BackgroundQuality indicators for nutritional therapy (QINT) are important in assessing care and monitoring of resources. Among the 30 indicators proposed by International Life Sciences Institute, Brazil, there is still no evaluation of the most pertinent for Pediatrics.ObjectiveTo list the 10 main quality indicators for nutritional therapies (QINTs) for Pediatrics.MethodsThis was a two-phase cross-sectional study. Firstly, a questionnaire was answered by physicians, nutritionists, nurses, and pharmacists, all with having experience in nutritional therapy (NT) with Pediatrics, in Rio de Janeiro, Brazil. Participants assessed four attributes of QINT by using the Likert scale. A Top 10 ranked QINT list for Pediatrics was established. To verify the consistency of the questionnaire, Cronbach’s Alpha coefficient was calculated. Secondly, the opinions of the participants on the results that were obtained were requested and the percentages of the positive responses were calculated.ResultsA total of 33 professionals participated in the first phase and 92% (n = 23 of 25) in the second phase approved the results of the selected indicators. Among the Top 10 QINTs, the three main ones were: #1: “Frequency of diarrhea in those patients on enteral nutrition” (mean = 13.194; α = 0.827); #2: “Frequency of dietary nutritional prescriptions upon the hospital discharge of the NT patients” (mean = 12.871; α = 0.822); #3: “Frequency of the NT patients who recovered their oral intake” (mean = 12.839; α = 0.859).ConclusionWhen considering the consistency and the concordance that were obtained, it can be suggested that the list of Top 10 QINTs as proposed in this study will help in the evaluation of NT quality indicators for Pediatrics.

Fructose intake is associated with cardiometabolic disorders, but few studies investigated its role on vascular reactivity and the potential effects of exercise training. Thus, we assessed the effect of fructose intake on vascular reactivity in trained rats. Therefore male Wistar rats (n=7/group) received tap water (control group, C) or Fructose 10% (F group) ad libitum for two weeks. Then, rats underwent treadmill exercise for eight weeks (FT group). Caloric intake was higher in fructose groups compared with C group (P<0.01), although we found no change in body weight and in lipid profile, except the higher HDL in FT group (P<0.01). Training increased serum NO (C=296.5±42.8; F=325.8±51.6; FT=718.4±151.2; P<0.01). Regarding body composition, F increased body fat content compared with C and FT groups (P=0.03), whereas the FT group showed higher protein content (P<0.01). Finally, vascular vasoconstrictor reactivity was increased by fructose since F group required lower concentrations of phenylephrine to promote 50% of the maximum contractile effect when compared to C and FT groups (C=1.31‐6±2.4‐7; F=2.43‐7±6.5‐8; FT= 7.99‐7±1.5‐7 M; P<0,01). Vasodilator response to acetylcholine was also impaired in F group and was preserved by exercise training (C= 3.13‐7±1.9‐7; F=3.64‐6±9.6‐7; FT=3.13‐7±1.9‐7M; P<0.01). Thus, aerobic exercise prevented fructose‐impaired vascular reactivity in rats. Grant Funding Source: CNPq, FAPERJ, CAPES, FINEP

During the onset of cardiovascular disease (CVD), disturbances in myocardial vascularization, cell proliferation and protein expression are observed. Aerobic training prevents CVD, but the underlying mechanisms behind left ventricle (LV) hypertrophy are not fully elucidated. The aim of this study was to investigate the mechanisms by which aerobic training protects the heart from LV hypertrophy during the onset of fructose-induced cardiometabolic disease. Male Wistar rats were allocated to four groups (n = 8/group): control sedentary (C), control training (CT), fructose sedentary (F) and fructose training (FT). The C and CT groups received drinking water, and the F and FT groups received D-fructose (10% in water). After 2 weeks, the CT and FT rats were assigned to a treadmill training protocol at moderate intensity for 8 weeks (60 min/day, 4 days/week). After 10 weeks, LV morphological remodelling, cardiomyocyte apoptosis, microRNAs and the insulin signalling pathway were investigated. The F group had systemic cardiometabolic alterations, which were normalised by aerobic training. The LV weight increased in the FT group, myocardium vascularisation decreased in the F group, and the cardiomyocyte area increased in the CT, F and FT groups. Regarding protein expression, total insulin receptor β-subunit (IRβ) decreased in the F group; phospho (p)-IRβ and phosphoinositide 3-kinase (PI3K) increased in the FT group; total-AKT and p-AKT increased in all of the groups; p-p70S6 kinase (p70S6K) protein was higher in the CT group; and p-extracellular signal-regulated kinase (ERK) increased in the CT and FT groups. MiR-126, miR-195 and cardiomyocyte apoptosis did not differ among the groups. Aerobic training activates p-p70S6K and p-ERK, and during the onset of a CVD, it can activate the IRβ-PI3K-AKT pathway.

L-Arginine and chronic exercise reduce oxidative stress. However, it is unclear how they affect cardiomyocytes during cardiovascular disease (CVD) development. The aim of this research was to investigate the possible effects of L-arginine supplementation and aerobic training on systemic oxidative stress and their consequences on cardiomyocytes during cardiometabolic disease onset caused by excess fructose. Wistar rats were allocated into four groups: control (C), fructose (F, 10% fructose in water), fructose training (FT; moderate running, 50-70% of the maximal velocity), and fructose arginine (FA; 880 mg/kg/day). Fructose was given for two weeks and fructose plus treatments for the subsequent eight weeks. Body composition, blood glucose, insulin, lipid profile, lipid peroxidation, nitrite, metalloproteinase-2 (MMP-2) activity, left ventricle histological changes, microRNA-126, -195, and -146, eNOS, p-eNOS, and TNF-α expressions were analyzed. Higher abdominal fat mass, triacylglycerol level, and insulin level were observed in the F group, and both treatments reversed these alterations. Myocardial vascularization was impaired in fructose-fed groups, except in FT. Cardiomyocyte hypertrophy was observed in all fructose-fed groups. TNF-α levels were higher in fructose-fed groups than in the C group, and p-eNOS levels were higher in the FA than in the C and F groups. Lipid peroxidation was higher in the F group than in the FT and C groups. During CVD onset, moderate aerobic exercise reduced lipid peroxidation, and both training and L-arginine prevented metabolic changes caused by excessive fructose. Myocardial vascularization was impaired by fructose, and cardiomyocyte hypertrophy appeared to be influenced by pro-inflammatory and oxidative environments.