Search

Menopausal transition and postmenopause are usually associated with changes in body composition and a decrease in physical activity energy expenditure (PAEE). This study investigated body composition, cardiometabolic risk factors, PAEE, and inflammatory markers in premenopausal women after a 10-year follow-up.In all, 102 premenopausal women participated in the 5-year observational longitudinal Montreal Ottawa New Emerging Team (MONET) study. This present substudy included 48 participants (age: 60.0 ± 1.7 years; body mass index: 23.2 ± 2.2 kg/m) 6.0 ± 0.3 years after completion of the initial MONET study. Measures included body composition, waist circumference (WC), fasting glucose and insulin levels, insulin sensitivity (QUICKI model), plasma lipid levels, PAEE, and inflammatory markers.Compared with baseline measures of the MONET study, analyses revealed no significant increase in body weight, although there were significant increases in WC, fat mass (FM), % FM, total cholesterol, low-density lipoprotein cholesterol and high-density lipoprotein cholesterol, haptoglobin, apolipoprotein B, ferritin, adiponectin, and soluble cluster of differentiation 14 (all P 0.001) after the 10-year follow-up. However, significant decreases were observed for fat-free mass, PAEE, fasting glucose levels, interleukin-8 levels, and soluble tumor necrosis factor receptors 1 and 2 (sTNFR-1 and sTNFR-2) levels (all P 0.05). To determine the effect of postmenopausal years, data were restructured based on final menstrual period (FMP), and one-way analyses of variance were performed.Waist circumference, % FM, total cholesterol, high-density lipoprotein cholesterol, apolipoprotein B, ferritin, adiponectin, and soluble cluster of differentiation 14 were higher in early and late postmenopausal periods in these women. sTNFR-1 and sTNFR-2 levels were higher at the FMP and early postmenopausal years as compared with the late postmenopausal periods. Finally, interleukin-8 levels were lower in years after FMP.The number of years elapsed since the FMP can affect body composition, cardiometabolic risk factors, and inflammatory markers in healthy premenopausal women going through menopausal transition and postmenopausal periods.

Transintestinal cholesterol excretion (TICE) is known as an alternate non-biliary route of cholesterol excretion from the body. The aim of this study was to determine whether exercise training has effects on intestinal membrane receptors involved in TICE in intact and ovariectomized (Ovx) rats. Sprague-Dawley rats were first divided into 4 groups: Sham operated and Ovx rats fed a standard diet (Sham-SD; Ovx-SD), or a high cholesterol diet (Sham-Chol; Ovx-Chol). These 4 groups were subsequently subdivided into either sedentary or voluntary wheel running groups for 6 weeks. The cholesterol diet resulted in increased hepatic cholesterol accumulation (p< 0.001) in both Sham and Ovx rats. Exercise training increased (p < 0.01) transcripts of intestinal low density lipoprotein receptor (LDL-R) and proprotein convertase subtilisin/kexin type 9 (PCSK9), which are involved in trans-intestinal cholesterol uptake from circulation, in both Sham and Ovx rats compared to rats remaining sedentary in all diet conditions. The up-regulation of intestinal gene expression of LDL-R and PCSK9 following voluntary wheel running in intact and Ovx rats suggests that exercise training may contribute to elimination of cholesterol through the TICE pathway.

The association between the energy density (ED) of foods and adiposity has been reported previously. However, whether the contribution of ED to adiposity remains significant when controlled for energy intake (EI) and physical activity energy expenditure (PAEE) remains to be clearly established. We aimed to investigate the independent contribution of ED to variations in body composition in women during the menopausal transition.Sixty-seven women from the MONET cohort study were analyzed. Seven-day food records were used to assess EI and ED. Body composition (body fat mass (FM) and trunk-fat mass (TFM)) was measured with dual-energy X-ray absorptiometry; PAEE was assessed with accelerometers. This secondary analysis of data included measurements obtained at years 1 and 5 of the study.Mean ED was correlated with FM (r = 0.22; P = 0.04) and TFM (r = 0.22; P = 0.04) at year 1, but not at year 5. The multiple regression analysis showed that EI and ED contributed to 14% of the variance in FM and TFM at year 1.These results suggest that ED is a modest but inconsistent determinant of adiposity in healthy women at the time of the menopause transition.

Made available in DSpace on 2019-10-06T15:34:22Z (GMT). No. of bitstreams: 0 Previous issue date: 2019-03-01 Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) Purpose: To compare the acute and chronic effects of high-intensity intermittent training (HIIT) and moderate-intensity continuous training (MICT) on indices of cardio-metabolic health: (HDL-c, total cholesterol, triglycerides, heart ratio, and phase angle/PhA) in physically active men. Methods: Twenty active men were randomly allocated to HIIT (n = 10), or MICT (n = 10) for 5 weeks, three times per week. HIIT consisted of running 5 km with 1-min at 100% of maximal aerobic speed interspersed by 1-min passive recovery while subjects in MICT group ran continuously the same 5 km at 70% of maximal aerobic speed. Blood samples were collected at different moments during the first and last exercise session. Before and after 5 weeks of both exercise training protocols, heart ratio (during exercise session) and PhA were measured pre and post-exercise training. Results: Fasting HDL-c levels did not change after 5 weeks of HIIT or MICT. Perceptual variation of HDL pre and post training (fed state) tended to differ between HIIT and MICT (p = 0.09). All lipoproteins parameters (HDL-c, total cholesterol, triglycerides and non-HDL) were increased in post-acute exercise session compared to pre-exercise during the first and last training session, these being observed after both training protocols. PhA and heart rate measured at different times during the first and last training session were not affected in both training protocols. Conclusion: These results indicate that HIIT and MICT modify the post-exercise lipoprotein profile acutely. On the other hand, only HIIT tended to increase HDL-c levels chronically. Exercise and Immunometabolism Research Group Department of Physical Education São Paulo State University (UNESP) School of Technology and Sciences Post Graduation Program in Motricity Sciences São Paulo State University (UNESP) Post Graduation Program in Physical Therapy São Paulo State University (UNESP) Department of Physical Education Federal University of Pernambuco School of Physical Education and Sport University of São Paulo Department of Exercise Sciences Université du Québec à Montréal Centre de Recherche du CHU Sainte-Justine Department of Kinesiology University of Montreal Exercise and Immunometabolism Research Group Department of Physical Education São Paulo State University (UNESP) School of Technology and Sciences Post Graduation Program in Motricity Sciences São Paulo State University (UNESP) Post Graduation Program in Physical Therapy São Paulo State University (UNESP) FAPESP: 20 15/23127-1 FAPESP: 2015/11302-3 FAPESP: 2016/16712-8

To determine the influence of cardiorespiratory fitness (hereafter “fitness”) and physical activity levels on cardiometabolic risk factors in premenopausal women going through the menopause transition. An ancillary study including 66 premenopausal women who participated to a 5-year observational, longitudinal study (2004 to 2009 in Ottawa) on the effects of menopause transition on body composition and cardiometabolic risk factors. Women underwent a graded exercise test on treadmill to measure peak oxygen uptake (VO2 peak) at year 1 and 5 and physical activity levels were measured using accelerometers. Cardiometabolic risk factors included: waist circumference, fasting plasma lipids, glucose and insulin levels, HOMA-IR score, c-reactive protein, apolipoprotein B (apoB) and resting systolic and diastolic blood pressure. Change in fitness was not associated with changes in cardiometabolic risk factors. The changes in total physical activity levels on the other hand showed a significant negative association with apoB levels. Three-way linear mixed model repeated measures, showed lower values of waist circumference, fasting triglycerides, insulin levels, HOMA-IR score, apoB and diastolic blood pressure in women with a fitness ≥ 30.0 mlO2 kg− 1 min− 1 compared to women with a fitness, Highlights • Fitness and physical activity levels are independent predictors of CVD. • Change in total physical activity levels was negatively association with apoB. • Fitness was associated with more favorable values of cardiometabolic risk factors.

OBJECTIVE Menopausal transition is usually associated with changes in body composition and a decrease in physical activity energy expenditure. Adipose tissue, especially visceral fat, is an important source of inflammatory markers, which contributes to the development of a proinflammatory state. Conversely, high levels of physical activity and exercise have an anti-inflammatory effect. This study aimed to investigate the impact of menopausal transition and physical activity on inflammatory makers. METHODS One hundred two healthy premenopausal women participated in a 5-year longitudinal study. The present secondary analyses were performed on 58 participants with a full set of data (age: 49.6 ± 1.7 y; body mass index: 23.3 ± 2.4 kg/m). Measures included body composition, waist circumference, fasting glucose and insulin levels, insulin sensitivity, plasma lipid levels, cardiorespiratory fitness, physical activity energy expenditure, and inflammatory markers. RESULTS Repeated measure analyses revealed, after the 5-year follow-up, significant increases in ferritin, interleukin-8 (IL-8), and soluble tumor necrosis factor-α receptor 1 and 2 (sTNFR1 and sTNFR2) (P

[Purpose] This study investigated the effects of ovariectomy (Ovx) and 12 weeks of resistance training (RT) on gene expression of GLUT2, the main glucose transporter in the liver, and on PPARγ, a transcription factor known to target GLUT2 expression. [Methods] Forty Holtzman rats were divided into 5 groups: Sham-sedentary (Sed), Sham- RT, Ovx-Sed, Ovx-RT, and Ovx-Sed with hormone replacement (E2). The RT protocol consisted of sessions held every 72 h for 12 weeks, during which the animals performed 4 to 9 vertical climbs (1.1 m) at 2 min intervals with progressively heavier weights (30 g after the fourth climb) tied to the tail. The E2 silastic capsule was inserted into the rats’ backs 48 hours before the first RT session. [Results] In addition to liver fat, GLUT2 protein levels and PPARγ transcripts were increased (P < 0.05) in Ovx compared to Sham-Sed animals, suggesting increased hepatic glucose uptake under estrogen deficient conditions. RT and E2 in Ovx rats decreased liver fat accumulation as well as GLUT2 and PPARγ gene expression to the level of Sham-Sed animals. [Conclusion] The results of this study suggest that liver GLUT2 as well as PPARγ expression in Ovx rats are accompanied by increased fat accumulation and glucose uptake, thus providing a substrate for increased de novo lipogenesis. RT appears to be an appropriate exercise model to circumvent these effects.

Objective Metabolic disorders are often associated with liver steatosis and increased plasma cholesterol levels. However, the link between excessive lipid accumulation and impairments in cholesterol metabolism remains uninvestigated in the liver. Hence, a short treatment with a high-fat diet (HFD) was previously shown to promote excessive lipid accumulation in liver prior to the development of metabolic disorders. The present study intended to characterize how increases in liver fat alter the expression of several key regulators of hepatic cholesterol metabolism in response to a short-term HFD. Methods Young Wistar rats were randomly submitted either to HFD (n = 8) or a regular chow diet (RCD; n = 8) for 14 days.Liver tissue and blood were sampled . Results Increases in triglycerides were highly significant (P< 0.01) in liver but marginal in plasma of HFD rats. In contrast, the HFD resulted in higher (P< 0.01) cholesterol levels in plasma but not in liver samples. Gene expression of key markers involved in cholesterol uptake (LDL particles) including low density lipoprotein receptor-related protein-1 (LRP-1) and protein convertase subtilisin/kexin type 9 (PCSK9) along with ATP-binding cassette, superfamily G, member 5 (ABCG5) involved in cholesterol exportation viabile ducts were found to be higher (P< 0.05) in response to the HFD. In contrast, expression of 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR), involved in cholesterol synthesis was down-regulated in liver Conclusions The data support the concept that excessive accumulation of lipids promptly alters the expression of key genes regulating cholesterol metabolism in liver. On a clinical point of view, this indicates that increases in plasma cholesterol occur after a short-term high fat diet.

Objective: To investigate if an exaggerated peak exercise systolic blood pressure (peak ESBP) is associated with alteration of cardiometabolic risk factors and predict future resting hypertension in middle aged women. Methods: Data analysis was performed in 95 healthy normotensive premeno-pausal women at baseline and 84 after 5-year follow-up (age, 49.9 ± 1.9 years; BMI, 23.3 ± 2.2 kg/m2; resting BP, 117/73 ± 11.8/7.6 mmHg). Blood pressure was measured at rest and during a progressive exercise test on treadmill. Women were divided into two groups according to their peak ESBP

It is unknown whether leptin and peptide YY (PYY) influence changes in resting energy expenditure (REE), independently of fat mass (FM) and fat-free mass (FFM) in addition to changes in other energy expenditure (EE) components during weight loss.The objective of the study was to examine the relationships between leptin, PYY, and body composition with different EE components before and after weight loss and whether changes in leptin and PYY were associated with differences in predicted vs measured REE after the intervention.This was a randomized controlled design.The study was conducted in a laboratory.Participants were ninety-three overweight/obese postmenopausal women (aged 58.1 ± 4.8 y; body mass index 32.1 ± 4.3 kg/m(2)).Interventions included a 6-month caloric restriction diet alone or caloric restriction diet+resistance training.Body composition (dual energy x-ray absorptiometry), REE (indirect calorimetry), total EE (TEE; doubly labeled water), and fasting leptin and total PYY before and after weight loss were measured.Both interventions yielded significant decreases in weight, FFM, REE, and leptin, whereas a significant time × group interaction was noted for FM (greater decrease in FM in the diet+resistance training group) (P.05 for all outcomes). No significant differences in TEE, physical activity EE, and PYY were noted between baseline and after the intervention. Age, FFM, leptin, and PYY were the best predictors of baseline REE (R(2) = 0.77; P = .0001), whereas age, FFM, and FM were associated with REE after the intervention (R(2) = 0.88; P = .0001). The same predictors, except for leptin, were significantly related to TEE at baseline (R(2) = 0.70; P = .0001) and after the intervention (R(2) = 0.29; P = .0001), whereas only PYY was a significant predictor of physical activity EE at baseline and after the intervention. Changes in FM and leptin accounted for 27% of the variance in ΔREE (P = .0001). Greater predicted vs measured REE was noted after the intervention (P = .02). However, Δ leptin and ΔPYY were not significant predictors of the differences between postintervention measurement and predicted REE.Δ Leptin and ΔFM were strong contributors to changes in REE. However, Δ leptin and ΔPYY were not significant predictors of the differences between predicted and measured REE after the intervention.

More than 1·4 billion individuals are overweight or obese worldwide. While complications often require therapeutic intervention, data regarding the impact of obesity on drug disposition are scarce. As the influence of diet-induced obesity on drug transport and metabolic pathways is currently unclear, the objective of the present study was to investigate the effect of high fat feeding for 13 weeks in female Sprague–Dawley rats on the hepatic expression of the nuclear receptors pregnane X receptor (PXR), constitutive androstane receptor (CAR), liver X receptor (LXR) and farnesoid X receptor (FXR) and several of their target genes. We hypothesised that high fat feeding would alter the gene expression of major hepatic transporters through a dysregulation of the expression of the nuclear receptors. The results demonstrated that, along with a significant increase in body fat and weight, a high-fat diet (HFD) induced a significant 2-fold increase in the expression of PXR as well as a 2-, 5- and 2·5-fold increase in the hepatic expression of the PXR target genes Abcc2, Abcb1a and Cyp3a2, respectively (PFXR were significantly increased in rats fed a HFD in addition to the increase in the expression levels of FXR target genes Abcb11 and Abcb4. The expression levels of both LXRα and LXRβ were slightly but significantly increased in rats fed a HFD, and the expression levels of their target genes Abca1 and Abcg5, but not Abcg8, were significantly increased. The expression of the nuclear receptor CAR was not significantly altered between the groups. This suggests that a HFD may induce changes in the hepatobiliary transport and metabolism of endogenous and exogenous compounds.

This study aims to investigate individual characteristics that explain interindividual variations in glucose disposal in response to a 6-month weight loss program in obese postmenopausal women.The cohort was divided into tertiles based on changes in glucose disposal after weight loss. Only women in the upper tertile (positive responders: Δ glucose disposal ≥ 0.92 mg/kg/min; n = 19) and lower tertile (negative responders: Δ glucose disposal ≤ -0.23 mg/kg/min; n = 19) were considered for analyses. Outcome measures included body weight, lean body mass (LBM), LBM index (= LBM / height [m]), fat mass (FM), FM index (= FM / height [m]), visceral fat, subcutaneous abdominal fat, high-sensitivity C-reactive protein (hsCRP) levels, interleukin-6, lipid profile, physical activity levels, fasting blood glucose and insulin levels, glucose disposal by hyperinsulinemic-euglycemic clamp technique, and resting blood pressure.At baseline, positive responders had higher triglycerides and hsCRP levels and lower glucose disposal (0.01P0.05) than negative responders. Except for visceral fat, the entire cohort showed significant decreases in all measures of body composition (P0.005) after weight loss, with greater decreases in body weight, body mass index, and FM index in positive responders (P0.005). Finally, data revealed that only positive responders showed decreases in LBM, LBM index, and hsCRP levels after weight loss (P between 0.01 and 0.001).An important interindividual variability in changes in glucose disposal after weight loss is observed. Interestingly, participants who display improvements in glucose disposal also show significant decreases in LBM, LBM index, and hsCRP after weight loss.

Resistance training (RT) has been shown to decrease fat mass (FM), and increase fat-free mass (FFM), which can be a useful for weight loss maintenance. Objective To examine the effects of a 1-year RT intervention on weight loss maintenance following a 6-month dietary weight loss intervention. Design Following a 6-month dietary weight loss intervention (−6% ± 5.8; 5.05 kg ± 4.45), 70 postmenopausal women living with overweight or obesity were randomized to a control group ( n = 34) or a RT group ( n = 36) (3×/week first 6 months, 2×/week last 6 months, 70–80% of 1-repetition maximum). Body composition (DXA), abdominal visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT) (CT scan), resting energy expenditure (EE) (indirect calorimetry), physical activity EE and total daily EE were measured (doubly-labelled water). Results A total of 54 participants completed the study (control group n = 29; RT group n = 25) and compliance to the RT program was on average 64%. Significant regains were noted for body weight 0.98 (3.71) kg vs. 1.33 (3.94) kg and FM regain 1.32 (2.69) kg vs. 0.81 (3.26) kg in control and RT groups after the 1-year weight maintenance phase. No group differences were noted. Resting EE and total daily EE did not change after the weight maintenance phase, and no differences were observed between groups. Both groups had significantly greater than predicted decrease in resting EE after the 6-month dietary intervention and at the end of the 1-year weight-loss maintenance phase. Conclusions Our results suggest that a 1-year RT intervention following a 6-month dietary weight loss intervention does not improve weight loss maintenance, body composition or EE in post-menopausal women living with overweight or obesity.

The aim of the present study was to identify molecular mechanisms involved in liver fat and cholesterol accumulation in ovariectomised (Ovx) rats fed with high-cholesterol diets. VLDL assembly and bile acid metabolism were specifically targeted. After being either Ovx or sham-operated, the rats were fed a standard diet or a high-fat diet containing 0, 0·25 or 0·5 % cholesterol for 6 weeks. Although Ovx rats exposed to dietary cholesterol intake accumulated the greatest amount of hepatic fat and cholesterol, plasma cholesterol levels were lower (PPP

Studies on normoglycemic ovariectomized Sprague-Dawley rats have provided insights about the effects of estrogen deficiency on insulin resistance in lean individuals. It is not completely clear if subjects with pre-established obesity and insulin resistance are at greater risk of developing type 2 diabetes when ovarian estrogens are no longer secreted, and if physical activity can protect against this susceptibility. Contrasting with their male counterparts, obese and insulin resistant female ZDF (Zucker diabetic fatty) rats do not become hyperglycemic when fed a standard diet. The aim of the study was to evaluate the hypothesis that withdrawal of ovarian estrogens in insulin resistant female ZDF rats would trigger overt hyperglycemia, provided they remain physically inactive. Female ZDF rats underwent either an ovariectomy (OVX) or a simulated surgery (SHAM). Thereafter, OVX rats engaged either in voluntary wheel cage running (OVX-Active), or like the Sham rats, remained sedentary (OVX-Sed) for 6 weeks. Fasting glycemia, insulinemia, and glucose tolerance were not altered in OVX-Sed as compared to SHAM-Sed rats. However, OVX-Sed rats showed altered liver triglyceride and glycogen contents, increased pancreatic insulin content and reduced insulin-stimulated muscle pAKT as compared to SHAM-Sed rats. Physical activity in OVX rats lowered fasting glucose and insulin levels, improved glucose tolerance and insulin-stimulated skeletal muscle glucose uptake as compared to OVX-Sed rats. OVX-induced alterations in pancreatic insulin content and liver glycogen and triglyceride contents were significantly improved by physical activity. Loss of ovarian estrogens did not cause overt hyperglycemia in insulin-resistant female ZDF rats. Physical activity improved glucose homeostasis despite estrogen deficiency.

It is unknown whether the satiety quotient (SQ) differs across the menopausal transition, and whether changes in SQ are related to changes in anthropometric/body composition variables. The objective of this study was to evaluate the changes in SQ and its association with energy intake and changes in anthropometric/body composition variables across the menopausal transition.At baseline, 102 premenopausal women (aged 49.9 ± 1.9 years, body mass index 23.3 ± 2.2 kg/m(2)) took part in a 5-year observational, longitudinal study. Body composition (DXA), appetite (visual analog scales), energy and macronutrient intakes (ad libitum lunch and 7-day food diary) were assessed annually. The SQ (mm/100 kcal) was calculated at 60 and 180 min post-breakfast consumption.Overall, the SQ increased at years 3 and 4 (p = 0.01-0.0001), despite no significant differences between menopausal status groups. Lower fullness, prospective food consumption and mean SQ values predicted overall increases in lunch energy and macronutrient intakes (p = 0.04-0.01), whereas only prospective food consumption and fullness SQ predicted energy intake and carbohydrate intake, respectively, when assessed with food diaries (p = 0.01). Delta SQs were negatively correlated with changes in waist circumference (p = 0.03-0.02), whereas delta SQs were positively (p = 0.04) and negatively (p = 0.02) associated with delta fat mass between years 1 and 5, and years 4 and 5, respectively.These results suggest that variations in SQ across the menopausal transition are related to energy and macronutrient intakes and coincide with changes in body composition and waist circumference.

Objective The purpose of this study was to investigate changes in dietary intake and appetite across the menopausal transition. Methods This was a 5-year observational, longitudinal study on the menopausal transition. The study included 94 premenopausal women at baseline (age: 49.9 ± 1.9 yrs; BMI: 23.3 ± 2.3 kg/m2). Body composition (DXA), appetite (visual analogue scale), eating frequency, energy intake (EI) and macronutrient composition (7-day food diary and buffet-type meal) were measured annually. Results Repeated-measures analyses revealed that total EI and carbohydrate intake from food diary decreased significantly over time in women who became postmenopausal by year 5 (P > 0.05) compared to women in the menopausal transition. In women who became postmenopausal by year 5, fat and protein intakes decreased across the menopausal transition (0.05 > P < 0.01). Although a decrease in % fat intake was observed during the menopausal transition (P < 0.05), this variable was significantly increased in the postmenopausal years (P < 0.05). Spontaneous EI and protein intake also declined over time and were higher in the years preceding menopause onset (P < 0.05). Desire to eat, hunger and prospective food consumption increased during the menopausal transition and remained at this higher level in the postmenopausal years (0.05 > P< 0.001). Fasting fullness decreased across the menopausal transition (P < 0.05). Conclusion These results suggest that menopausal transition is accompanied with a decrease in food intake and an increase in appetite.

Objectives Factors that influence weight gain during the menopausal transition are not fully understood. The purpose of this study was to investigate changes in energy expenditure (EE) across the menopausal transition. Methods One hundred and two premenopausal women (age: 49.9 ± 1.9 yrs; BMI: 23.3 ± 2.2 kg/m2) were followed for 5 years. Body composition (DXA), physical activity EE (accelerometer), resting EE and thermic effect of food (indirect calorimetry) were measured annually. Results Total EE decreased significantly over time in postmenopausal women (P < 0.05), which was mostly due to a decrease in physical activity EE (P < 0.05). Although average resting EE remained stable over time in postmenopausal women, a significant increase, over the 5-year period, was noted in women who were in the menopausal transition by year 5 (P < 0.05). Finally, the time spent in moderate physical activity decreased and the time spent in sedentary physical activity increased during the menopausal transition (P < 0.05). Conclusion These results suggest that menopausal transition is accompanied with a decline in EE mainly characterized by a decrease in physical activity EE and a shift to a more sedentary lifestyle.

The present study measured the impact of adding resistance training to an energy-restricted diet on the components of energy expenditure in overweight or obese postmenopausal women.Participants (n = 137) were randomly divided into two groups: (1) a diet and resistance training (DRT) group and (2) a diet-only (DO) group. Women followed a 6-month energy-restricted diet consisting of 2,100 to 3,360 kJ less than daily needs. The DRT group also followed a resistance training program (three times a week). Resting energy expenditure (REE) was measured by indirect calorimetry. Total energy expenditure was measured with doubly labeled water. Body composition was measured by dual-energy x-ray absorptiometry.Eighty nine women were included in the analyses for this study (DRT, n = 21; DO, n = 68). REE in both groups was significantly lower after the intervention (mean difference ± SD: DO, -0.26 ± 0.4 MJ d; DRT, -0.33 ± 0.4 MJ d; P ≤ 0.05). Relative REE, expressed per kilogram of lean body mass corrected for fat mass change, remained stable in both groups. Physical activity energy expenditure remained stable in both groups (mean difference ± SD: DO, 0.02 ± 1 MJ d, P = 0.91; DRT, -0.14 ± 1 MJ d, P = 0.64).Adding resistance training to an energy-restricted diet does not significantly alter any compartment of energy expenditure. REE is lower owing to reduction in body composition compartments, but relative REE is not significantly altered.

The aim of this study was to determine the effects of an atherogenic diet (AD; 40 % lipid, 1.25 % cholesterol, kcal) on triglyceride (TAG) and cholesterol accumulation in liver and on gene expression of liver X receptor (LXR) and farnesoid X receptor (FXR) and their target genes and to observe if these responses are affected by endurance training. Sprague–Dawley rats (n = 32) were divided into two groups and randomly assigned to an AD or a standard diet (SD) for 7 weeks. Half of the rats in each group were assigned to an exercise training program for 5 days/week. The AD resulted in a large (P

Objective: Cardiovascular disease is the first cause of mortality in women in North America. The risk of car-diovascular disease increases sharply after middle age in women, especially after menopause. The aim was toinvestigate changes in body composition and cardiometabolic profile throughout the menopausal transition.Methods: This was a 5-year observational, longitudinal study on the menopausal transition. The study included102 premenopausal women at baseline (age, 49.9 T1.9 y; body mass index, 23.3 T2.2 kg/m 2 ). Outcome measuresinclude menopause status, body composition by dual-energy x-ray absorptiometry (total fat mass [FM], trunk FM,and total fat-free mass), waist circumference, visceral and abdominal subcutaneous fat, fasting glucose and insulinlevels, homeostasis model assessment of insulin resistance, plasma lipid levels (triglycerides, total cholesterol, andhigh- and low-density lipoprotein cholesterol), and resting blood pressure.Results: Repeated-measure analyses revealed significant increases for FM, percentage FM, trunk FM, visceralfat, plasma fasting glucose, and high-density lipoprotein cholesterol (0.05 9P G0.01) and a significant decrease forplasma glucose levels after follow-up. Those who were in perimenopause or postmenopause by year 3 of the studyshowed a significant increase in visceral fat (P G0.01) compared with baseline. Despite some significant changes inthe metabolic profile among the menopause statuses, the women did not show any cardiometabolic deterioration bythe end of the study.Conclusions: Our results suggest that changes in body composition and fat distribution can occur in nonobesewomen as they go through the menopausal transition. However, these changes were not accompanied by car-diometabolic deteriorations in the present study.Key Words: Menopause YBody composition YCardiometabolic risk factors YVisceral fat.

Healthy diet and physical activity are associated with a lower cardiometabolic risk (CMR). Little is known about whether they interact to improve CMR. The purpose of the present study was to determine the synergistic associations of diet quality and physical activity energy expenditure (PAEE) on CMR factors. The present study was ana posteriorianalysis of two cross-sectional studies on 124 inactive non-diabetic postmenopausal women with a BMI ≥ 27 kg/m2. The following factors were measured: diet quality (assessed by the Canadian Healthy Eating Index (C-HEI) from a 3 d food record); PAEE (doubly labelled water); body composition (dual-energy X-ray absorptiometry, computed tomography scan); lipoprotein profile (total, HDL- and LDL-cholesterol (HDL-C and LDL-C), non-HDL-C, total cholesterol:HDL-C, TAG, apoA1, apoB, apoA1:apoB and LDL-C:apoB); insulin sensitivity (homeostasis model assessment of insulin resistance and hyperinsulinaemic–euglycaemic clamp); inflammatory markers (high-sensitivity C-reactive protein (hs-CRP), haptoglobin, orosomucoid, IL-6 and leucocyte count). The association of the interaction PAEE × C-HEI and CMR factors was evaluated by hierarchical regressions. Fat mass-adjusted ANCOVA determined the interaction between PAEE and the C-HEI. In hierarchical regressions, the interaction PAEE × C-HEI was a correlate of more favourable values of HDL-C, apoB, apoA1:apoB and LDL-C:apoB ratios, and hs-CRP, while only PAEE was a negative correlate of haptoglobin. Compared with those in the low-PAEE/low-C-HEI group, women in the high-PAEE/high-C-HEI group had 10 % higher HDL-C, 13 % lower apoB, 11 % larger LDL particles and 28 % lower hs-CRP concentrations (P

The purpose of the present study was to establish a model of rats prone and resistant to intra-abdominal fat accumulation in response to ovariectomy (Ovx-P and Ovx-R) and to determine its relationship with molecular biomarkers.Two experiments were conducted in which female rats were either sham-operated (Sham) or ovariectomized (Ovx). In the first experiment, ovariectomized rats were stratified into three tertiles based on intra-abdominal adipose tissue mass. To strengthen the Ovx-P/Ovx-R model, we conducted a second experiment in which the numbers of rats in each group were extended and in which different molecular markers were measured. At the end of a 6-8-week period, ovariectomized rats that displayed the lower abdominal fat accumulation (lower tertile) were labelled as Ovx-R and those in the upper tertile as Ovx-P.Ovx-R rats displayed similar abdominal fat gain to Sham rats whereas Ovx-P rats depicted abdominal fat mass twice as high as that of Sham and Ovx-R rats. Despite the difference in abdominal adiposity, liver fat content was ~50% higher (p0.01) in both Ovx-R and Ovx-P rats compared to Sham rats. In addition, both Ovx-R and Ovx-P rats depicted higher HOMA-IR scores (p0.05) and lower (p0.01) hepatic gene expression of leptin receptor-b and -e, microsomal transfer protein (MTP), and diacylglycerol acyltransferase-2 (DGAT-2) compared to Sham rats.The present findings indicate that estrogen withdrawal-induced hepatic steatosis and associated insulin resistance may be dissociated from abdominal fat accumulation and suggest that a decrease in leptin action through a down-regulation of leptin receptors and a decrease in very low density lipoprotein production through a down-regulation of MTP and DGAT-2 may be factors responsible for this observation in the absence of peripheral fat gain.

Background and aims The purpose of this study was to compare the relationship of several insulin sensitivity indices with cardiometabolic risk factors in overweight and obese postmenopausal women. Methods and results This was a cross-sectional study involving 137 overweight and obese postmenopausal women (age: 57.7 ± 4.8 yrs; body mass index: 32.4 ± 4.6 kg/m 2 ; body fat: 38.6 ± 9.2 kg). Insulin sensitivity was determined by the euglycaemic–hyperinsulinemic (EH) clamp technique as well as by oral glucose tolerance test (OGTT) derived indices (Stumvoll, Matsuda and SI is ) and fasting surrogate indices (HOMA, QUICKI). Cardiometabolic risk factors included: body composition and visceral fat that were measured using dual energy X-ray absorptiometry and computed tomography, respectively. Peak oxygen consumption, lower body muscle strength (using weight training equipment), physical activity energy expenditure (doubly labeled water), plasma lipids and C-reactive protein were also measured. Correlations of insulin sensitivity indices with metabolic risk factors showed some similarities, however, a wide range of variations were also observed. Furthermore, our results showed that visceral fat was the primary predictor for surrogate and OGTT indices, explaining 15–28% of the variance and the triglycerides/HDL-C ratio was the primary predictor for the EH clamp indices, explaining 15–17% of the variance. Conclusion The present study indicates that the different methods of measuring and/or expressing insulin sensitivity display variations for associations with cardiometabolic risk factors. Therefore, interpretations of relationships between insulin sensitivity indices and cardiometabolic risk factors should take into account the method used to estimate and express insulin sensitivity.

The main objective of this study was to establish whether a stable measurement of strength could be obtained without prior exercise familiarization in postmenopausal women who were overweight or obese. A second objective was to evaluate the influence of physical activity on the variability of strength measurement. Thirty postmenopausal women (age: 57.9 yr; SD: 5 yr; body mass index: 31.0 kg/m2; SD: 4 kg/m2) underwent 3 strength testing sessions (48 hr apart) each including 3 exercises (leg press, chest press, and lat pull down). Energy expenditure was measured before the strength testing week with the doubly labelled water method over a 10-day period. Resting metabolic rate was measured by indirect calorimetry. Physical activity energy expenditure was calculated as follows: total energy expenditure x 0.9, minus the resting metabolic rate. Repeated analysis of variance and paired t-test were used to assess the difference and the reliability of the testing sequence. Results from leg press and chest press exercises indicated no significant difference among the 3 testing sessions. The lat pull down exercise was associated with a significant systematic bias between sessions 1 and 2 (mean difference: 1.4 kg; SD: 3 kg; 95% confidence intervals; 0.2-2.7 kg), but the difference disappeared at the third testing session (mean difference: 0.7 kg; SD: 3 kg; 95% confidence intervals; 0.5-2 kg). Physical activity did not influence the variability of the strength results. Overall, our results showed that a relatively stable strength measurement can be obtained within a maximum of 3 testing sessions without prior familiarization. In addition, physical activity did not influence strength testing in postmenopausal women who were overweight or obese.

Regular physical activity is beneficial in preventing the risk of cardiovascular complications of diabetes. Recent studies showed a cardioprotective role of oxytocin (OT) to induce natriuretic peptides (NPs) and nitric oxide (NO) release. It is not known if the diabetic state is associated with a reduced OT–NPs–NO system and if exercise training improves this system. To address this, we investigated the effects of treadmill running using the db/db mouse model of type 2 diabetes. Eight-week-old db/db mice were subjected to running 5 days per week for a period of 8 weeks. The lean db/+ littermates were used as controls. Sedentary db/db mice were obese and hyperglycaemic, and exercise training was not effective in reducing body weight and the hyperglycaemic state. Compared to control mice, db/db mice had lower heart weight and heart-to-body weight ratios. In these mice, this was associated with augmented cardiac apoptosis, cardiomyocyte enlargement and collagen deposits. In addition, db/db mice displayed significant downregulation in gene expression of OT (76%), OT receptors (65%), atrial NP (ANP; 43%), brain NP (BNP; 87%) and endothelial nitric oxide synthase (eNOS) (54%) in the heart (P < 0.05). Exercise training had no effect on expression of these genes which were stimulated in control mice. In response to exercise training, the significant increment of anti-apoptotic Bcl-2 gene expression was observed only in control mice (P < 0.05). In conclusion, downregulation of the OT–NPs–NO system occurs in the heart of the young db/db mouse. Exercise training was not effective in reversing the defect, suggesting impairment of this cardiac protective system in diabetes.

The aim of the present study was to investigate the effects of maintaining only one of the two components of a food restriction (FR)+resistance training (RT) regimen on the regain of body weight and fat mass (liver and adipocytes) in ovariectomized (Ovx) rats.Five week Ovx rats were submitted to a weight loss program consisting of a 26% FR combined with RT (OvxFR+RT) for 8 weeks. RT consisted of climbing a 1.5m vertical grid with a load attached to the tail, 20-40 times with progressively increasing loads 4 times/week. Following this weight loss intervention, OvxFR+RT rats were sub-divided into 3 groups for an additional 5 weeks: 2 groups went back to a normal ad libitum feeding with or without RT and the other group kept only FR.Combined FR+RT program in Ovx rats led to lower body mass gain, liver triacylglycerol (TAG) levels, and fat mass gain compared to sedentary normally fed Ovx rats (P0.01). Stopping both FR and RT over a 5 week period resulted in the regain of body weight, intra-abdominal fat pad weight and liver TAG (P0.01). When only FR was maintained, the regain of body and fat pad weight as well as liver and plasma TAG concentrations was completely prevented. However, when only RT was maintained, regain in the aforementioned parameters was attenuated but not prevented (P0.05).It is concluded that following a FR+RT weight loss program, continuation of only RT constitutes an asset to attenuate body weight and fat mass regain in Ovx rats; although the impact is less than the maintaining FR alone. These results suggest that, in post-menopausal women, RT is a positive strategy to reduce body weight and fat mass relapse.

Skeletal muscle capillarisation responds to physiological and pathological conditions with a remarkable plasticity. Angiomotin was recently identified as a new pro-angiogenic molecule. Angiomotin is expressed as two protein isoforms, p80 and p130. Whereas p80 stimulates endothelial cell migration and angiogenesis, p130 is rather characteristic of stabilized and matured vessels. To date, how angiomotin expression is physiologically regulated in vivo remains largely unknown. We thus investigated (1) whether angiomotin was physiologically expressed in skeletal muscle; (2) whether exercise training, known to stimulate muscle angiogenesis, affected angiomotin expression; and (3) whether such regulation was altered in obesity, a pathological situation often associated with an impaired angiogenic activity and some capillary rarefaction in skeletal muscle. Two models of obesity were used: a high fat diet regime and Zucker Diabetic Fatty rats (ZDF). Our results provide evidence that angiomotin was expressed both in capillaries and myofibres. In non-obese rats, the p80 isoform was increased in plantaris muscle in response to endurance training whereas p130 was unaffected. In obese animals, no change was observed for p80 whereas training significantly decreased p130 expression. Exercise training induced angiogenesis in plantaris from both obese and non-obese rats, possibly through the modulation of angiomotin level and its consequences on RhoA–ROCK signalling. In conclusion, any increase in p80 or decrease in p130, as respectively observed in non-obese and obese animals, led to an increased ratio between p80 and p130 isoforms. This increased angiomotin p80/p130 ratio might then directly reflect the enhanced angiogenic ability of skeletal muscle in response to exercise training.

Acylation-stimulating protein (ASP) has been shown to positively stimulate fatty acid esterification and glucose uptake in adipocytes. In vitro studies demonstrate that insulin stimulates ASP secretion from adipocytes. Individuals with obesity and/or metabolic disturbances (insulin resistance and type 2 diabetes) have increased plasma ASP.The present study was designed to evaluate whether ASP levels are influenced by the metabolic profiles of overweight and obese postmenopausal women during a euglycaemic/hyperinsulinaemic clamp (EHC). Patients The study population consisted of 76 overweight and obese sedentary postmenopausal women.We evaluated insulin sensitivity, plasma ASP levels, body composition including visceral adipose tissue area, blood lipid profiles, liver enzymes, peak aerobic capacity, resting metabolic rate (RMR) and total energy expenditure (TEE).We observed wide interindividual variations of ASP levels during the EHC. Therefore, subjects were divided into three groups based on ASP changes. Negative ASP Responders (NAR; n = 24) showed a -20% or greater decrease in ASP levels while Positive ASP Responders (PAR; n = 42) displayed ASP fluctuations superior to +20%. Ten subjects had little or no ASP change and were considered as Zero ASP responders (ZAR). PAR women displayed a worse metabolic profile than NAR women, including higher BMI, visceral adipose tissue, fasting insulin levels, lean body mass, and alanine aminotransferase (ALT), a marker of impaired liver function. After adjustment for BMI, only ALT remained significantly different, while lean body mass (P = 0.08) and visceral adipose tissue (P = 0.07) remained marginally higher. Correlation analysis of all subjects demonstrated that fasting ASP levels correlated positively with albumin and VO(2 peak) and this association remained significant after adjustments for the effect of BMI. In addition, the percentage maximal change in ASP levels during the EHC was positively associated with BMI, lean body mass, visceral adipose tissue, fasting insulin, HOMA, TEE, RMR, ALT and AST.Overall these results suggest that an elevated ASP response during the EHC is associated with metabolic disturbances in overweight and obese postmenopausal women.

Fat mass gain and regain following weight loss are major concerns and may be even more critical after menopause. The present study was undertaken to evaluate the effect of a resistance training protocol on body weight and fat mass in ovariectomized Sprague-Dawley rats following diet-induced weight loss.Rats were randomly divided into ovariectomized (Ovx) and sham-operated (Sham) groups. Five weeks after ovariectomy, Ovx rats were subjected to a 26% food restriction (OvxFR) for 8 weeks. Following this period, OvxFR rats went back to a normal ad libitum feeding and were divided into two groups: either sedentary or undergoing a resistance training program for an additional 5 weeks, which consisted of climbing a 6-m vertical grill, 20-40 times, with progressively increasing load four times/week.The food restriction program decreased (p0.01) body mass, fat pad weight (intra-abdominal and subcutaneous), and liver triacylglycerol (TAG) levels as compared to normally fed Ovx rats. Stopping the food restriction program over a 5-week period resulted in a partial regain in body weight and intra-abdominal fat pad weight (p0.05), and in an almost complete regain in liver TAG compared to normally fed Ovx rats. On the other hand, no significant increases in these variables were noted when the food restriction was replaced by resistance training over the same 5-week period.These results indicate that a resistance training program could be useful in preventing body weight as well as adipose tissue and liver fat regain in Ovx rats, following diet-induced weight loss. It is suggested that changing from a food restriction regimen to a resistance training program can be an interesting strategy to promote successful long-term weight reduction in postmenopausal women.

OBJECTIVE To investigate whether estrogen deficiency modifies the expression of important genes involved in hepatic lipid regulation, PPAR alpha, SREBP-1c, and SCD-1, in association with fat accumulation in the liver of ovariectomized rats. DESIGN Thirty female Sprague-Dawley rats were divided into three groups: sham-operated (n = 12), ovariectomized (n = 12), and ovariectomized with 17beta-estradiol replacement (n = 6). All animals were killed 8 weeks after surgery. In addition to liver triacylglycerol determination, transcripts levels and protein content of peroxisome proliferator-activated receptor alpha, liver sterol regulatory element-binding protein 1c, and stearoyl coenzyme Adesaturase 1 were quantified by quantitative real-time polymerase chain reaction and Western blot, respectively. RESULTS As expected, liver triacylglycerol levels were higher (51%; 21.9 +/- 2.6 vs 14.5 +/- 1.2 mg/g; P < 0.01) in ovariectomized compared with sham-operated rats. Peroxisome proliferator-activated receptor alpha mRNA levels were 66% lower (P < 0.01), whereas sterol regulatory element-binding protein 1 and stearoyl coenzyme A desaturase 1 transcript levels were 80% and 41% higher (P < 0.05), respectively, after estrogen removal. Our data on gene expression obtained with quantitative real-time polymerase chain reaction for peroxisome proliferator-activated receptor alpha and sterol regulatory element-binding protein 1c were confirmed by Western blots. All the effects of ovariectomy were prevented by 17beta-estradiol replacement, indicating a role for estrogens in the prevention of hepatic fat accumulation. CONCLUSIONS Our results suggest that a reduction in lipid oxidation and an increase in lipogenesis are defective mechanisms leading to lipid accumulation in the liver of ovariectomized rats. We conclude that estrogen deficiency induced by ovariectomy changes the expression of genes that favor the development of a steatotic phenotype.

The purpose of this study was to investigate the effects of three weeks of rosuvastatin (Ros) treatment alone and in combination with voluntary training (Tr) on expression of genes involved in cholesterol metabolism (LDLR, PCSK9, LRP-1, SREBP-2, IDOL, ACAT-2 and HMGCR) in the liver of eight week-old ovariectomized (Ovx) rats. Sprague Dawley rats were Ovx or sham-operated (Sham) and kept sedentary for 8 weeks under a standard diet. Thereafter, rats were transferred for three weeks in running wheel cages for Tr or kept sedentary (Sed) with or without Ros treatment (5mg/kg/day). Six groups were formed: Sham-Sed treated with saline (Sal) or Ros (Sham-Sed-Sal; Sham-Sed-Ros), Ovx-Sed treated with Sal or Ros (Ovx-Sed-Sal; Ovx-Sed-Ros), Ovx trained treated with Sal or Ros (Ovx-Tr-Sal; Ovx-Tr-Ros). Ovx-Sed-Sal rats depicted higher (P < 0.05) body weight, plasma total cholesterol (TC) and LDL-C, and liver TC content compared to Sham-Sed-Sal rats. In contrast, mRNA levels of liver PCSK9, LDLR, LRP-1 as well as plasma PCSK9 concentrations and protein levels of LRP-1 were reduced (P < 0.01) in Ovx-Sed-Sal compared to Sham-Sed-Sal rats. However, protein levels of LDLR increased (P < 0.05) in Ovx-Sed-Sal compared to Sham-Sed-Sal rats. Treatment of Ovx rats with Ros increased (P < 0.05) mRNA and protein levels of LRP-1 and PCSK9 but not mRNA levels of LDLR, while its protein abundance was reduced at the level of Sham rats. As a result, plasma LDL-C was not reduced. Exercise alone did not affect the expression of any of these markers in Ovx rats. Overall, Ros treatment corrected Ovx-induced decrease in gene expression of markers of cholesterol metabolism in liver of Ovx rats, but without reducing plasma LDL-C concentrations. Increased plasma PCSK9 levels could be responsible for the reduction of liver LDLR protein abundance and the absence of reduction of plasma LDL-C after Ros treatment.

The present study was undertaken to determine the time course of liver lipid infiltration in ovariectomized (Ovx) rats and the impact of high-fat (HF; 42% kJ) feeding on this response.In a first step, Ovx rats were compared to Sham-operated (Sham) and Ovx rats supplemented with 17beta-estradiol (OvxE2) to evaluate the effect of estrogen removal. In a second time, Ovx rats fed a HF diet (OvxHf) were compared with normally fed Ovx rats. Animals were killed after 3, 8, and 13 weeks of their respective treatment (n=8 rats/group). We measured liver triacylglycerol (TAG) content, fat pad mass, and several other plasma parameters.Ovariectomy resulted in the typical increase in energy intake and body weight. Liver TAG accumulation was 35, 43, and 99% higher in Ovx than in Sham rats after 3, 8, and 13 weeks, respectively. The ovariectomy-induced liver lipid infiltration was completely prevented by estrogen replacement. On the opposite, plasma TAG concentrations were lower in Ovx than in Sham and OvxE2 rats. HF feeding in Ovx rats resulted in a significant (P0.05; 38 versus 22 mg/g at 13-week) accumulation of fat in liver as compared to normally fed Ovx rats.Ovariectomy results in a progressive accumulation of fat in liver over a 13-week period. In addition, HF feeding in Ovx rats lead to an even more severe liver lipid infiltration. These data indicate that the absence of estrogens in rat favours fat accretion in liver, which is highly amplified by a HF diet.

Exercise training results in cardiovascular and metabolic adaptations that may be beneficial in menopausal women by reducing blood pressure, insulin resistance, and cholesterol level. The adaptation of the cardiac hormonal systems oxytocin (OT), natriuretic peptides (NPs), and nitric oxide synthase (NOS) in response to exercise training was investigated in intact and ovariectomized (OVX) rats. Ovariectomy significantly augmented body weight (BW), left ventricle (LV) mass, and intra-abdominal fat pad weight and decreased the expression of oxytocin receptor (OTR), atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and guanylyl cyclase-A (GC-A), in the right atrium (RA) and LV, indicating estrogenic control of these genes. These effects of ovariectomy were counteracted by 8-wk-long exercise training which decreased fat pad weight (33.4 ± 2.3 to 23.4 ± 3.1 g, n = 8, P < 0.05), plasma free fatty acids (0.124 ± 0.033 to 0.057 ± 0.010 mM, n = 8, P < 0.01), and plasma triacylglycerol (0.978 ± 0.174 to 0.588 ± 0.115 mM, n = 8, P < 0.05). Chronic exercise tended to decrease BW and stimulated ANP (4- to 5-fold) and OTR gene expression in the LV and RA and BNP and inducible NOS (iNOS) mRNA in the LV. In sham-operated rats, exercise augmented ANP expression in the RA, downregulated GC-A mRNA in the LV and RA, but increased its expression threefold in the RA of OVX animals. Endothelial NOS and iNOS expression was enhanced in the left atrium of sham-operated rats. Altogether, these data indicate that in OVX animals, chronic exercise significantly enhances cardiac OT, NPs, and NOS, thus implicating all three hormonal systems in the beneficial effects of exercise training.

The purpose of the present study was to investigate the effects of a high-fat diet (HFD) in previously trained rats that have been detrained for different periods. Two groups of female rats were, first, either treadmill trained for 8 weeks or remained sedentary (Sed). Trained animals, thereafter, remained inactive for 4 weeks (Inact-4 weeks), while fed a standard diet, before being submitted to a high-fat diet (42% kcal of fat) for an additional 2 or 6 weeks. The order was reversed in a 3rd group in which rats were first kept sedentary for 4 weeks before being submitted to the same 8-week training program that ended with the initiation of the HFD (Inact-0 week). Fat accumulation in the mesenteric depot (P0.05) and in the sum of 3 intra-abdominal (urogenital, retroperitoneal, and mesenteric; P=0.065) tissues in response to the HF feeding was higher in trained rats kept inactive for 4 weeks than in Sed and Inact-0 week animals. Liver triacylglycerol accumulation also showed a tendency to be higher (P0.07) in Inact-4 weeks than in Inact-0 week rats. These changes were not associated with significant changes in fat cell diameter and number in the mesenteric adipose tissue. When rats in all groups were subdivided into obesity prone (OP) and obesity resistant (OR) on the basis of the change in body weight gain in response to the HFD, liver lipid infiltration was higher (P0.01) in OP Inact-4 weeks rats than in all other groups. The present results indicate that previously trained rats that have been inactive for a while maintain higher body adiposity in response to a HFD than in freshly inactive and sedentary rats.

Studies have revealed that high-fat (HF) diets promote hyperglycaemia, whole-body insulin resistance and non-alcoholic fatty liver disease (NAFLD). Recently, hepatic glucagon resistance has been shown to occur in rats fed a HF diet. More precisely, diet-induced obesity (DIO) reduces the number of hepatic plasma membrane glucagon receptors (GR), which results in a diminished response to glucagon during a hyperglucagonaemic clamp. The present study was undertaken to test the hypothesis that a HF-DIO is associated with a desensitization and destruction of the hepatic GR. We also hypothesized that a single bout of endurance exercise would modify the GR cellular distribution under our DIO model. Male rats were either fed a standard (SD) or a HF diet for two weeks. Each group was subdivided into a non-exercised (Rest) and an acute exercised (EX) group. The HF diet resulted in a reduction of total hepatic GR (55%) and hepatic plasma membrane GR protein content (20%). These changes were accompanied by a significant increase in endosomal and lysosomal GR content with the feeding of a HF diet. The reduction of GR plasma membrane as well as the increase in endosomal GR was strongly correlated with an increase of PKC-alpha, suggesting a role of PKC-alpha in GR desensitization. EX increased significantly PKC-alpha protein content in both diets, suggesting a role of PKC-alpha in EX-induced GR desensitization. The present results suggest that liver lipid infiltration plays a role in reducing glucagon action in the liver through a reduction in total cellular and plasma membrane GR content. Furthermore, the GR desensitization observed in our in vivo model of HF diet-induced hepatic steatosis and in EX individuals may be regulated by PKC-alpha.

Background The purpose of the study was to evaluate the effects of high dietary cholesterol in ovariectomized (Ovx) rats on several key markers of hepatic cholesterol and bile acid metabolism. Method Ovx and sham operated (Sham) rats were given either a standard diet (SD), a SD diet supplemented with 0.25 % cholesterol (SD + Chol), or a high fat diet supplemented with 0.25 % cholesterol (HF + Chol) for 5 weeks. Results Ovx was associated with higher (P

The purpose of the present study was to determine the time course of changes inin vitrolipolysis and in perilipin content (Western blot) in the mesenteric and/or the retroperitoneal fat depots in relation to the development of hepatic steatosis in high-fat diet-fed rats. Female Sprague-Dawley rats were submitted to a high-fat diet (HF diet; 42% as kJ) or a standard diet (SD diet) for 1, 2, 3 or 8 weeks. Fat accretion in the mesenteric and retroperitoneal tissues was higher (PP−4to 10−7m-isoproterienol) in the mesenteric and retroperitoneal fat depots was not changed during the first 3 weeks, regardless of the diet. Lipolysis in the mesenteric adipose tissue in the basal and stimulated states was, however, higher (PP>0·05) effects of diet and time on perilipin content of mesenteric tissue. In spite of a rapid fat accretion, the present results do not provide any evidence of a rapid (3 weeks) increase inin vitrolipolysis in intra-abdominal fat depots upon the undertaking of an HF diet at a time where liver lipid infiltration is the most significant.

The purpose of the present study was to test the hypothesis that short-term alternations of high-fat with normal chow feeding result in higher fat accumulation in liver than continuous intake of the same high-fat diet. Male Sprague-Dawley rats (7 weeks of age) were divided into 3 groups according to diet composition: standard chow (SD; 12,5% kcal as fat), high-fat (HF; 42% kcal as fat), and food cycles (FC) consisting of 10-day alternations between HF and SD diets beginning with the high-fat diet. Rats in each of these 3 groups were sacrificed after 10, 30, and 50 days (n = 10 rats/sub-groups). Energy intake, body weight, liver and muscle relative weights were not significantly (P0.05) different between FC- and HF-fed rats. Using the total energy intake for the 50-day period, it was calculated that approximately 30% less calories as fat was ingested in the FC- compared to the HF-fed rats. In spite of this, liver lipid infiltration as well as fat accretion in abdominal adipose tissues were increased (P0.01) similarly in FC- and HF-fed rats. Plasma FFA and insulin levels depicted strong tendencies (P0.07) to be higher in FC- than in continuous HF-fed rats at the end of the 50-day period. These results indicate that, despite a 30% reduction in ingested lipids, alternations of HF with normal chow diet compared to the continuous hyperlipidic diet caused the same level of infiltration of lipids in the liver and in the abdominal adipose tissues and, to a certain extent, may even result in a larger deterioration of the metabolic profile.

Previous data have demonstrated that, to handle the oxidative stress encountered with training at high intensity, skeletal muscle relies on an increase in mitochondrial biogenesis, a reduced H(2)O(2) production, and an enhancement of antioxidant enzymes. In the present study, we evaluated the influence of voluntary running on mitochondrial O(2) consumption and H(2)O(2) production by intermyofibrillar mitochondria (IFM) and subsarcolemmal mitochondria (SSM) isolated from oxidative muscles in conjunction with the determination of antioxidant capacities. When mitochondria are incubated with succinate as substrate, both maximal (state 3) and resting (state 4) O(2) consumption were significantly lower in SSM than in IFM populations. Mitochondrial H(2)O(2) release per unit of O(2) consumed was 2-fold higher in SSM than in IFM. Inhibition of H(2)O(2) formation by rotenone suggests that complex I of the electron transport chain is likely the major physiological H(2)O(2)-generating system. In Lou/C rats (an inbred strain of rats of Wistar origin), neither O(2) consumption nor H(2)O(2) release by IFM and SSM were affected by long-term, voluntary wheel training. In contrast, glutathione peroxidase and catalase activity were significantly increased despite no change in oxidative capacities with long-term, voluntary exercise. Furthermore, chronic exercise enhanced heat shock protein 72 accumulation within skeletal muscle. It is concluded that the antioxidant status of muscle can be significantly improved by prolonged wheel exercise without necessitating an increase in mitochondrial oxidative capacities.