Biomedical subjects

S Lemieux

Publications and source records attributed to S Lemieux.

At least 37 records · Page 2Linked to original sources

PubMed2001

[Fat distribution and metabolism].

It is well known that adipose tissue distribution is an important factor involved in the etiology of type 2 diabetes and cardiovascular diseases. Adipose tissue distribution is obviously different between men and women, men being prone to accumulate their excess of energy in the abdominal region, more specifically in the intra-abdominal depot (visceral) whereas women show a selective deposition of adipose tissue in the gluteo-femoral region. Several studies have demonstrated an association between age and adipose tissue distribution and a selective deposition of visceral adipose tissue has been reported with age, in both men and women. In this regard, the menopause transition also appears to be a factor associated with an accelerated accumulation of abdominal adipose tissue. This increase in visceral adipose tissue has been suggested to play a significant role in the etiology of metabolic complications increasing the risk of type 2 diabetes and cardiovascular diseases. However, a selective mobilization of visceral adipose tissue in response to a weight loss program has been noted among viscerally obese patients, this reduction in visceral adipose tissue being associated with improvements in the lipoprotein-lipid profile and insulin sensitivity. Thus, the distribution of adipose tissue is an important factor to take into account in the evaluation of the patient. Furthermore, the amount of abdominal adipose tissue should also be considered as an important therapeutic target for the optimal management of cardiovascular disease risk.

Abdomen↗

PubMed2000

Contribution of visceral obesity to the deterioration of the metabolic risk profile in men with impaired glucose tolerance.

AIMS/HYPOTHESIS: Impaired glucose tolerance is associated with metabolic alterations which increase cardiovascular disease risk. The contribution of hyperglycaemia to this increased risk is, however, not clear. Abdominal obesity is often observed in subjects with impaired glucose tolerance; our objective was therefore to find the contribution of visceral adipose tissue to the deterioration of the metabolic risk profile noted in subjects with impaired glucose tolerance. METHODS: We studied 284 men with a normal glucose tolerance and 66 men with impaired glucose tolerance which was defined as a glycaemia between 7.8 and 11.1 mmol/l 2 h after a 75-g glucose load. RESULTS: Men with impaired glucose tolerance had more visceral adipose tissue and higher concentrations of plasma glucose and insulin in the fasting state and following a 75-g oral glucose load than men with a normal glucose tolerance. They also had higher concentrations of plasma cholesterol, triglycerides, apolipoprotein B and lower concentrations of HDL-cholesterol as well as higher cholesterol:HDL-cholesterol ratios than men with a normal glucose tolerance. The two groups of men were then compared after a statistical adjustment for the amount of visceral adipose tissue. Although men with impaired glucose tolerance still had higher fasting plasma glucose and insulin concentrations after the adjustment for visceral adipose tissue, differences in all the variables of the lipid-lipoprotein profile were eliminated. CONCLUSION/INTERPRETATION: Visceral adipose tissue accumulation is an important factor in the deterioration of the plasma lipid-lipoprotein noted in men with impaired glucose tolerance.

Abdomen↗

PubMed1999

Ly-49CB6 NK inhibitory receptor recognizes peptide-receptive H-2Kb.

NK-mediated cytotoxicity involves two families of receptors: activating receptors that trigger lysis of the target cells being recognized and inhibitory receptors specific primarily for MHC I on the target cell surface that can override the activating signal. MHC I molecules on the cell surface can be classified into molecules made stable by the binding of peptide with high affinity or unstable molecules potentially capable of binding high affinity peptide (hence, peptide receptive) and being converted into stable molecules. It has been previously shown that the Ly-49A inhibitory receptor recognizes stable Dd molecules. We show in this study that the inhibitory receptor Ly-49CB6 recognizes peptide-receptive Kb molecules, but does not recognize Kb molecules once they have bound high affinity peptide.

Animals↗

PubMed1999

Tolerance and alloreactivity of the Ly49D subset of murine NK cells.

Class I-specific stimulatory and inhibitory receptors expressed by NK cell subsets contribute to the alloreactive potential of the self-tolerant murine NK cell repertoire. In this report, we have studied potential mechanisms of tolerance to the function of the positive signaling Ly49D receptor in mice that express one of its ligands, H2-Dd. Our results demonstrate that H2-Dd-expressing mice possess a large Ly49D+ subset of NK cells that is functionally capable of rejecting bone marrow cell (BMC) allografts in vivo and lysing allogeneic Con A lymphoblasts in vitro. Also, we show that the Ly49D receptor is responsible for the ability of H2b/d F1 hybrid mice to reject H2d/d parental BMC (hybrid resistance). Thus, deletion or anergy of Ly49D+ cells in H2-Dd+ hosts cannot explain self tolerance. Our functional studies revealed that coexpression of the Dd-specific Ly49A or Ly49G2 inhibitory receptors by Ly49D+ cells resulted in tolerance to Dd+ targets, while coexpression of Kb-specific inhibitory receptors Ly49C/I resulted in tolerance to Kb+ targets. Only in H2d/d cells did Ly49C/I dominantly inhibit Ly49D-Dd stimulation. This correlated with an increased mean fluorescence intensity of Ly49C expression, as well as an increased percentage of Ly49C+ cells in the Ly49D+A/G2- compartment. Therefore, we conclude that self tolerance of the Ly49D subset can be achieved through coexpression of a sufficient level of self-specific inhibitory receptors.

Animals↗

PubMed1999

Elevated plasma lipids in patients with binge eating disorders are found only in those who are anorexic.

OBJECTIVE: We have previously shown that patients with restricting type anorexia nervosa (AN-R) have low plasma lipid levels, which increase with refeeding. In this study, we investigated plasma lipid levels in patients with eating disorders, distinguishing between individuals with bulimia nervosa (BN) and anorexia nervosa of the binge eating/purging type (AN-B). METHODS: We examined the fasting lipid levels in individuals with BN (n = 10) and AN-B (n = 9), and compared these findings with a group of age-matched normal weight healthy controls (C) (n = 10). RESULTS: The AN-B group had significantly higher concentrations of total plasma cholesterol, apolipoprotein (apo) B, apoA1, and low-density lipoprotein (LDL)-cholesterol than both control and BN groups (p < .05). The AN-B group also had higher plasma triglycerides and intermediate-density lipoprotein (IDL)-apo B levels (p < .05) than controls. DISCUSSION: In conclusion, the issue of hyperlipidemia in patients with eating disorders is a complex one and this study, taken together with the findings of our previous study, demonstrates the importance of carefully distinguishing between the major types of eating disorders (AN-R, BN, and AN-B) when examining plasma lipid levels.

Adult↗

PubMed1999

Relationship of visceral adipose tissue to metabolic risk factors for coronary heart disease: is there a contribution of subcutaneous fat cell hypertrophy?

Visceral adipose tissue (VAT) accumulation is an important correlate of the metabolic complications found in obese patients. The aim of this study was to evaluate the respective contribution of VAT deposition versus subcutaneous abdominal or femoral fat cell hypertrophy as correlates of the metabolic risk profile in 69 men and 65 premenopausal women (aged 35+/-5 years) with a wide range of fatness (body mass index, 18 to 57 kg/m2). In both genders, VAT accumulation was positively correlated with fasting plasma insulin, triglyceride (TG), and low-density lipoprotein (LDL)-apolipoprotein B (apo B) levels and the cholesterol (CHOL)/high-density lipoprotein (HDL)-CHOL ratio (.24 < or = r < or = .71, P < .05). A similar pattern of positive relationships was found between subcutaneous abdominal fat cell weight and metabolic risk variables in men and women (.33 < or = r < or = .60, P < .01). Positive associations were also observed in women between femoral fat cell weight and fasting plasma insulin, TG, and CHOL levels and the CHOL/HDL-CHOL ratio (.29 < or = r < or = .42, P < .05). However, only plasma TG concentrations and the CHOL/HDL-CHOL ratio were positively correlated with femoral fat cell weight in men (r = .30, P < .05). To better investigate the relationships between the metabolic risk profile and hypertrophic subcutaneous obesity, individuals with small versus large subcutaneous abdominal adipocytes were matched according to VAT accumulation. Men with large abdominal fat cells displayed higher plasma TG and LDL-apo B levels compared with men characterized by small abdominal adipocytes (P < .05). Stepwise multiple regression analyses showed that subcutaneous abdominal fat cell weight was the best independent variable predicting plasma TG and LDL-apo B levels in men. No significant difference was found in the metabolic profile of subjects displaying small versus large femoral adipocytes. Taken together, these results suggest that for a given VAT deposition, the presence of hypertrophied subcutaneous abdominal adipocytes in men appears to be associated with further deterioration in the metabolic risk profile. On the other hand, the hypertrophy of femoral adipocytes does not further alter the metabolic complications generally related to obesity in both men and women.

Adipocytes↗

PubMed1999

Assessment of Cmv1 candidates by genetic mapping and in vivo antibody depletion of NK cell subsets.

The mouse chromosome 6 locus Cmv1 controls resistance to infection with murine cytomegalovirus (MCMV). We have previously shown that Cmv1 is tightly linked to members of the NK gene complex (NKC) including the Ly49 gene family. To assess the candidacy of individual NKC members for the resistance locus, first we followed the co-segregation of Cd94, Nkg2d, and the well-characterized Ly49a, Ly49c and Ly49g genes with respect to Cmv1 in pre-existing panels of intraspecific backcross mice. Gene order and intergene distances (in cM) were: centromere-Cd94/Nkg2d-(0.05)-Ly49a/Ly49c/Ly49 g/Cmv1-(0. 3)-Prp/Kap/D6Mit13/111/219. This result excludes Cd94 and Nkg2d as candidates whereas it localizes the Ly49 genes within the minimal genetic interval for Cmv1. Second, we monitored the cell surface expression of individual Ly49 receptors in MCMV-infected mice over 2 weeks. The proportion of Ly49C(+) and Ly49C/I(+) cells decreased, the proportion of Ly49A(+) and Ly49G2(+) remained constant, and the cell surface density of Ly49G2 increased during infection, suggesting that NK cell subsets might have different roles in the regulation of MCMV infection. Third, we performed in vivo antibody depletion of specific NK cell subsets. Depletion with single antibodies did not affect the resistant phenotype suggesting that Ly49A(+), Ly49C(+), Ly49G2(+) and Ly49C/I(+) populations are not substantial players in MCMV resistance, and arguing for exclusion of the respective genes as candidates for Cmv1. In contrast, mice depleted with combined antibodies showed an intermediate phenotype. Whether residual NK cells, post-depletion, belong to a particular subset expressing another Ly49 receptor, or a molecule encoded by a yet to be identified gene of the NKC, is discussed.

Animals↗

PubMed1999

Correction of hyperandrogenemia by laparoscopic ovarian cautery in women with polycystic ovarian syndrome is not accompanied by improved insulin sensitivity or lipid-lipoprotein levels.

Polycystic ovarian syndrome (PCOS) is a common disorder associated with hyperandrogenemia and infertility. Abdominal obesity, insulin resistance, and dyslipoproteinemias are other common metabolic disorders typically found in women with PCOS. The cause-effect relationship between hyperandrogenemia and insulin resistance-dyslipoproteinemia remains unclear. In this study, we have investigated the changes in androgenemia, insulin sensitivity, and plasma lipid-lipoprotein levels after laparoscopic ovarian cautery (LOC) for ovulation induction in eight infertile women with clomiphene citrate-resistant PCOS. After LOC, significant decreases in androstenedione (43%), testosterone (48%), and free testosterone (48%) concentrations were observed (P < 0.05). Glucose utilization during an euglycemic-hyperinsulinemic clamp did not change after LOC. In addition, no significant changes after the surgical procedure were observed for cholesterol, triglycerides, and apolipoprotein concentrations measured in total plasma and in different lipoprotein fractions. In conclusion, within the short duration of observation of this study, our findings demonstrate that insulin resistance and lipoprotein abnormalities associated with PCOS are not secondary to hyperandrogenemia. The clinician, therefore, must be cognizant of the persistence of these metabolic risk factors for cardiovascular disease once successful ovulation and fertility is restored, and institute appropriate monitoring, counseling, and medical intervention as required.

Adult↗

PubMed1999

Is visceral adiposity a significant correlate of subcutaneous adipose cell lipolysis in men?

The aim of the present study was to examine whether site differences in s.c. adipose tissue (AT) lipolysis may be considered a contributing factor to the altered metabolic risk profile of visceral compared to peripheral obese men once the concomitant variation in adipose cell size is taken into account. For this purpose, sc abdominal and femoral fat cell lipolytic responses were investigated in two groups of men (body mass index, 28 +/- 2 kg/m2), aged 36 +/- 3 yr, who were matched for both s.c. abdominal AT area (256 +/- 64 cm2) and s.c. abdominal adipose cell weight (0.55 +/- 0.08 microg lipid/cell) but were characterized by either a high (162 +/- 29 cm2; n = 18) or a low (101 +/- 21 cm2; n = 18) visceral AT deposition. The maximal lipolytic response to epinephrine or to isoproterenol (beta-adrenergic agonist) as well as the maximal antilipolytic effect of either epinephrine or clonidine (alpha2-adrenergic agonist) assessed in s.c. adipocytes were similar among men with low vs. high levels of visceral AT. However, the beta-adrenoceptor sensitivity was increased in s.c. abdominal adipose cells of individuals with a high visceral AT accumulation compared to those with a low intraabdominal fat deposition. Positive relationships were also found between the lipolytic sensitivity of s.c. abdominal adipocytes and plasma insulin concentrations measured in the fasting state and after an oral glucose load. These results suggest that variation in the degree of visceral adiposity in men does not seem to be associated with differences in regional adipose cell maximal lipolytic capacity once fat cell size is taken into account. However, the greater beta-adrenoceptor lipolytic sensitivity of s.c. abdominal adipocytes could be considered a significant correlate of the increased insulinemia observed among men characterized by high levels of visceral AT.

Abdomen↗

PubMed1999

Age-related increase in visceral adipose tissue and body fat and the metabolic risk profile of premenopausal women.

OBJECTIVE: Age-related differences in body fat and, more specifically, in the accumulation of abdominal visceral adipose tissue (AT) were examined as potential covariates of the age-related difference in the metabolic profile predictive of cardiovascular disease (CVD) risk observed in young, as compared with middle-aged, premenopausal women. RESEARCH DESIGN AND METHODS: Body composition, AT distribution, plasma lipoprotein-lipid levels, glucose tolerance, and plasma insulin concentrations were assessed in a sample of 122 young women (27.4+/-7.5 years, mean +/- SD) and compared with a sample of 52 middle-aged premenopausal women (49.5+/-5.3 years) who still had a normal menstrual cycle. RESULTS: Middle-aged women were characterized by elevated levels of total abdominal and visceral AT and greater body fat mass and waist circumference, as well as by higher plasma levels of total cholesterol, LDL cholesterol, apolipoprotein (apo)B, and LDL-apoB compared with younger women. Furthermore, middle-aged women showed a greater glycemic response to a 75-g oral glucose load than young women (P < 0.01). In both young and middle-aged subjects, visceral AT accumulation was significantly correlated with plasma triglyceride, apoB, and LDL-apoB levels and with the cholesterol/HDL cholesterol ratio, as well as with plasma glucose, insulin, and C-peptide levels measured in the fasting state and after the oral glucose load, and negatively correlated with HDL cholesterol levels (-0.41 < or = r < or = 0.65, P < 0.05). When variables were adjusted for levels of visceral AT and fat mass, age-related differences that were initially found in plasma apoB and LDL-apoB levels, as well as in fasting glycemia and glucose tolerance, were eliminated. CONCLUSIONS: Results of the present study suggest that even before the onset of menopause there is an age-related deterioration in the metabolic risk profile and an increase in visceral AT deposition in middle-aged women compared with young control subjects. Furthermore, our results provide support for the notion that the age-related increase in visceral AT accumulation is a significant factor involved in the deterioration of the CVD risk profile noted in premenopausal women with age.

Adipose Tissue↗

PubMed1999

A stable isotope method using a [(2)H(5)]glycerol bolus to measure very low density lipoprotein triglyceride kinetics in humans.

We have developed a method using a bolus of [(2)H(5)]glycerol to determine parameters of VLDL-triglyceride (VLDL-TG) turnover and have compared the data to that obtained using simultaneously a bolus of [2-(3)H]glycerol in six young normolipidemic men. No measurable enrichment was found after 12 h for [(2)H(5)]glycerol; therefore, we could only perform a monoexponential analysis of its data. No differences in fractional catabolic rate (FCR) were seen when comparing the multicompartmental modeling of [2-(3)H]glycerol data (modeled over 48 h) either to the monoexponential analyses of the [2-(3)H]glycerol or that of the [(2)H(5)]glycerol data. The two monoexponential approaches were highly correlated (r = 0.96 for FCR), however, FCR was 18% higher with the [(2)H(5)]glycerol than with the [2-(3)H]glycerol data (P < 0.003). In all six subjects, a 10-h infusion of [1-(13)C]acetate was started at the same time as the glycerol boluses were given. In two men we were able reliably to detect VLDL-TG-fatty acid enrichment. The measurement of FCR in these two subjects using the mass isotopomer distribution analysis (MIDA) approach was in good agreement (within 10%) with FCRs determined with the labeled glycerol methods. In conclusion, our results have shown that results obtained with the [(2)H(5)]glycerol bolus were highly correlated with those obtained with the [2-(3)H]glycerol, but the FCRs were slightly higher with the former. We have also demonstrated that FCRs determined from monoexponential modeling were in good agreement with those determined from the multicompartmental modeling of the TG-glycerol data.

Acetates↗

PubMed1998

MHC class I mosaic mice reveal insights into control of Ly49C inhibitory receptor expression in NK cells.

We have analyzed lymphocyte development in natural MHC class I chimeric mice, generated through a transgenic approach in beta2-microglobulin (beta2m)-/- mice. In these mice, MHC class I+ cells coexist with an equal proportion of MHC class I-deficient cells. These MHC class I mosaic mice had normal numbers of CD8+ T cells, which had a target cell specificity similar to that of wild-type mice. Consequently, the mice did not develop any signs of autoimmunity. They also had normal numbers of NK cells. This allowed an examination of the MHC class I influence on the expression of the Ly49C inhibitory receptor on NK cells. This receptor binds to H-2Kb. It is expressed at low levels on NK cells in wild-type mice of the H-2b haplotype, but at markedly higher levels on NK cells in beta2m-/- mice and other strains of mice lacking expression of H-2Kb. Relatively little is known about how MHC class I molecules affect expression of the Ly49 receptors. Through the analysis of the present MHC class I mosaic mice, we demonstrate that the expression levels of Ly49C on NK cells is a consequence not only of MHC class I expression in the environment, but also of the expression of MHC class I molecules by the NK cells themselves. These findings are discussed in relation to the biological role of the calibration of the Ly49 inhibitory receptor expression in relation to self-MHC class I.

Animals↗

PubMed1998

Fine tuning of natural killer cell specificity and maintenance of self tolerance in MHC class I-deficient mice.

TAP1-/-, beta2-microglobulin (beta2m)-/- and TAP1/beta2m-/- mice all express low but quantitatively different levels of MHC class I molecules. Using these mice, we have addressed questions relating to the fine tuning of natural killer (NK) cell specificity and maintenance of self tolerance in the NK cell system. NK cells from B6 wild-type mice killed target cells from TAP1-/-, beta2m-/- and TAP1/beta2m-/- mice in vivo and rejected bone marrow grafts from the same mice in vivo at equivalent levels. NK cells from TAP1-/-, beta2m-/- mice did not kill target cells or reject bone marrow grafts from TAP1/beta2m-/- mice. NK cells in all MHC class I-deficient mice were tolerant to autologous MHC class I-deficient cells, as revealed by in vitro cytotoxicity assays using NK cell effectors activated with the interferon-inducing agent Tilorone, or by in vivo bone marrow graft experiments. However, the self-tolerant state of MHC class I-deficient NK cells was broken by in vitro stimulation with IL-2 for 4 days. Under these conditions, NK cells from the MHC class I-deficient mice killed autologous MHC class I-deficient cells while MHC class I-positive targets were spared. The C-type lectin inhibitory receptor Ly49C has a specificity for H-2Kb and is expressed on a subset of NK1.1+ cells in B6 mice. Wild-type and all MHC class I-deficient mice had similar numbers of Ly49C-positive NK1.1+ cells. However, Ly49C expression was markedly down-regulated on NK1.1+ cells from B6 mice, as compared to TAP1-/-, beta2m-/- and TAP1/beta2m-/- mice. In vitro stimulation of NK cells with IL-2 for 4 days did not significantly change this pattern. The present results are discussed in relation to the role of MHC class I molecules and Ly49 receptors in shaping the NK cell repertoire and raise new questions about maintenance of self tolerance in the NK cell system.

Animals↗

PubMed1998

Visceral obesity and the risk of ischaemic heart disease: insights from the Québec Cardiovascular Study.

There is no doubt that visceral obesity increases the susceptibility to IHD, emphasizing the need to consider this condition in the risk management of IHD. The use of CT or MRI as clinical tools to assess visceral adipose tissue accumulation does not appear to be justified, however, mostly because of the costs of the procedures and the limited availability of the necessary apparatus. The waist:hip ratio has been used extensively as an indicator of body fat distribution. However, it has been shown that the waist:hip ratio is less accurate than the waist circumference alone or the sagittal diameter in predicting visceral adipose tissue accumulation, particularly when monitoring changes in visceral adipose tissue mass over time.79 Also, the prediction of visceral adipose tissue levels by the waist circumference alone, as opposed to the waist:hip ratio, does not appear to be affected by gender or by the degree of obesity.80 For these reasons we have proposed that the waist circumference should be systematically measured in managing the risk of IHD. It is a simple and inexpensive measurement to perform, while providing potentially critical information on the risk profile of both men and women.80 We believe that identification of viscerally obese patients, a high-risk population for IHD, should be considered as a critical step in the risk management of IHD.

Cholesterol, LDL↗

PubMed1998

Function of hexameric RNA in packaging of bacteriophage phi 29 DNA in vitro.

A cyclic hexamer of the 120-base prohead RNA (pRNA) is needed for efficient in vitro packaging of the B. subtilis bacteriophage phi 29 genome. This capacity of pRNA to form higher multimers by intermolecular base pairing of identical subunits represents a new RNA structural motif. Dimers of pRNA are likely intermediates in formation of the cyclic hexamer. A three-dimensional model of the pRNA hexamer is presented.

Bacillus Phages↗

PubMed1998

Modeling active RNA structures using the intersection of conformational space: application to the lead-activated ribozyme.

The Pb2+ cleavage of a specific phosphodiester bond in yeast tRNA(Phe) is the classical model of metal-assisted RNA catalysis. In vitro selection experiments have identified a tRNA(Phe) variant, the leadzyme, that is very active in cleavage by Pb2+. We present here a three-dimensional modeling protocol that was used to propose a structure for this ribozyme, and is based on the computation of the intersection of conformational space of sequence variants and the use of chemical modification data. Sequence and secondary structure data were used in a first round of computer modeling that allowed identification of conformations compatible with all known leadzyme variants. Common conformations were then tested experimentally by evaluating the activity of analogues containing modified nucleotides in the catalytic core. These experiments led to a new structural hypothesis that was tested in a second round of computer modeling. The resulting proposal for the active conformation of the leadzyme is consistent with all known structural data. The final model suggests an in-line SN2 attack mechanism and predicts two Pb2+ binding sites. The protocol presented here is generally applicable in modeling RNAs whenever the catalytic or binding activity of structural analogues is known.

Catalysis↗

PubMed1998

Apolipoprotein B-48 and retinyl palmitate are not equivalent markers of postprandial intestinal lipoproteins.

This study compared retinyl palmitate and apolipoprotein (apo) B-48 as markers of postprandial triglyceride-rich lipoproteins. Nine non-diabetic men received an oral vitamin A-containing fat load. We measured retinyl palmitate, apoB-48, apoB-100, and triglyceride levels in Sf > 400, Sf 60-400 and Sf 20-60 lipoproteins. The peak retinyl palmitate concentration was delayed compared to the peak apoB-48 concentration in each fraction. The discrepancy between retinyl palmitate and apoB-48 was further investigated in another study of 12 men. In that study, a fat load was given and 5 h later, lipolysis was stimulated in vivo with heparin (60 U/kg, i.v.) and the same parameters were followed. Thirty minutes after heparin, triglyceride levels decreased significantly in the three triglyceride-rich lipoprotein fractions (Sf > 400, Sf 60-400 and Sf 20-60). ApoB-48 levels also fell significantly in the three triglyceride-rich lipoprotein fractions. In contrast, retinyl palmitate concentrations did not change significantly in Sf > 400 and Sf 60-400 fractions and increased significantly in the Sf 20-60 fraction. Our results indicate that retinyl palmitate and apolipoprotein B-48 do not mark the same properties of postprandial intestinal lipoproteins. The metabolic pattern of apolipoprotein B-48 parallels that of triglyceride. One possible explanation for these observations is that the apoB-48-containing triglyceride-rich lipoproteins are metabolically heterogeneous and that older particles, those in circulation for a longer period of time, may be cleared more rapidly than newer ones.

Adult↗

PubMed1997

Fat gain in female swimmers.

The association between diet and body composition was investigated in 6 elite female swimmers subjected to a 13-month nutritional supervision and in 11 female untrained subjects matched for fat-free mass. The impact of a 2-month interruption of training on diet and body composition was also studied in the swimmers. A positive correlation was observed between the percentage of dietary energy as fat and percent body fat in the untrained subjects (r = 0.68, p < 0.05). When values of the swimmers were incorporated in the regression analysis, the correlation coefficient remained the same. Following detraining for 2 months, a 4.8-kg body weight gain, including 4.3 kg fat mass, was observed. The energy equivalent of these morphological changes was 170 MJ and corresponded to about the amount of energy that would have been normally expended during this detraining period. In conclusion, these results suggest that the association between diet and body composition is not altered by exercise training, and that body fat gain occurs in response to detraining, perhaps to promote the restoration of energy and fat balance.

Adolescent↗