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Biomedical subjects

J P Despres

Publications and source records attributed to J P Despres.

At least 19 recordsLinked to original sources
PubMed1997

Endurance training with constant energy intake in identical twins: changes over time in energy expenditure and related hormones.

The effects of exercise training and of its interaction with the genotype on components of energy expenditure and related hormones were examined in young male monozygotic twins. Energy intake was maintained at the pretraining level for a 93-day training period. The estimated net energy deficit induced by training was 244 MJ and was associated with a 5-kg body weight loss that was almost entirely explained by body fat loss. Resting metabolic rate (RMR) was significantly decreased by 8% after training despite the preservation of fat-free mass (FFM). Accordingly, plasma norepinephrine (NE) concentrations, NE appearance rate, and plasma levels of triiodothyronine (T3), free T3, and total thyroxine (T4) were lower after training. The energy cost of standardized exercise was also reduced after the training program. A modest to significant within-twin-pair resemblance was observed for absolute changes in the RMR, thermic effect of food, energy cost of exercise, NE clearance, and plasma concentrations of thyroid hormones. These results suggest that when exercise training is associated with a substantial negative energy balance, energy expenditure and levels of related hormones are decreased, and this effect is partly accounted for by heredity.

Adult↗
PubMed1997

Reproducibility of the HERITAGE Family Study intervention protocol: drift over time.

PURPOSE: The primary goal of the HERITAGE Family Study was to document the role of the genotype in the response to aerobic exercise training. Toward this end, nuclear families were enrolled in a 20-week exercise training program, with a large variety of tests performed before and after the training. Since study drift has the potential to adversely affect the results, reproducibility and potential bias over six consecutive 4-month periods were examined for selected test. METHODS: Intraclass correlations (ICC), technical errors (TE), coefficients of variation within subject (CV), and means were calculated with use of the pretraining test results for each of the six time periods. To check for homogeneity, hypothesis tests were performed on the intraclass correlations and means. If homogeneity was not found across all six periods, further tests were performed to assess differences between pairs of time periods. RESULTS: There was little evidence for real drifts in reproducibility, with most tests having ICCs of 0.8 or better. Only a few tests showed any change over time, and in no case was there evidence of a systematic drift in mean values. CONCLUSIONS: Overall, the reproducibility of the HERITAGE Family Study tests and assays considered in this paper was found to be very good, with no evidence of any systematic drift over time.

Adolescent↗
PubMed1991

Further evidence for the presence of "small eaters" and "large eaters" among women.

One hundred thirty-four women, aged 36 +/- 4 (mean +/- SD) y, BMI 20 +/- 3 kg/m2, perceiving themselves as having either a low or high energy intake (EI), participated in a study to determine variations in EI. Information on EI and activity level was obtained from repeated 7-d records. The 40 subjects with the lowest EI (in kcal/kg body wt) were categorized as small eaters (SEs); the 40 subjects with the highest EI were considered to be large eaters (LEs). The absolute (in kcal) and relative (in kcal/kg body wt) EIs of the SE and LE groups were 1488 +/- 312 and 27 +/- 4 for the SE group, respectively and 2393 +/- 509 and 47 +/- 6 for the LE group, respectively. There was no significant difference in activity level or fat-free mass (FFM) between the groups. However, LEs weighed significantly less (51 vs 55 kg) and were leaner (22% body fat vs 33%) than were SEs. Individuals with similar FFM and activity level can vary significantly in EI needs.

Adult↗
PubMed1989

Impact of dietary fat content and fat oxidation on energy intake in humans.

Three studies were performed to assess the effects of a high-fat diet and exercise-induced changes in fat oxidation on energy intake in humans. In the first study the short-term effect of a high-fat diet on spontaneous energy intake was investigated. The second study evaluated the long-term effect of a high-fat diet on adiposity and the third study evaluated the effect of exercise-induced changes in fat oxidation on short-term regulation of energy intake when subjects were consuming a high-fat diet. The results of these studies indicate that a high-fat diet induces a short-term hyperphagia, a high percentage of lipids in the usual diet is associated with a higher adiposity, and exercise may attenuate or amplify the high-fat, diet-induced hyperphagia, depending on the magnitude of the exercise-induced increase in fat oxidation.

Adaptation, Physiological↗
PubMed1989

Effect of massive obesity on low and high density lipoprotein binding to human adipocyte plasma membranes.

Adipose tissue is a major cholesterol storage organ in man, and turnover of this slowly exchangeable pool is dependent on low and high density lipoproteins which deliver and remove cholesterol from this site. To determine whether lipoprotein binding is altered in the obese state, we examined the binding of low density lipoprotein (LDL) and high density lipoprotein (HDL2 and HDL3) to purified adipocyte plasma membranes obtained from omental fat depots of massively obese patients (BMI greater than 40 kg/m2) and lean subjects. The specific binding and uptake of 125I-HDL2 and 125I-HDL3 were greater for obese than for lean adipocytes. Scatchard analysis of binding studies using purified adipocyte plasma membranes and varying amounts of labeled HDL2 or HDL3 demonstrated a higher binding affinity (lower Kd) for HDL2 and higher binding capacity (Bmax) value for both HDL2 and HDL3 in obese as compared to lean. 125I-LDL specific binding was somewhat lower in obese than in lean membranes but this difference was not statistically significant. The cholesterol content of isolated omental adipocytes expressed on a cellular basis or as the cholesterol/triglyceride ratio (mg chol/g of lipid) were similar in the obese and lean subjects. Furthermore, 125I-LDL, 125I-HDL2 or 125I-HDL3 specific binding did not correlate with cellular cholesterol content or with cholesterol/triglyceride ratio. These findings indicate that lipoprotein binding to adipocytes is altered in obesity and is characterized by up-regulation of HDL (particularly HDL2) binding with little change in LDL binding. We conclude from this study that obesity has a profound effect on the expression of HDL binding sites in human adipocytes and that LDL and HDL binding in fat cells are regulated differently.

Adipose Tissue↗
PubMed1989

Evidence for the existence of small eaters and large eaters of similar fat-free mass and activity level.

The objective of this study was to identify individuals of the same age, sex, activity level and fat-free mass who differed in their level of energy intake (EI). Estimates of energy intake and physical activity level were derived from three-day food and activity records from 430 individuals 17-54 years of age. Body composition was measured by underwater weighing and body fat and fat-free mass were obtained. Subjects were grouped into four categories based on age and sex (females aged 17-34 and 35-54 years and males aged 17-34 and 35-54 years). Subjects were identified as small eaters (SE) or large eaters (LE) according to kJ of EI per kg body weight, SE being from the lower quartile and LE from the upper quartile of their distributions. The results showed that, on average, LE consumed almost twice as many kJ per kg body weight as SE (about 200 versus 100). In addition middle-aged male and female SE were significantly (P less than 0.001) heavier than middle-aged male and female LE respectively. The mean body weight for the male SE was 82 +/- 12 kg (mean +/- s.d.) against 69 +/- 9 kg for the LE, while it was 66 +/- 10 kg against 52 +/- 5 kg for the female SE and LE. The male and female SE also had a significantly higher percentage body fat in both age groups. In general, there was no difference in fat-free mass and activity level between the SE and LE. It is concluded that there exist groups of individuals who have a considerable difference in their EI and adiposity even though they have similar levels of activity and fat-free mass.

Activities of Daily Living↗
PubMed1989

Scanning electron microscopy of very small fat cells and mature fat cells in human obesity.

To determine the effect of obesity on the size distribution of fat cell populations in human adipose tissue, omental fat tissue biopsies were obtained from lean, moderately obese, and massively obese patients. The size distributions of adipocytes from lean and obese fat tissues examined by the scanning electron microscopic method were bimodal, consisting of populations of very small fat cells and mature fat cells, in contrast to collagenase-derived isolated cells that showed only the large mature fat cells. The very small fat cell population represented 21 to 26% of the total fat cell number in the lean and in both obese groups. In contrast, preparations of human fat cells isolated by the collagenase method systematically excluded the very small fat cells. In massive obesity, both cell populations participated in the hyperplastic growth but only the larger mature fat cells increased in size, implying that these two cell populations differ in their physiological role.

Adipose Tissue↗
PubMed1988

Weight loss in massive obesity: reciprocal changes in plasma HDL cholesterol and HDL binding to human adipocyte plasma membranes.

Human obesity is frequently associated with elevated plasma triglyceride and cholesterol concentrations and reduced high density lipoprotein (HDL) cholesterol, abnormalities that commonly revert to normal levels with weight loss. This study was undertaken to examine possible mechanism(s) associated with the changes in plasma HDL cholesterol concentrations in massively obese patients after weight loss. Ten massively obese patients (two men and eight women, age = 37.8 +/- 2.4 years) were studied before, during, and after 1 year of weight loss and weight maintenance following gastric stapling. Total cholesterol and low density lipoprotein cholesterol were within the normal range for sex and age before weight loss and did not change significantly during or after weight reduction. In the females, HDL cholesterol concentrations increased from 0.96 +/- 0.06 mmol/L to 1.23 +/- 0.3 mmol/L (mean +/- SEM, n = 8, P less than .05) with weight reduction. In the two men, plasma HDL cholesterol concentrations were, respectively, 1.22 and 0.65 mmol/L before and 1.23 and 0.98 mmol/L after weight loss. Specific binding of 125I-HDL2 and 125I-HDL3 to purified plasma membranes was determined using abdominal and omental fat depot before and after weight loss in six of the ten obese patients. An average reduction of 30% to 40% in 125I-HDL2 and 125I-HDL3 binding capacity to these membranes occurred after weight loss. Furthermore, a positive correlation (r = .65, n = 10, P less than .05) was observed between plasma HDL cholesterol and triglyceride concentrations before weight loss but not after weight loss (r = .01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue↗
PubMed1988

Selective uptake of HDL cholesterol ester by human fat cells.

In humans, high-density lipoprotein (HDL)-cholesterol ester turnover exceeds that of HDL apoproteins by severalfold or more, suggesting an independent catabolic fate of these constituents. The present study investigated the cellular uptake and dissociation of HDL labeled in its apoproteins with 125I and in its cholesterol ester with [3H]cholesteryl palmityl ether, a nonhydrolyzable cholesterol ester analogue. Approximately 50% of cell-associated 125I-HDL2 and 125I-HDL3 was released from prelabeled adipose cells by incubating the latter in the presence or absence of unlabeled lipoproteins for 2 h. The uptake of HDL-cholesterol ester by human fat cells as reflected by [3H]cholesteryl palmityl ether was 5-18 times greater than that predicted from the uptake of 125I-HDL2 and 125I-HDL3 and was irreversible. Analysis of dissociated 125I-HDL3 demonstrated changes to both higher and lower density fractions compared with the starting material. There was a high correlation between the cellular uptake of HDL3-cholesterol ester and HDL3-apoprotein uptakes (r = 0.90, P less than 0.01), suggesting that HDL-cholesterol ester uptake requires a specific apoprotein interaction or binding step. The selective uptake and retention of HDL-cholesterol ester by isolated adipocytes implies that human fat tissue may play a role in regulating the lipid composition of plasma HDL.

Adipose Tissue↗
PubMed1988

Sensitivity to overfeeding: the Quebec experiment with identical twins.

The role of the genotype in the response to short-term overfeeding was assessed by submitted six pairs of male monozygotic twins to a 4.2 MJ (1000 kcal) per day energy intake surplus for a period of 22 consecutive days. Individual differences in fat mass and fat-free mass gains were observed in response to overfeeding but they were not randomly distributed. Indeed, the within-pair resemblance in the response was striking when compared to the heterogeneity found among the pairs in adiposity and fat-free mass gains. The intrapair resemblance in the response to overfeeding as assessed by the intraclass coefficient computed with the individual changes, reached 0.88 for total fat mass and 0.76 for fat-free mass. A similar trend for a genetically determined pattern of adaptation to overfeeding was observed for resting metabolic rate (intraclass = 0.63), thermic effect of a meal (intraclass = 0.62), and energy cost of submaximal exercise (intraclass = 0.78) when the data were analysed in terms of changes in oxygen uptake. On the other hand, no major alterations in glucose and insulin response to a glucose load or a test meal, in cardio-pulmonary adaptation to submaximal exercise and in maximal exercise tolerance were found with overfeeding. In contrast, the response of suprailiac fat cell lipolysis (intraclass of about 0.7) and heparin releasable adipose tissue lipoprotein lipase (intraclass - 0.82) varied among individuals but was highly homogeneous within genotypes. Similarly, a genotype-overfeeding interaction effect was seen for serum triglycerides (intraclass = 0.69), HDL-cholesterol (intraclass = 0.85), and the HDL-cholesterol to total cholesterol ratio (intraclass = 0.82). Multiple correlation analyses suggest that much of the variance in the response of fat mass (R = 0.65) and fat-free mass (R = 0.81) is accounted for by alterations in the energy expenditure components assessed in the study. If one takes into account the measurement errors always present in such complex studies and the fact that only a limited fraction of the energy expenditure of activity was considered by design, one can conclude that the genotype determines to a large extent the response variation to short-term overfeeding. In particular, the genotype-overfeeding interaction effect for body composition changes seems to be mediated by the various energy expenditure components, themselves characterized by significant genotype-overfeeding interaction effects.(ABSTRACT TRUNCATED AT 400 WORDS)

Adipose Tissue↗
PubMed1988

A new porcine bioprosthesis: design rationale and early clinical experience.

The Medtronic Intact valve is a third-generation porcine bioprosthesis produced using a leaflet fixation process which imposes virtually zero hydrostatic pressure. This fixation method provides optimal preservation of the original leaflet structure and integrity and should result in an improvement in durability compared to conventional preservation techniques. The biomechanical basis for this hypothesis is presented along with early experience with 118 patients (125 valves). There have been no complications related to primary valve failure and the incidence of other valve related events is acceptable.

Aortic Valve↗
PubMed1988

Interactions of high density lipoprotein subclasses (HDL2 and HDLc) with dog adipocytes: selective effects of cholesterol and saturated fat feeding.

Adipose tissue is a cholesterol storage organ and derives its cholesterol primarily from circulating lipoproteins. The present study shows that adipocytes isolated from canine omental fat tissue interact specifically with high density lipoprotein subfractions lacking or enriched in apolipoprotein E, namely canine high density lipoprotein-2 (HDL2) and HDLc, respectively. While 125I-labeled HDL2 binding was inhibited similarly by both excess unlabeled HDLc and HDL2, 125I-labeled HDLc interaction was inhibited by its homologous ligand only. Paired studies showed that the amount of HDLc associated with adipocytes was significantly higher compared to HDL2. The effect of a short-term cholesterol and saturated fat feeding on adipocyte-HDL interaction was examined using fat cells obtained from dogs before and again 3 weeks after a diet supplemented with cholesterol (1% w/w) and saturated fat (30% lard, w/w). Significant increases in body weight and omental fat cell weight occurred after fat feeding. The amount of 125I-labeled HDL2 that could be bound to adipocytes increased after the diet, whether expressed on a per cell basis (P less than 0.005) or per unit cell surface (P less than 0.025). The amount of cell-associated 125I-labeled HDLc, however, was not significantly affected by the cholesterol-rich diet. The characteristics of HDLc and HDL2 dissociation were assessed by examining the release of labeled lipoproteins from adipocytes preincubated with 125I-labeled HDLc and 125I-labeled HDL2. HDL2 dissociation from adipocytes was significantly decreased (P less than 0.05) following the diet and may explain in part the apparent increase in cell-associated 125I-labeled HDL2.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue↗
PubMed1987

Regional variation in HDL metabolism in human fat cells: effect of cell size.

Abdominal obesity is related to reduced plasma high-density lipoprotein (HDL) cholesterol, and both are associated with cardiovascular disease risk. We have observed that plasma membranes from abdominal subcutaneous adipocytes have a greater HDL binding capacity than omental fat cell plasma membranes. The present study examined whether these binding characteristics could be due to differences in fat cell size or cholesterol concentration between the two adipose depots. Abdominal subcutaneous and deep omental fat were obtained from massively obese patients at surgery. Subcutaneous abdominal fat cells were significantly larger and their cellular cholesterol content greater than omental adipocytes. The uptake of HDL by collagenase-isolated fat cells was studied by incubating the cells for 2 h at 37 degrees C with 10 micrograms/ml 125I-HDL2 or 125I-HDL3. In both depots, the cellular uptake of 125I-HDL2 and 125I-HDL3 was specifically inhibited by addition of 25-fold excess unlabeled HDL and a close correlation was observed between the cellular uptake of 125I-HDL2 and 125I-HDL3. In obese patients, the uptake of 125I-HDL was higher in subcutaneous cells than in omental cells [5.85 +/- 0.53 vs. 2.74 +/- 0.30 pmol X 2 h-1. (10(6) cells)-1]. The cellular 125I-HDL uptake was significantly correlated with adipocyte size and fat cell cholesterol content but not with adipocyte cholesterol concentration. These results suggest that the higher HDL uptake observed in subcutaneous cells compared with omental cells in obesity is the result of differences in adipocyte size rather than differences in the cholesterol concentration (cholesterol-to-triglyceride ratio).(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue↗
PubMed1987

Interaction of high density lipoprotein with adipocytes in a new patient with Tangier disease.

A 56-year-old man, the offspring of a consanguineous first cousin marriage, presented with clinical, morphological, and biochemical features of familial deficiency of high-density lipoproteins (Tangier disease). Of 8 first- and second-degree relatives examined, 4 had either plasma apo A-I or HDL cholesterol concentrations 2 standard deviations below normal population mean on at least 1 occasion. The patient and a majority of his relatives also had high plasma apo B concentrations relative to their levels of cholesterol. Adipose tissue biopsy was undertaken to study HDL interaction with the patients' cells. Specific uptake of HDL3 was demonstrated in adipocytes of this patient, but was decreased relative to a control of similar fat cell size. However, no marked difference in fat cell cholesterol content was observed between the Tangier patient and the control. Thus it appears unlikely that adipocytes play a role in the etiology of Tangier disease.

Adipose Tissue↗
PubMed1986

The role of body fat in insulin sensitivity of endurance athletes.

The purpose of the study was to assess the role of adiposity in the enhanced insulin sensitivity observed in endurance athletes (EA). An oral glucose tolerance test (75 g glucose) was administered to nine EA and to 23 sedentary subjects (SS). Two different strategies were used to investigate the problem. First, body composition indicators and Vo2max were correlated with the delta insulin and delta glucose areas measured for 180 minutes following glucose ingestion. These correlation analyses were performed for the two groups combined (n = 32). No significant correlations were observed between either fat weight or percent body fat versus delta insulin, delta glucose or delta glucose/delta insulin areas. Moreover, no significant correlation was observed between the several subcutaneous fat indicators and delta insulin, delta glucose and delta glucose/delta insulin areas. The second strategy consisted of comparing EA to SS when percent body fat difference was eliminated. This was achieved by two different methods, first by covariance analysis and second by comparing subsamples of trained and non-trained subjects paired with respect to percent body fat. These two comparisons revealed that even when adiposity was equal between the groups, a significantly greater insulin sensitivity was observed in the EA group (p less than 0.01). The present results suggest that adiposity is not the determining factor for the increased insulin sensitivity of trained subjects.

Adipose Tissue↗
PubMed1985

Characterization of high density lipoprotein binding to human adipocyte plasma membranes.

Freshly isolated human adipocytes showed specific uptake of 125I-labeled human high density lipoprotein (HDL2 and HDL3), a portion of which could be released by subsequent incubation with excess unlabeled ligand. To study the mechanism of HDL binding, sucrose gradient-purified adipocyte plasma membranes were incubated with radioiodinated lipoprotein particles under equilibrium conditions in the absence (total binding) or presence (nonspecific binding) of 100-fold excess unlabeled ligand. Specific binding of HDL2 and HDL3, calculated by subtracting nonspecific from total binding, was Ca++ independent, unaffected by EDTA, and not abolished by pronase treatment of the membranes. Modification of HDL3 by reductive methylation or cyclohexanedione treatment also failed to affect its binding to adipocyte plasma membranes. High salt concentration (200 mM NaCl) inhibited specific binding of HDL2 and HDL3 but had no effect on LDL binding. A significant portion of 125I-HDL2 or 125I-HDL3 binding was consistently inhibited by adding excess unlabeled LDL, but this inhibition was incomplete as compared with a similar molar excess of unlabeled HDL2 or HDL3. The role of apoproteins (apo) in HDL binding to adipocyte membranes was examined by comparing binding of HDL2 and HDL3 isolated from normal, abetalipoproteinemic (abeta) and apo E-deficient (apo E0) plasma. Specific binding was observed with all normal and mutant HDL particles. Furthermore, a significant portion (61-78%) of abeta-HDL2, apo E0-HDL2, and apo E0-HDL3 binding was inhibited by adding 100-fold excess of unlabeled low density lipoproteins (LDL). The cross-competition of LDL and HDL binding was confirmed by the ability of normal, abeta, and apo E0-HDL2 to completely inhibit 125I-LDL binding. These data suggest that HDL binding is independent of apo E and that the responsible apoprotein(s) of HDL complete with LDL-apo B for binding to the same or closely related site in the adipocyte plasma membrane. Normal and apo E0-HDL3 binding was also completely inhibited by normal HDL2, which suggested that HDL2 and HDL3 probably bind to the same site. Scatchard analysis of normal HDL2, normal HDL3, and apo E0-HDL3 binding data best fitted a one-component binding profile with similar equilibrium dissociation constants (40-96 nM). HDL3 binding was found to be effectively inhibited by anti-human apo AI or anti-human apo AII, but not by anti-human apo B antisera. This binding was also unaffected by monoclonal anti-human apo B or E antibodies known to inhibit binding of apo B or apo E containing lipoprotein to the LDL receptor of cultured fibroblasts. These findings, taken together, suggest that human fat cells possess HDL binding sites with apo AI and /or apo AII specificity. The significant but partial inhibition of HDL2 and HDL3 binding by LDL along with the complete inhibition of LDL binding by HDL2 and HDL3 tends to exclude a single binding site that interacts both lipoproteins and favors the interpretation that LDL and HDL particles bind to multiple recognition sites or to different conformation of the same lipoprotein binding domain on the human fat cell.

Adipose Tissue↗