Differential Impact of Calcium and Vitamin D on Body Composition Changes in Post-Menopausal Women Following a Restricted Energy Diet and Exercise Program

Vitamin D and calcium supplementation have been posited to improve body composition and different formulations of calcium may impact bioavailability. However, data are lacking regarding the combinatorial effects of exercise, diet, and calcium and/or vitamin D supplementation on body composition changes in post-menopausal women. Herein, 128 post-menopausal women (51.3 ± 4.5 years, 36.4 ± 5.7 kg/m2, 46.2 ± 4.5% fat) were assigned to diet and supplement groups while participating in a supervised circuit-style resistance-training program (3 d/week) over a 14-week period. Diet groups included: (1) normal diet (CTL), (2) a low-calorie, higher protein diet (LCHP; 1600 kcal/day, 15% carbohydrates, 55% protein, 30% fat), and (3) a low-calorie, higher carbohydrate diet (LCHC; 1600 kcal/day, 55% carbohydrates, 15% protein, 30% fat). Supplement groups consisted of: (1) maltodextrin (PLA), (2) 800 mg/day of calcium carbonate (Ca), and (3) 800 mg/day of calcium citrate and malate and 400 IU/day of vitamin D (Ca+D). Fasting blood samples, body composition, resting energy expenditure, aerobic capacity, muscular strength and endurance measures were assessed. Data were analyzed by mixed factorial ANOVA with repeated measures and presented as mean change from baseline [95% CI]. Exercise training promoted significant improvements in strength, peak aerobic capacity, and blood lipids. Dieting resulted in greater losses of body mass (CTL −0.4 ± 2.4; LCHC −5.1 ± 4.2; LCHP −3.8 ± 4.2 kg) and fat mass (CTL −1.4 ± 1.8; LCHC −3.7 ± 3.7; LCHP −3.4 ± 3.4 kg). When compared to LCHC-PLA, the LCHC + Ca combination led to greater losses in body mass (PLA −4.1 [−6.1, −2.1], Ca −6.4 [−8.1, −4.7], Ca+D −4.4 [−6.4, −2.5] kg). In comparison to LCHC-Ca, the LCHC-Ca+D led to an improved maintenance of fat-free mass (PLA −0.3 [−1.4, 0.7], Ca −1.4 [−2.3, −0.5], Ca+D 0.4 [−0.6, 1.5] kg) and a greater loss of body fat (PLA −2.3 [−3.4, −1.1], Ca −1.3 [−2.3, −0.3], Ca+D −3.6 [−4.8, −2.5]%). Alternatively, no significant differences in weight loss or body composition resulted when adding Ca or Ca+D to the LCHP regimen in comparison to when PLA was added to the LCHP diet. When combined with an energy-restricted, higher carbohydrate diet, adding 800 mg of Ca carbonate stimulated greater body mass loss compared to when a PLA was added. Alternatively, adding Ca+D to the LCHC diet promoted greater% fat changes and attenuation of fat-free mass loss. Our results expand upon current literature regarding the impact of calcium supplementation with dieting and regular exercise. This data highlights that different forms of calcium in combination with an energy restricted, higher carbohydrate diet may trigger changes in body mass or body composition while no impact of calcium supplementation was observed when participants followed an energy restricted, higher protein diet

Effects of Adherence to a Higher Protein Diet on Weight Loss, Markers of Health

Resistance training and maintenance of a higher protein diet have been recommended to help older individuals maintain muscle mass. This study examined whether adherence to a higher protein diet while participating in a resistance-based exercise program promoted more favorable changes in body composition, markers of health, and/or functional capacity in older females in comparison to following a traditional higher carbohydrate diet or exercise training alone with no diet intervention. In total, 54 overweight and obese females (65.9 ± 4.7 years; 78.7 ± 11 kg, 30.5 ± 4.1 kg/m2, 43.5 ± 3.6% fat) were randomly assigned to an exercise-only group (E), an exercise plus hypo-energetic higher carbohydrate (HC) diet, or a higher protein diet (HP) diet. Participants followed their respective diet plans and performed a supervised 30-min circuit-style resistance exercise program 3 d/wk. Participants were tested at 0, 10, and 14 weeks. Data were analyzed using univariate, multivariate, and repeated measures general linear model (GLM) statistics as well as one-way analysis of variance (ANOVA) of changes from baseline with [95% confidence intervals]. Results revealed that after 14 weeks, participants in the HP group experienced significantly greater reductions in weight (E −1.3 ± 2.3, [−2.4, −0.2]; HC −3.0 ± 3.1 [−4.5, −1.5]; HP −4.8 ± 3.2, [−6.4, −3.1]%, p = 0.003), fat mass (E −2.7 ± 3.8, [−4.6, −0.9]; HC −5.9 ± 4.2 [−8.0, −3.9]; HP −10.2 ± 5.8 [−13.2, –7.2%], p \u3c 0.001), and body fat percentage (E −2.0 ± 3.5 [−3.7, −0.3]; HC −4.3 ± 3.2 [−5.9, −2.8]; HP −6.3 ± 3.5 [−8.1, −4.5] %, p = 0.002) with no significant reductions in fat-free mass or resting energy expenditure over time or among groups. Significant differences were observed in leptin (E −1.8 ± 34 [−18, 14]; HC 43.8 ± 55 [CI 16, 71]; HP −26.5 ± 70 [−63, −9.6] ng/mL, p = 0.001) and adiponectin (E 43.1 ± 76.2 [6.3, 79.8]; HC −27.9 ± 33.4 [−44.5, −11.3]; HP 52.3 ± 79 [11.9, 92.8] µg/mL, p = 0.001). All groups experienced significant improvements in muscular strength, muscular endurance, aerobic capacity, markers of balance and functional capacity, and several markers of health. These findings indicate that a higher protein diet while participating in a resistance-based exercise program promoted more favorable changes in body composition compared to a higher carbohydrate diet in older females

Atg9 establishes Atg2-dependent contact sites between the endoplasmic reticulum and phagophores

The autophagy-related (Atg) proteins play a key role in the formation of autophagosomes, the hallmark of autophagy. The function of the cluster composed by Atg2, Atg18, and transmembrane Atg9 is completely unknown despite their importance in autophagy. In this study, we provide insights into the molecular role of these proteins by identifying and characterizing Atg2 point mutants impaired in Atg9 binding. We show that Atg2 associates to autophagosomal membranes through lipid binding and independently from Atg9. Its interaction with Atg9, however, is key for Atg2 confinement to the growing phagophore extremities and subsequent association of Atg18. Assembly of the Atg9-Atg2-Atg18 complex is important to establish phagophore-endoplasmic reticulum (ER) contact sites. In turn, disruption of the Atg2-Atg9 interaction leads to an aberrant topological distribution of both Atg2 and ER contact sites on forming phagophores, which severely impairs autophagy. Altogether, our data shed light in the interrelationship between Atg9, Atg2, and Atg18 and highlight the possible functional relevance of the phagophore-ER contact sites in phagophore expansion