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Objetivo: Identificar os verdadeiros efeitos da restrição calórica (RC) sobre o consumo máximo de oxigênio (VO2máx) relativo e absoluto e força muscular. Métodos: Uma revisão sistemática foi conduzida em 5 bancos de dados, até novembro de 2019. Vinte e oito ensaios controlados foram incluídos nas meta-análises comparando RC sozinho vs. Dieta padrão (RC vs. controle) ou comparando RC mais treinamento físico vs. treinamento de exercício sozinho (RC + EX vs. EX) sobre o VO2máx e a força muscular. Resultados: RC + EX teve um efeito positivo para o VO2máx relativo (1,13 [0,49; 1,78]ml/kg/min, p

Low-density lipoprotein receptor-related protein-1 (LRP1) plays an important role in regulating energy homeostasis, the integrity of the blood-brain barrier, and metabolic signal transport across the brain, while its dysfunction has been associated with cognitive decline, dementia, and Alzheimer’s disease. However, the impact of LRP1 in GABAergic neurons on neurodegeneration and memory is poorly understood. Mice lacking LRP1 in GABAergic neurons (Vgat-Cre; LRP1loxP/loxP) were subjected to behavioral tests for memory and learning. Here we show that the loss of LRP1 in GABAergic neurons causes significant impairment in short-term memory. The spatial Y-maze test revealed that Vgat-Cre; LRP1loxP/loxP mice exhibited decreased travel distance and duration in the novel arm compared to the controls (LRP1loxP/loxP mice). A reduction in correct responses to find the escape platform in the water T-maze test was found when LRP1 is absent in GABAergic neurons. Moreover, the distance and duration in the novel arm as well as the performance of the reversal water T-maze test were negatively correlated with body weight as well as serum levels of leptin, insulin, and ApoJ. Mice lacking LRP1 in GABAergic neurons displayed decreased freezing time in the contextual and cued fear conditioning test. Histopathological evaluation of the hippocampus revealed that Vgat-Cre; LRP1loxP/loxP mice had greater neuronal necrosis and neuroinflammation than those of LRP1loxP/loxP mice. These findings suggest that LRP1 in GABAergic neurons may play a crucial role in maintaining normal memory function and could be a molecular target for neurodegenerative diseases such as Alzheimer’s disease.

Obesity is a chronic, non-transmissible and multifactorial disease commonly associated with systemic inflammation and damage to health. This disorder has been pointed out as leading to the development of a diversity of eye diseases and, consequently, damage to visual acuity. More specifically, cardiometabolic risk is associated with lacrimal gland dysfunctions, since it changes the inflammatory profile favoring the development and worsening of dry eye disease. In more severe and extreme cases, obesity, inflammation, and diabetes mellitus type 2 can trigger the total loss of vision. In this scenario, besides its numerous metabolic functions, clusterin, an apolipoprotein, has been described as protective to the ocular surface through the seal mechanism. Thus, the current review aimed to explain the role of clusterin in dry eye disease that can be triggered by obesity and diabetes.

Obesity is a chronic, non-transmissible and multifactorial disease commonly associated with systemic inflammation and damage to health. This disorder has been pointed out as leading to the development of a diversity of eye diseases and, consequently, damage to visual acuity. More specifically, cardiometabolic risk is associated with lacrimal gland dysfunctions, since it changes the inflammatory profile favoring the development and worsening of dry eye disease. In more severe and extreme cases, obesity, inflammation, and diabetes mellitus type 2 can trigger the total loss of vision. In this scenario, besides its numerous metabolic functions, clusterin, an apolipoprotein, has been described as protective to the ocular surface through the seal mechanism. Thus, the current review aimed to explain the role of clusterin in dry eye disease that can be triggered by obesity and diabetes.

Obesity is closely related to insulin resistance and type 2 diabetes genesis. The liver is a key organ to glucose homeostasis since insulin resistance in this organ increases hepatic glucose production (HGP) and fasting hyperglycemia. The protein-tyrosine phosphatase 1B (PTP1B) may dephosphorylate the IR and IRS, contributing to insulin resistance in this organ. Aerobic exercise is a great strategy to increase insulin action in the liver by reducing the PTP1B content. In contrast, no study has shown the direct effects of strength training on the hepatic metabolism of PTP1B. Therefore, this study aims to investigate the effects of short-term strength exercise (STSE) on hepatic insulin sensitivity and PTP1B content in obese mice, regardless of body weight change. To achieve this goal, obese Swiss mice were submitted to a strength exercise protocol lasting 15 days. The results showed that STSE increased Akt phosphorylation in the liver and enhanced the control of HGP during the pyruvate tolerance test. Furthermore, sedentary obese animals increased PTP1B content and decreased IRS-1/2 tyrosine phosphorylation, however, STSE was able to reverse this scenario. Therefore, we conclude that STSE is an important strategy to improve the hepatic insulin sensitivity and HGP by reducing the PTP1B content in the liver of obese mice, regardless of changes in body weight.

Obesity is a disease characterized by the exacerbated increase of adipose tissue. A possible way to decrease the harmful effects of excessive adipose tissue is to increase the thermogenesis process, to the greater energy expenditure generated by the increase in heat in the body. In adipose tissue, the thermogenesis process is the result of an increase in mitochondrial work, having as substrate H+ ions, and which is related to the increased activity of UCP1. Evidence shows that stress is responsible for increasing the greater induction of UCP1 expression via β-adrenergic receptors. It is known that physical exercise is an important implement for sympathetic stimulation promoting communication between norepinephrine/epinephrine with membrane receptors. Thus, the present study investigates the influence of short-term strength training (STST) on fatty acid composition, lipolysis, lipogenesis, and browning processes in the subcutaneous adipose tissue (sWAT) of obese mice. For this, Swiss mice were divided into three groups: lean control, obesity sedentary, and obese strength training (OBexT). Obese animals were fed a high-fat diet for 14 weeks. Trained obese animals were submitted to 7 days of strength exercise. It was demonstrated that STST sessions were able to reduce fasting glycemia. In the sWAT, the STST was able to decrease the levels of the long-chain fatty acids profile, saturated fatty acid, and palmitic fatty acid (C16:0). Moreover, it was showed that STST did not increase protein levels responsible for lipolysis, the ATGL, ABHD5, pPLIN1, and pHSL. On the other hand, the exercise protocol decreased the expression of the lipogenic enzyme SCD1. Finally, our study demonstrated that the STST increased browning process-related genes such as PGC-1α, PRDM16, and UCP1 in the sWAT. Interestingly, all these biomolecular mechanisms have been observed independently of changes in body weight. Therefore, it is concluded that short-term strength exercise can be an effective strategy to initiate morphological changes in sWAT.

Obesity is linked to a reduction in the control of hepatic glucose production, which is the primary mechanism related to fasting hyperglycemia and the development of type 2 diabetes mellitus (T2DM). The main system involved in hepatic gluconeogenesis synthesis is controlled by pyruvate carboxylase (PC), which increases in obesity conditions. Recently, we showed that short-term strength training is an important tool against obesity-induced hyperglycemia. As aerobic exercise can reduce the hepatic PC content of obese animals, we hypothesized that strength exercise can also decrease this gluconeogenic enzyme. Therefore, this study investigated whether the metabolic benefits promoted by short-term strength training are related to changes in hepatic PC content. Swiss mice were divided into three groups: lean control (Ctl), obese sedentary (ObS), and obese short-term strength training (STST). The STST protocol was performed through one session/day for 15 days. The obese exercised animals had reduced hyperglycemia and insulin resistance. These results were related to better control of hepatic glucose production and hepatic insulin sensitivity. Our bioinformatics analysis showed that hepatic PC mRNA levels have positive correlations with glucose levels and adiposity, and negative correlations with locomotor activity and muscle mass. We also found that hepatic mRNA levels are related to lipogenic markers in the liver. Finally, we observed that the obese animals had an increased hepatic PC level; however, STST was efficient in reducing its amount. In conclusion, we provide insights into new biomolecular mechanisms by showing how STST is an efficient tool against obesity-related hyperglycemia and T2DM, even without body weight changes.

Excess of adipose tissue increases the concentration of proinflammatory cytokines, triggering a subclinical inflammatory condition. This inflammatory profile contributes to retina damage, which can lead to retinal dysfunction and reduced vision. Regularly practicing both aerobic and strength exercises is well known for promoting anti-inflammatory effects on different organs in the peripheral and central regions. However, the effects of combined physical exercise (CPE, strength + aerobic) on the inflammatory process in the retina tissue are not yet known. This study aimed to investigate the effects of CPE on the inflammatory profile of the retina in obese mice. Swiss mice were distributed into control, sedentary obese, and trained obese groups. The trained obese group was subjected to short-term CPE, 1 h/day, for 7 days. The CPE was composed of aerobic and strength exercises in the same exercise session. The strength exercise protocol consisted of 10 climbing series, with 12 &plusmn, 1 dynamic climbing movements at 70% of the maximum voluntary carrying capacity (MVCC), and the aerobic exercise protocol consisted of 30 min of treadmill running, with an intensity of 75% of the exhaust velocity. Subsequently, the retina was excised and analyzed by Western blot. Obese animals presented impairment on glucose homeostasis and elevated levels of proinflammatory proteins in the serum and retina, however, CPE was effective in reversing these parameters, independently of changes in body adiposity. Therefore, for the first time, we have shown that short-term CPE can be an important strategy to treat an inflammatory profile in the retina.

Made available in DSpace on 2022-04-28T19:47:02Z (GMT). No. of bitstreams: 0 Previous issue date: 2021-12-15 Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) Hepatic steatosis is directly associated with hepatic inflammation and insulin resistance, which is correlated with hyperglycemia and type 2 diabetes mellitus (T2DM). Aerobic and strength training have been pointed out as efficient strategies against hepatic steatosis. However, little is known about the effects of the combination of those two protocols on hepatic steatosis. Therefore, this study aimed to evaluate the impact of short-term combined training (STCT) on glucose homeostasis and in the synthesis and oxidation of fat in the liver of obesity-induced mice with hepatic steatosis. Swiss mice were distributed into three groups: control lean (CTL), sedentary obese (OB), and combined training obese (CTO). The CTO group performed the STCT protocol, which consisted of strength and aerobic exercises in the same session. The protocol lasted seven days. The CTO group reduced the glucose levels and fatty liver when compared to the OB group. Interestingly, these results were observed even without reductions in body adiposity. CTO group also showed increased hepatic insulin sensitivity, with lower hepatic glucose production (HGP). STCT reduced the expression of the lipogenic genes Fasn and Scd1 and hepatic inflammation, as well as increased the ACC phosphorylation and the oxidative genes Cpt1a and Ppara, reverting the complications caused by obesity. Since this protocol increased lipid oxidation and reduced hepatic lipogenesis, regardless of body fat mass decrease, it can be considered an effective non-pharmacological strategy for the treatment of hepatic steatosis. Exercise Cell Biology Lab Faculty of Applied Sciences University of Campinas Laboratory of Nutritional Genomics Faculty of Applied Sciences University of Campinas Motricity Sciences Institute of Biosciences São Paulo State University Julio de Mesquita Filho Multidisciplinary Laboratory of Food and Health Faculty of Applied Sciences University of Campinas School of Physical Education and Sport of Ribeirão Preto University of São Paulo (USP) Postgraduate Program in Rehabilitation and Functional Performance Ribeirão Preto Medical School USP Laboratory of Molecular Biology of Exercise Faculty of Applied Sciences University of Campinas Motricity Sciences Institute of Biosciences São Paulo State University Julio de Mesquita Filho FAPESP: 2015/07199-2 FAPESP: 2016/12569-6 FAPESP: 2016/24406-4

Loss of cardiomyocytes occurs with aging and contributes to cardiovascular complications. In the present study, we highlighted the role of clusterin, a protein that has recently been associated with the protection of cardiomyocytes from apoptosis. Clusterin protects cardiac cells against damage from myocardial infarction, transplant, or myocarditis. Clusterin can act directly or indirectly on apoptosis by regulating several intracellular pathways. These pathways include (1) the oxidant and inflammatory program, (2) insulin growth factor 1 (IGF-1) pathway, (3) KU70 / BCL-2-associated X protein (BAX) pathway, (4) tumor necrosis factor alpha (TNF-α) pathway, (5) BCL-2 antagonist of cell death (BAD) pathway, and (6) mitogen-activated protein kinase (MAPK) pathway. Given the key role of clusterin in preventing loss of cardiac tissue, modulating the expression and function of this protein carries the potential of improving cardiovascular care in the future.

The present study verified the responses of proteins related to the autophagy pathway after 10 h of fast with resistance exercise and protein ingestion in skeletal muscle and liver samples. The rats were distributed into five experimental groups: control (CT, sedentary and without gavage after fast), exercise immediately (EXE-imm, after fast, rats were submitted to the resistance protocol and received water by gavage immediately after exercise), exercise after 1 h (EXE-1h, after fast, rats were submitted to the resistance protocol and received water by gavage 1 h after exercise), exercise and supplementation immediately after exercise (EXE/Suppl-imm, after fast, rats were submitted to the resistance protocol and received a mix of casein: whey protein 1:1 (w/w) by gavage immediately after exercise), exercise and supplementation 1 h after exercise (EXE/Suppl-1h, after fast, rats were submitted to the resistance protocol and received a mix of casein: whey protein 1:1 (w/w) by gavage 1 h after exercise). In summary, the current findings show that the combination of fasting, acute resistance exercise, and protein blend ingestion (immediately or 1 h after the exercise stimulus) increased the serum levels of leucine, insulin, and glucose, as well as the autophagy protein contents in skeletal muscle, but decreased other proteins related to the autophagic pathway in the liver. These results deserve further mechanistic investigations since athletes are combining fasting with physical exercise to enhance health and performance outcomes.

A obesidade pode ser responsavel pela perda da acuidade visual. Recentemente uma proteina conhecida como Clusterina tem sido descrita como protetora de superficie ocular. No entanto, ainda nao esta claro se o exercicio fisico e capaz de modular os niveis de clusterina na retina. Buscamos investigar o papel do exercicio combinado no metabolismo da clusterina na retina de camundongos obesos. Camundongos Swiss foram distribuidos em grupos controle (CT), obesos sedentarios (OBS) e obesos treinados (OBC). Os animais foram submetidos a um protocolo de exercicios combinados de curta duracao que consistiu em treinamento de forca em escada seguido de exercicio aerobio em esteira por 7 dias, totalizando 1h / dia. Posteriormente, a retina foi excisada e analisada por Western Blot e RT-PCR. O grupo OBC melhorou a sinalizacao de insulina em comparacao com CTS e OBS. Alem disso, o grupo OBC apresentou um aumento no conteudo de IL-10 e reducao do perfil pro-inflamatorio. Os niveis de clusterina reduziram-se, em media, 18% nos grupos OBC vs OBS. Em suma, o treinamento combinado mostrou-se eficiente na reducao do perfil inflamatorio atraves da diminuicao do conteudo das proteinas envolvidas e por consequencia melhora na acao da insulina. Alem disso, o exercicio foi capaz de reduzir os niveis de clusterina tecidual. Esta similaridade no comportamento, sugere que esta diminuicao se relacione com a acao anti-inflamatoria de clusterina.

E comprovado que a pratica de exercicio fisico e de jejum causam modificacoes morfofisiologicas no tecido adiposo branco (TAB) como o aumento na concentracao de mitocondrias e no conteudo de UCP-1, levando assim, ao begeamento desse tecido. Entretanto, ainda nao se sabe se a combinacao destas estrategias poderia potencializar tais efeitos. Diante disso, este projeto objetivou avaliar os efeitos agudos de tres protocolos gradativos de jejum (4h, 8h e 16h) no desempenho do exercicio de forca e em marcadores do begeamento do TAB. Para isto, camundongos C57BL/6J foram submetidos aos protocolos de jejum + exercicio de forca e tiveram os dados fisiologicos coletados, posteriormente, os animais foram eutanasiados para avaliar a expressao do mRNA do TAB. Os resultados fisiologicos encontrados, apontam que, o grupo 16HJ obteve um consumo maior do que os demais grupos num periodo de 24h apos o exercicio. Alem disso, em relacao ao teste de forca de resistencia, o grupo 16HJ apresentou um melhor desempenho que os grupos 4HJ e 8HJ, entretanto, nenhum dos grupos de jejum foi diferente do CT, indicando assim que a nao ha reducao da performance apos a pratica de jejum. Alem do mais, as analises biomoleculares de mRNA revelaram que os tempos de jejum de 8h e 16h poderiam ser melhor conciliados com o exercicio de forca para estimular o begeamento do TAB, uma vez que eles aumentaram os niveis de UCP1 e PGC1a, respectivamente.

A sarcopenia e cada vez mais recorrente sendo a reducao progressiva em todas as partes do corpo da forca e massa muscular,pode levar a uma disfuncao metabolica prejudicando a mobilidade, equilibrio e locomocao.Por outro lado o exercicio fisico de forca e uma ferramenta nao farmacologica importante na prevencao a sarcopenia,atua de maneira a promover contracoes musculares que estimulam a sintese proteica,aumentam a area de seccao transversa do musculo,resistencia,forca e atenua a perda de massa magra no processo de envelhecimento.O jejum melhora a sinalizacao da insulina, aumenta a secrecao do hormonio de crescimento e cortisol.Diante disso o objetivo do trabalho foi avaliar o efeito agudo de diferentes protocolos de jejum aliados ao exercicio de forca na performance de animais.Para isso camundongosC57BL/6J foram submetidos protocolos de jejum de 4h 8h e 16h,posteriormente, realizaram uma sessao de exercicio de forca.Os dados fisiologicos foram coletados,os animais foram eutanasiados para que analises biomoleculares fossem realizadas no tecido muscular.Ate o momento encontrou-se que o protocolo de jejum aliado ao treinamento de forca atuou de forma positiva em relacao ao teste de resistencia,promovendo um aumento de performance do grupo 16HJ em relacao aos grupos 4HJ E 8HJ.Houve reducao na ingestao alimentar do grupo 16 HJ em relacao aos outros grupos,nao houve perda de performance de nenhum dos grupos,indicando que a restricao alimentar nao prejudicou o desempenho dos animais.

Air pollution is comprised of several substances, including particulate matter (PM). Exposure to air pollution may trigger alterations in DNA methylation thus modifying gene expression patterns. This phenomenon is likely to mediate the relationship between exposure to air pollution and adverse health effects. The purpose of this study was analyzing the effects of exposure to PM2.5 during pregnancy or lactation and whether it would cause multigenerational epigenetic alterations in the promoter region of the genes Pdx1 and NEUROG3 within mouse pancreatic islets. Our results show that maternal exposure to PM2.5 led to an elevation in blood glucose levels within the two following generations (F1 and F2). There was also an increase in DNA methylation in the aforementioned promoter regions accompanied by reduced gene expression in generations F1 and F2 upon F0 exposure to PM2.5 during pregnancy. These data suggest that maternal exposure to PM2.5 from air pollution, particularly during pregnancy, may lead to a multigenerational and lifelong negative impact on glucose homeostasis mediated by an increase in DNA methylation within the promoter region of the genes Pdx1 and NEUROG3 in pancreatic islets.

Obesity and cardiovascular diseases are worldwide public health issues. In this review, we discussed the participation of ROCK protein in cardiac hypertrophy, mainly through the modulation of leptin and insulin signaling pathways. Leptin plays a role in cardiovascular disease development and, through the Rho-associated protein kinase (ROCK), promotes cardiac hypertrophy. ROCK protein, is regulated by small Rho-GTPases and has two isoforms with high homology. ROCK is able to activate the MAP kinase (MAPK) pathway and modulate insulin signaling in the heart, participating in cardiac hypertrophy development of concentric and eccentric left ventricle growth. Although different types of stimulus can lead to morphologically antagonistic heart growth, physical exercise promotes improvements in hemodynamic function, emerging as a promising non-pharmacological tool to improve overall health. Leptin can activate ROCK in a pathological way, increasing MAPK activity and decreasing insulin signaling via insulin receptor substrate 1 (IRS1) serine 307 residue phosphorylation, phosphatase and tensin homolog, and protein kinase Cβ2. In turn, physical exercise decreases leptin levels and positively modulates insulin signaling as well as increases ROCK-dependent IRS1 (Ser632/635) phosphorylation, improving phosphatidylinositol 3-kinase/protein kinase B axis and promoting physiologic heart growth. Currently, there is a lack of studies about differences in ROCK isoforms, especially during exercise and/or obesity. However, the understanding of its biological function and the complex mechanism underlying the distinct types of cardiac hypertrophy development can be a useful tool in the improvement and treatment of cardiovascular outcomes.

Obesity is a public health issue that affects more than 600 million adults worldwide. The disease is characterized by fat accumulation, mainly in the abdominal area. The human body is mainly composed of two types of adipose tissue: white adipose tissue (WAT) and brown adipose tissue (BAT); however, the browning process generates a different type of brown fat-like adipocyte in WAT, which similar to BAT has thermogenic capacity by activating UCP-1. The hypothalamic arcuate nucleus plays an important role in WAT browning via POMC neurons, which are influenced by synergistic insulin and leptin signaling. On the other hand, stimulation of AgRP neurons suppresses WAT browning. The hypothalamic inflammatory process that occurs in obesity impairs insulin and leptin signaling in this tissue and, consequently, can decrease WAT browning. In addition, practicing physical exercise may be a great strategy for triggering the browning process since it reduces hypothalamic inflammation and increases POMC neurons gene expression. Moreover, physical exercise stimulates irisin gene expression, which has an important impact on thermogenesis, which in turn culminates in increased gene expression of proteins such as UCP-1 and Cidea, which are related to WAT browning. Furthermore, thermogenetic activation of WAT leads to increased energy expenditure, favoring obesity treatment. Therefore, this mini-review aimed to highlight the most recent studies that link the control of hypothalamic activity with the browning metabolism of adipose tissue in response to physical exercise.

The study of zinc bioavailability in foods is important because this mineral intake does not meet the recommended doses for some population groups. Also, the presence of dietary factors that reduce zinc absorption contributes to its deficiency. Rice fortified with micronutrients (Ultra Rice®) is a viable alternative for fortification since this cereal is already inserted into the population habit. The aim of this study was to evaluate the bioavailability of zinc (Zn) in rice fortified with zinc oxide. During 42 days, rats were divided into four groups and fed with diets containing two different sources of Zn (test diet: UR® fortified with zinc oxide, or control diet: zinc carbonate (ZnCO3)), supplying 50% or 100%, respectively, of the recommendations of this mineral for animals. Weight gain, food intake, feed efficiency ratio, weight, thickness and length of femur; retention of zinc, calcium (Ca) and magnesium (Mg) in the femur and the concentrations of Zn in femur, plasma and erythrocytes were evaluated. Control diet showed higher weight gain, feed efficiency ratio, retention of Zn and Zn concentration in the femur (p < 0.05). However, no differences were observed (p > 0.05) for dietary intake, length and thickness of the femur, erythrocyte and plasmatic Zn between groups. Although rice fortified with zinc oxide showed a lower bioavailability compared to ZnCO3, this food can be a viable alternative to be used as a vehicle for fortification.

Fructose consumption has been growing exponentially and, concomitant with this, the increase in the incidence of obesity and associated complications has followed the same behavior. Studies indicate that fructose may be a carbohydrate with greater obesogenic potential than other sugars. In this context, the liver seems to be a key organ for understanding the deleterious health effects promoted by fructose consumption. Fructose promotes complications in glucose metabolism, accumulation of triacylglycerol in the hepatocytes and alterations in the lipid profile, which, associated with an inflammatory response and alterations in the redox state, will imply a systemic picture of insulin resistance. However, physical exercise has been indicated for the treatment of several chronic diseases. In this review, we show how each exercise protocol (aerobic, strength or a combination of both) promote improvements in the obesogenic state created by fructose consumption as an improvement in the serum and liver lipid profile (HDL increase and decrease TG and LDL levels) and a reduction of markers of inflammation caused by an excess of fructose. Therefore, it is concluded that the practice of aerobic physical exercise, strength or a combination of both is essential for attenuating the complications developed by the consumption of fructose.

Feeding is indicative of the nutritional status of children, however micronutrient deficiency is common in this age group. We evaluated the impact of inclusion of rice (Ultra Rice® (UR®)) fortified with iron, zinc, thiamin and folic acid on laboratory measurements and the nutrient intake of children. Ninety-nine preschoolers (2–6 years; 42.6% male) from two preschools participated, one of which received UR® added to polished rice as part of school meals (test preschool) and the other received only polished rice (control preschool). Biochemical evaluations were performed before and after four months of intervention. Feeding was assessed by direct weighing of food, complemented by 24-h recalls, and the diet was assessed by the Healthy Eating Index (HEI) adapted to the Brazilian reality. The fortified rice improved the levels of zinc (p < 0.001), thiamine (p < 0.001), folic acid (p = 0.003), mean corpuscular hemoglobin (p < 0.001) and mean corpuscular hemoglobin concentration (p < 0.001). The inadequacy percentages of thiamine, folic acid and iron were lower among preschoolers from the test preschool. This study demonstrated the effectiveness of using UR® on laboratory measurements of children. The inadequate intake of thiamine, folic acid and iron was also reduced, making the fortified rice an interesting strategy in school feeding programs.

Fructose consumption has been growing exponentially and, concomitant with this, the increase in the incidence of obesity and associated complications has followed the same behavior. Studies indicate that fructose may be a carbohydrate with greater obesogenic potential than other sugars. In this context, the liver seems to be a key organ for understanding the deleterious health effects promoted by fructose consumption. Fructose promotes complications in glucose metabolism, accumulation of triacylglycerol in the hepatocytes, and alterations in the lipid profile, which, associated with an inflammatory response and alterations in the redox state, will imply a systemic picture of insulin resistance. However, physical exercise has been indicated for the treatment of several chronic diseases. In this review, we show how each exercise protocol (aerobic, strength, or a combination of both) promote improvements in the obesogenic state created by fructose consumption as an improvement in the serum and liver lipid profile (high-density lipoprotein (HDL) increase and decrease triglyceride (TG) and low-density lipoprotein (LDL) levels) and a reduction of markers of inflammation caused by an excess of fructose. Therefore, it is concluded that the practice of aerobic physical exercise, strength training, or a combination of both is essential for attenuating the complications developed by the consumption of fructose.