body composition, fasting plasma glucose and insulin levels, glycosylated hemoglobin, and the lipid profile were determined at baseline, in the middle (3 months), and at the end (6 months) of the training program. When the subjects were considered as a group, the only significant effect of training was on Vo2max, which increased from 32.2 +/- 1.2 mL/kg/min at baseline to 38.0 +/- 1.7 mL/kg/min at 6 months (P < .001). When the data were analyzed on an individual basis, significant associations were observed between changes in body fat mass and changes in the low-density lipoprotein (LDL) cholesterol/high-density lipoprotein (HDL) cholesterol ratio (r = .62,P = .04) or triglyceride (TG) levels (r = .64,P = .03). These data indicate that fat loss, not training per se, favorably alters the lipid profile of subjects with NIDDM who participate in an aerobic physical-conditioning program.

Adipose Tissue↗
PubMed1996

Plasma high-density lipoprotein cholesterol but not apolipoprotein A-I is a good correlate of the visceral obesity-insulin resistance dyslipidemic syndrome.

Apolipoprotein (apo) A-I is a major component of high-density lipoproteins (HDLs), and it has been suggested that measurement of apo A-I may provide additional information in the assessment of coronary heart disease (CHD) risk. In the present study in a sample of 111 men (age [mean +/- SD], 35.3 +/- 6.6 years), we determined whether a low apo A-I concentration is associated with the cluster of metabolic abnormalities that characterize the visceral obesity-insulin resistance dyslipidemic syndrome. For this purpose, the first and fourth quartiles of apo A-I and HDL cholesterol (HDL-C) concentrations were compared in relation to body fat distribution, glucose tolerance, and plasma insulin and lipoprotein levels. Men in the first quartile (< the 25th percentile) of HDL-C, as compared with men in the fourth quartile (> the 75th percentile), were characterized by an elevated visceral adipose tissue (AT) accumulation (P < .05), as well as by increased plasma levels of triglycerides ([TGs] P < .0001), apo B (P < .0005), and insulin (P < .01). These differences were not found when the first and fourth quartiles of plasma apo A-I concentrations were compared. These results suggest that plasma levels of HDL-C are more closely associated with the various features of the visceral obesity-insulin resistance syndrome than plasma apo A-I.

Adipose Tissue↗
PubMed1996

Overfeeding in identical twins: 5-year postoverfeeding results.

From a total of 12 pairs of young male identical twins who were overfed by an estimated 84,000 kcal over a period of 100 days, several pairs (eight to 11, depending on variables) were remeasured for body weight, body composition with the underwater weighing technique, regional fat distribution from skinfolds, girths, computed tomography (CT) fat areas in the abdominal region, and fasting plasma glucose, insulin, total cholesterol, high-density lipoprotein (HDL) cholesterol, and triglycerides 4 months and 5 years after completion of the overfeeding protocol. At 4 months, the twins had lost approximately 7 of 8 kg that they had gained with overfeeding. However, 5 years later, body weight had increased by 5 kg over the preoverfeeding level. Fluctuations in fat mass were greater than those in fat-free mass. The younger twins gained approximately twice as much as the older twins in the late recovery period, a difference attributed to the late phase of growth in body mass in the former. Upper-body fat was reduced at 4 months of follow-up study, but was increased in the late recovery phase. All blood values were normalized in the postoverfeeding periods. A within-pair resemblance was generally observed for the changes noted in the recovery periods, but it was more striking when variations between preoverfeeding and 4-month or 5-year values were considered. We conclude from these observations that there were no persistent effects of exposure to the overfeeding protocol over the expected age-associated increases in body mass, body fat, upper-body fat, abdominal visceral fat (AVF), and metabolic variables predictive of risk for common diseases in individuals of normal body weight and with no family history of obesity. The intrapair resemblance suggests that the genotype contributes to the alterations observed in the recovery from overfeeding and in the age-associated changes.

Adipose Tissue↗
PubMed1996

RNA-labelled Ro and La ribonucleoprotein complexes reassembled in vitro; characterization by gel shift analysis.

Ro and La RNP complexes were reassembled from in vitro labelled hY5 RNA and HeLa cell extracts. These complexes were then visualized through retardation of migration of labelled hY5 RNA in non-denaturing polyacrylamide gels. Three major complexes (named A, B, and C) were formed when crude cellular extracts (S100 fraction) were used. Using monospecific anti-60-kD Ro (Ro60) and anti-La antibodies to retard RNPs containing these antigens during migration in the gels, the three major complexes were shown to contain Ro60 (C), La (B), or both proteins (A). The specificity of RNA-protein interactions in the reassembled complexes was further demonstrated using two 3'-shortened hY5 RNA transcripts lacking the La-binding site (hY5-Alu I RNA) and both the Ro60 and La-binding sites (hY5-Hha I RNA). hY5-Hha I RNA still formed a single, minor complex when incubated with S100 extract, suggesting interaction with a yet undefined protein. In addition, we used the capacity of specific antibodies to retard the migration of the reassembled complexes to design a detection assay for anti-Ro and anti-La autoantibodies. Using 84 human sera, our assay was shown to approximate the specificity and sensitivity of an immunoprecipitation assay where 32P-labelled cell extracts are used as source of antigens. Our assay may be used to detect low levels of antibodies to conformational determinants on Ro60 and La proteins in human sera and antibody preparations.

Autoantigens↗
PubMed1996

The hyperphagic effect of a high-fat diet and alcohol intake persists after control for energy density.

This study was performed to investigate the effect of a high-fat diet and alcohol (high-fat, alcohol) intake on subsequent spontaneous energy intake when controlling for food energy density. Twelve adults males participated in two 1-d randomly assigned sessions that only differed by the macronutrient composition of the appetizer served at lunchtime. Dietary energy was mainly provided by lipid and alcohol in one appetizer whereas carbohydrate was the main source of energy in the other appetizer. The energy density, content, and weight of the foods were comparable in the two appetizers. Ad libitum energy intake measured at lunchtime after ingestion of the high-fat, alcohol appetizer exceeded that observed after the high-carbohydrate appetizer by >812kJ (P<0.01). This overfeeding had no detectable effect on postprandial hunger and was not compensated by changes in energy intake at dinnertime. In conclusion, this study demonstrates that a high-fat diet and alcohol favor subsequent overfeeding, which is not due to their higher energy density.

Adult↗