Diet In Adulthood Research Articles

Adolescent food insecurity in female rodents and susceptibility to diet-induced obesity

Food insecurity is defined as having limited or uncertain access to nutritious foods, and adolescent food insecurity is associated with obesity and disordered eating behaviors in humans. We developed a rodent model of adolescent food insecurity to determine whether adolescent food insecurity per se promotes increased susceptibility to diet-induced obesity and altered eating behaviors during adulthood. Female juvenile Wistar rats were singly housed and assigned to three experimental diets: food-secure with standard chow (CHOW), food-secure with a high-fat/sugar Western diet (WD), and food-insecure with WD (WD-FI). Food-secure rats (CHOW and WD) received meals at fixed feeding times (9:00, 13:00, and 16:00). WD-FI rats received meals at unpredictable intervals of the above-mentioned feeding times but had isocaloric amounts of food to WD. We investigated the impact of adolescent food insecurity on motivation for sucrose (Progressive Ratio), approach-avoidance behavior for palatable high-fat food (Approach-Avoidance task), and susceptibility to weight gain and hyperphagia when given an obesogenic choice diet. Secondary outcomes were the effects of food insecurity during development on anxiety-like behaviors (Open Field and Elevated Plus Maze) and learning and memory function (Novel Location Recognition task). Rodents with adolescent food insecurity showed a greater trend of weight gain and significantly increased fat mass and liver fat accumulation on an obesogenic diet in adulthood, despite no increases in motivation for sucrose or high-fat food. These data suggest that adolescent unpredictable food access increases susceptibility to diet-induced fat gain without impacting food motivation or food intake in female rodents. These findings are among a small group of recent studies modeling food insecurity in rodents and suggest that adolescent food insecurity in females may have long-term implications for metabolic physiology later in life.

Chronic high-sugar diet in adulthood protects Caenorhabditis elegans from 6-OHDA-induced dopaminergic neurodegeneration

BackgroundDiets high in saturated fat and sugar, termed “Western diets,” have been associated with several negative health outcomes, including increased risk for neurodegenerative disease. Parkinson’s disease (PD) is the second most prevalent neurodegenerative disease and is characterized by the progressive death of dopaminergic neurons in the brain. We build upon previous work characterizing the impact of high-sugar diets in Caenorhabditis elegans to mechanistically evaluate the relationship between high-sugar diets and dopaminergic neurodegeneration.ResultsAdult high-glucose and high-fructose diets, or exposure from day 1 to 5 of adulthood, led to increased lipid content, shorter lifespan, and decreased reproduction. However, in contrast to previous reports, we found that adult chronic high-glucose and high-fructose diets did not induce dopaminergic neurodegeneration alone and were protective from 6-hydroxydopamine (6-OHDA) induced degeneration. Neither sugar altered baseline electron transport chain function and both increased vulnerability to organism-wide ATP depletion when the electron transport chain was inhibited, arguing against energetic rescue as a basis for neuroprotection. The induction of oxidative stress by 6-OHDA is hypothesized to contribute to its pathology, and high-sugar diets prevented this increase in the soma of the dopaminergic neurons. However, we did not find increased expression of antioxidant enzymes or glutathione levels. Instead, we found evidence suggesting downregulation of the dopamine reuptake transporter dat-1 that could result in decreased 6-OHDA uptake.ConclusionsOur work uncovers a neuroprotective role for high-sugar diets, despite concomitant decreases in lifespan and reproduction. Our results support the broader finding that ATP depletion alone is insufficient to induce dopaminergic neurodegeneration, whereas increased neuronal oxidative stress may drive degeneration. Finally, our work highlights the importance of evaluating lifestyle by toxicant interactions.

Early Life Polychlorinated Biphenyl 126 Exposure Disrupts Gut Microbiota and Metabolic Homeostasis in Mice Fed with High-Fat Diet in Adulthood.

Evidence supports the potential influence of persistent organic pollutants (POPs) on the pathogenesis and progression of obesity and diabetes. Diet-toxicant interactions appear to be important in diet-induced obesity/diabetes; however, the factors influencing this interaction, especially the early life environmental exposure, are unclear. Herein, we investigated the metabolic effects following early life five-day exposure (24 μg/kg body weight per day) to 3,3′,4,4′,5-pentacholorobiphenyl (PCB 126) at four months after exposure in mice fed with control (CTRL) or high-fat diet (HFD). Activation of aryl hydrocarbon receptor (AHR) signaling as well as higher levels of liver nucleotides were observed at 4 months after PCB 126 exposure in mice, independent of diet status. Inflammatory responses including higher levels of serum cytokines and adipose inflammatory gene expression caused by early life PCB 126 were observed only in HFD-fed mice in adulthood. Notably, early life PCB 126 exposure worsened HFD-induced impaired glucose homeostasis characterized by glucose intolerance and elevated gluconeogenesis and tricarboxylic acid (TCA) cycle flux without worsening the effects of HFD related to adiposity in adulthood. Furthermore, early life PCB 126 exposure resulted in diet-dependent changes in bacterial community structure and function later in life, as indicated by metagenomic and metabolomic analyses. These data contribute to a more comprehensive understanding of the interactions between diet and early life environmental chemical exposure.

Trpc5-regulated AMPKα/mTOR autophagy pathway is associated with glucose metabolism disorders in low birth weight mice under overnutrition

Previous studies have shown that low birth weight (LBW) individuals are at higher risk of glucose metabolism disorders compared with normal birth weight (NBW) individuals under overnutrition conditions, but the mechanism remains unclear. To explore the underlying mechanism of glucose metabolism disorders induced by LBW under overnutrition in adulthood, the prenatal malnutrition method was applied to ICR mice to establish the LBW mice model and high-fat diets were used to mimic overnutrition conditions. Then the mechanism was further explored on Hepg2 cells treated with nutritional deprivation plus palmitic acid. The results showed that LBW plus high-fat interventions will cause glucose metabolism disorders and inhibit autophagy flux in adulthood. Moreover, the expression of TRPC5-regulated AMPK/mTOR autophagy pathway was downregulated by LBW with high-fat interventions. Collectively, LBW plus high-fat intervention increased the risk of glucose metabolism disorders, which may be related to the alteration of TRPC5 expression level and its regulation of the AMPKα/mTOR autophagy pathway. This study may provide a fundamental basis for the molecular mechanism of glucose metabolism disorders induced by LBW with high-fat diets in adulthood and a new target for the treatment of metabolic diseases in LBW individuals.

Maternal Consumption of a Cafeteria Diet during Lactation Leads to Altered Diet-Induced Thermogenesis in Descendants after Exposure to a Western Diet in Adulthood.

This study investigates the ability of a maternal cafeteria diet during lactation to program brown adipose tissue (BAT) metabolic responses to an obesogenic diet re-exposure in the adult offspring after consuming a standard diet (SD). Nursing rats were fed an SD or a cafeteria diet during lactation. Their offspring (O-C and O-CAF, respectively) were weaned onto an SD, and at 16 weeks of age they were switched to a Western diet until week 24. Gene and protein expression in BAT were measured at PN22 and at 24 weeks. At PN22, compared to controls, O-CAF rats displayed lower mRNA levels of lipogenesis-related genes (Fasn), and higher expression of genes related to lipolysis (Pnpla2), fatty acid uptake (Cd36, Lpl), and oxidation (Cpt1b). Additionally, O-CAF animals displayed increased mRNA levels of Adrb3, Ucp1, and Cidea. In adulthood, these animals maintained lower mRNA levels of lipogenesis-related genes (Pparg, Srebf1, Fasn), but displayed lower expression of genes related to fatty acid uptake (Cd36), fatty acid oxidation (Cpt1b), lipolysis (Pnpla2), Adrb3, Ucp1, and Cidea. Thus, exposure to an obesogenic diet in nursing rats can affect long-term lipid metabolism and attenuate diet-induced thermogenesis in BAT in response to a new obesogenic dietary challenge later in life.

Restoring Impaired Fertility Through Diet: Observations of Switching From High-Fat Diet During Puberty to Normal Diet in Adulthood Among Obese Male Mice.

BackgroundObesity is associated with a decrease in testicular function, yet the effects and mechanisms relative to different stages of sexual development remain unclear. The aim of this study is to determine whether high-fat diet-induced obesity impairs male fertility during puberty and in adulthood, and to ascertain its underlying mechanisms. This study aims to further reveal whether restoring to a normal diet can improve impaired fertility.MethodsMale mice were divided into 6 groups: the group N and H exposed to a normal diet or high-fat diet during puberty. The group NN or NH were further maintained a normal diet or exposed to high-fat diet in adulthood, the group HH or HN were further maintained high-fat diet or switched to normal diet in adulthood. Metabolic parameters, fertility parameters, testicular function parameters, TUNEL staining and testicular function-related proteins were evaluated, respectively.ResultsThe fertility of the mice in the high-fat diet group was impaired, which validated by declines in pregnancy rates and litter weight loss. Further analysis demonstrated the increased level of oxidative stress, the increased number of spermatogenic cell apoptosis and decreased number of sperm and decreased acrosome integrity. The expression of steroidogenic acute regulatory (StAR) and spermatogenesis related proteins (WT-1) decreased. Fertility among the HN group recovered, accompanied by the recovery of metabolism, fertility and testicular function parameters, StAR and WT-1 expression.ConclusionsThe findings suggest that high-fat diet-induced obesity impairs male fertility during puberty and in adulthood. The loss of acrosome integrity, the increase of oxidative stress, the increase of cells apoptosis and the down-regulation of StAR and WT-1 may be the underlying mechanisms. Switching from high-fat diets during puberty to normal diets in adulthood can improve male fertility.

Adolescent and early adulthood inflammation-associated dietary patterns in relation to premenopausal mammographic density

BackgroundAdolescence and early adulthood has been identified as a critical time window for establishing breast cancer risk. Mammographic density is an independent risk factor for breast cancer that may be influenced by diet, but there has been limited research conducted on the impact of diet on mammographic density. Thus, we sought to examine the association between adolescent and early adulthood inflammatory dietary patterns, which have previously been associated with breast cancer risk, and premenopausal mammographic density among women in the Nurses’ Health Study II (NHSII).MethodsThis study included control participants with premenopausal mammograms from an existing breast cancer case-control study nested within the NHSII who completed a Food Frequency Questionnaire in 1998 about their diet during high school (HS-FFQ) (n = 685) and/or a Food Frequency Questionnaire in 1991 (Adult-FFQ) when they were 27–44 years old (n = 1068). Digitized analog film mammograms were used to calculate the percent density, absolute dense, and non-dense areas. Generalized linear models were fit to evaluate the associations of a pro-inflammatory dietary pattern and the Alternative Healthy Eating Index (AHEI, an anti-inflammatory dietary pattern) with each breast density measure.ResultsSignificant associations were observed between an adolescent pro-inflammatory dietary pattern and mammographic density in some age-adjusted models; however, these associations did not remain after adjustment for BMI and other breast cancer risk factors. No associations were observed with the pro-inflammatory pattern or with the AHEI pattern in adolescence or early adulthood in fully adjusted models.ConclusionsTo our knowledge, this is the first study to evaluate the dietary patterns during adolescence and early adulthood in relation to mammographic density phenotypes. Our findings do not support an association between adolescent and early adulthood diet and breast density in mid-adulthood that is independent of BMI or other breast cancer risk factors.

New home, new diet? Reconstruction of diet at the 10th century CE Hungarian Conquest period site of Kenézlő-Fazekaszug from stable carbon and nitrogen isotope analyses

The first Hungarians settled the Carpathian Basin in the 9th and 10th centuries CE, during the Hungarian Conquest. The 10th century CE Kenézlő-Fazekaszug is one of several cemeteries from this period that exist across present-day Hungary. Although stable isotope studies have investigated the diet of medieval Europeans, this paper details the first dietary research performed on a Hungarian Conquest period population. Stable carbon and nitrogen isotope analyses were undertaken on dental enamel (n = 18) and dentin (n = 17) to determine childhood diet. Enamel apatite δ13C values average at −9.5‰ and dentin collagen δ13C values at −16.0‰. Dentin collagen δ15N values have a mean of 11.9‰. Additionally, stable carbon and nitrogen isotope analyses were performed on bone apatite (n = 21) and collagen (n = 22) to determine adulthood diet. Bone apatite δ13C values average at −11.1‰. Bone collagen δ13C and δ15N values have an average of −17.0‰ and 11.5‰, respectively. These results suggest that C3 plants were the primary plant type utilized by the population but also that C4 plants were consumed in varying quantities. This data supports the archaeological evidence that C3 plants dominated C4 plants in early medieval Europe. The δ15N values show that this population consumed moderate amounts of animal protein, as well as that adult males had preferential access to animal protein. This study reveals new information about diet during a formative time in Hungarian history.

Sex-Specific Effects of Myo-Inositol Ingested During Lactation in the Improvement of Metabolic Health in Adult Rats.

To examine the effects of myo-inositol supplementation during lactation in male and female rats on metabolic parameters and its potential to reverse metabolic alterations associated with a moderate gestational calorie restriction. The offspring of control and 25% gestational calorie-restricted rats are supplemented with myo-inositol or vehicle throughout lactation and exposed to a Western diet (WD) from 5 to 7 months of age. Blood parameters are measured and gene expression and protein levels in retroperitoneal white adipose tissue (rWAT) and liver are analyzed. In male offspring, but not in females, myo-inositol supplementation resulted in lower fasting triglyceride and insulin levels and HOMA-IR at 7 months, and reversed the alterations in these parameters due to gestational calorie restriction. The expression pattern of key genes in metabolism in rWAT and liver support the beneficial effect of myo-inositol supplementation in reversing metabolic alterations programmed by gestational calorie restriction in male rats. Myo-inositol supplementation at physiological doses during lactation improves metabolic health and prevents the programmed trend to develop insulin resistance and hypertriglyceridemia in male rats acquired by inadequate fetal nutrition and exacerbated by a diabetogenic diet in adulthood. The absence of clear effects in females deserves further investigation.

Perinatal exposure to low doses of glyphosate-based herbicide combined with a high-fat diet in adulthood causes changes in the jejunums of mice

AimExposure to pesticides and consumption of high-fat diets are widespread in society. Reports have shown that exposure to glyphosate and a high-fat diet can cause gastrointestinal disorders and increase susceptibility to obesity. Thus, this study evaluated the impacts of perinatal exposure to glyphosate followed by consumption of a high-fat diet in adulthood on the histology and morphometry of jejunums and enteric nervous system of C57BL/6 mice. Material and methodsAfter mating, 20 C57BL/6 female mice were separated into a control group (CG) and a glyphosate group (GLY) that received water with 0.5% glyphosate. After the lactation period, some male offspring were randomly separated into CG-SD and GLY-SD (standard diet) groups or CG-HD and GLY-HD (high-fat diet) groups. After 12 weeks, jejunum samples were collected and submitted to histological analysis. Key findingsIndirect exposure to glyphosate changed the morphometry of the intestinal wall, increased the proportion of intraepithelial lymphocytes (IELs) and goblet cells, and altered the area occupied by collagen fibers. The hyperlipidemic diet hypertrophied the jejunal total wall, total muscular and submucosal layers, decreased IELs, and increased the proportion of goblet cells. GLY-HD mice had shallower crypts, shorter villi, and less goblet cells and IELs than mice from GLY-SD group. GLY-HD also showed an increased number of neurons in myenteric and submucosal plexuses. Groups exposed to glyphosate and/or fed a high-fat diet had atrophied submucosal neurons. SignificanceThis study suggests that perinatal glyphosate exposure combined with a high-fat diet in adulthood increases the risk of jejunum inflammation and dysfunction.

Dietary exposures in childhood and adulthood and cardiometabolic outcomes: a systematic scoping review.

Associations between diet and cardiometabolic outcomes are often based on a single measurement of diet in adulthood. Dietary exposures in childhood are thought to influence cardiometabolic disease development and individuals' diets can change over time, therefore dietary exposure in childhood and over long periods are both important to consider. This scoping review aimed to identify and characterise the literature on associations between diet measured in both childhood and adulthood and cardiometabolic outcomes. Seven databases were searched; eligible evidence sources were original analyses published as a journal article in English. Exposures included measures of dietary intake, diet quality and eating behaviours measured in both childhood and adulthood with at least five years between first and last measurements. Cardiometabolic outcomes included measures of anthropometry, biochemistry, vascular structure/function and disease states/scores. We identified 37 eligible articles from nine cohort studies. Dietary exposures were measured between two and eight times and most often assessed by food frequency questionnaire or diet history. The dietary exposures most frequently examined were protein, fat, carbohydrate, fruit, vegetables, sugar-sweetened beverages and breakfast. Cardiometabolic outcomes were predominantly based on risk markers. Authors utilised a variety of analytical approaches to transform and analyse repeated measures of diet, providing insights relevant to different lifespan nutrition concepts. The literature on associations between diet in childhood and adulthood and cardiometabolic outcomes is limited, but such studies have great potential to extend our knowledge in ways only possible with repeated measures of diet over time. Further research is needed to develop the evidence base for diet-disease relationships from a life course perspective, accounting for diet in both childhood and adulthood.

Prenatal maternal vitamin D deficiency sex-dependently programs adipose tissue metabolism and energy homeostasis in offspring.

In utero environment is crucial to ensure normal development of the fetus and to program metabolic health throughout the life. Beside macronutrients, the role of micronutrients, including vitamin D, begins to be explore. The aim of this study was to decipher the impact of maternal vitamin D deficiency (VDD), in normal and high-fat (HF) diet context, on adipose tissue metabolism and energy homeostasis in offspring, considering sex-specific responses. Body weight, energy expenditure, and spontaneous activity was differential impacted in juvenile male and female offspring born from VDD mice. In adulthood, a HF diet combined with maternal VDD disrupted glucose homeostasis and adiposity in male offspring but not in females. Such phenotypes were associated to different transcriptomic profiles in adipose tissue, which could be related to differential modulation of plasma 17β-estradiol concentrations. Thus, maternal VDD sex-dependently modulated metabolic fate of the offspring, especially when associated with HF diet in adulthood.

Enduring effects of an unhealthy diet during adolescence on systemic but not neurobehavioural measures in adult rats

ABSTRACT Introduction: Adolescence is an important stage of maturation for various brain structures. It is during this time therefore that the brain may be more vulnerable to environmental factors such as diet that may influence mood and memory. Diets high in fat and sugar (termed a cafeteria diet) during adolescence have been shown to negatively impact upon cognitive performance, which may be reversed by switching to a standard diet during adulthood. Consumption of a cafeteria diet increases both peripheral and central levels of interleukin-1β (IL-1β), a pro-inflammatory cytokine which is also implicated in cognitive impairment during the ageing process. It is unknown whether adolescent exposure to a cafeteria diet potentiates the negative effects of IL-1β on cognitive function during adulthood. Methods: Male Sprague-Dawley rats consumed a cafeteria diet during adolescence after which time they received a lentivirus injection in the hippocampus to induce chronic low-grade overexpression of IL-1β. After viral integration, metabolic parameters, circulating and central pro-inflammatory cytokine levels, and cognitive behaviours were assessed. Results: Our data demonstrate that rats fed the cafeteria diet exhibit metabolic dysregulations in adulthood, which were concomitant with low-grade peripheral and central inflammation. Overexpression of hippocampal IL-1β in adulthood impaired spatial working memory. However, adolescent exposure to a cafeteria diet, combined with or without hippocampal IL-1β in adulthood did not induce any lasting cognitive deficits when the diet was replaced with a standard diet in adulthood. Discussion: These data demonstrate that cafeteria diet consumption during adolescence induces metabolic and inflammatory changes, but not behavioural changes in adulthood.

Severity of Villous Atrophy at Diagnosis in Childhood Does Not Predict Long-term Outcomes in Celiac Disease.

Current pediatric guidelines allow noninvasive diagnosis of celiac disease in selected children. We investigated in a large cohort study whether the severity of villous atrophy at diagnosis is associated with clinical characteristics or long-term health outcomes, thus having a prognostic significance. Comprehensive medical data on 906 children with celiac disease were analyzed. Long-term health outcomes of 503 adult patients diagnosed in childhood were moreover assessed with a specific study questionnaire and validated Gastrointestinal Symptom Rating Scale (GSRS) and Psychological General Well-Being (PGWB) questionnaires. Patients were classified into 3 groups according to the severity of villous atrophy at diagnosis, and all variables were compared. Altogether 34% of the patients had partial, 40% subtotal, and 26% total villous atrophy. Children with milder lesions were diagnosed more recently (median year 2007 vs 2006 vs 2001, respectively, P < 0.001), more often by screening (30% vs 25% vs 17%, P < 0.001) and they suffered less often from anemia (16% vs 21% vs 32%, P < 0.001) and growth disturbances (22% vs 36% vs 54%, P < 0.001) and had lower transglutaminase-2 antibody levels (median 64 U/L vs 120 U/L vs 120 U/L, P < 0.001). There was no difference in other disease features.Altogether 212 adults diagnosed in childhood completed the questionnaires. Severity of villous atrophy at childhood diagnosis did not predict presence of complications or comorbidities, persistent symptoms, and self-perceived health, quality of life or adherence to a gluten-free diet in adulthood. Presence of advanced villous atrophy at diagnosis is associated with more severe clinical characteristics but not with poorer long-term health and treatment outcomes.

212-LB: Gestational Exposure to Low-Dose Benzene Predisposes to Diabetes in Adulthood

Benzene is a well-known human carcinogen that is one of the major components of air pollution. Sources of benzene in ambient air include cigarette smoke, e-cigarettes, vaping, and evaporation of benzene-containing petrol processes. Epidemiological studies demonstrated the association with type 2 diabetes (T2D) and the development of insulin resistance (IR). Because maternal environmental stressors can greatly affect offspring health, we hypothesized that exposure to low concentrations of benzene during critical windows of development may contribute to the escalating prevalence of metabolic imbalance and diabetes in offspring. Specifically, we tested the hypothesis that prenatal exposure to benzene at concentrations relevant to cigarette smoking or vaping, would prime hypothalamic gliosis, resulting in exacerbated metabolic outcomes following exposure to a high-fat diet in adulthood. Pregnant C57BL/6JB dams were exposed to benzene at 50ppm or filtered air throughout gestation, and offspring metabolic phenotype was evaluated before and after high-fat-diet (HFD) feeding for 6 months. The male offspring of benzene-exposed dams exhibited exaggerated hyperglycemia on a chow diet compared to the male offspring of control dams, whereas female offspring did not differ according to prenatal treatment. No changes in body weight, body composition, or early postnatal hypothalamic glial activation were observed between groups. Regardless, adult male offspring of benzene-exposed dams exhibited severe impairment in the parameters of energy homeostasis (Vo2, VCO2, and heat production), suggesting the effect of metabolic reprogramming in whole-body metabolic regulation in adult offspring. In summary, prenatal benzene exposure at low dose programs offspring for increased susceptibility to diet induced metabolic changes in adulthood in a sexually dimorphic manner. Disclosure L. Koshko: None. L.K. Debarba: None. O. Didyuk: None. P.I. Fakhoury: None. M. Sadagurski: None. U. Klueh: Research Support; Self; Abbott. Other Relationship; Self; Cell and Molecular Tissue Engineering, LLC.

Raising girls and boys in early China: Stable isotope data reveal sex differences in weaning and childhood diets during the eastern Zhou era.

ObjectivesUsing stable isotope analysis of incremental dentin segments, we reconstruct breastfeeding, weaning, and childhood dietary patterns of Eastern Zhou period (771–221 BC) individuals from the Central Plains of China. Previous isotopic research on the Eastern Zhou demonstrated dietary difference between male and female diets in adulthood via bone collagen analysis. To understand the development of gendered dietary patterns we must examine the early life period. We aim to identify the timing of the weaning process, whether childhood diets were the same as adulthood diets, and if there were differences between the diets of boys and girls during childhood.Materials and MethodsWe present incremental dentin and bone collagen δ13C and δ15N isotope data from 23 individuals from two Eastern Zhou archaeological sites (Xiyasi 西亚斯and Changxinyuan 畅馨苑).ResultsWeaning was completed between ages 2.5 and 4 years. Females were weaned slightly earlier than males. Early childhood diets show significant incorporation of C3 foods, such as wheat and soybean, for almost all children, while later adulthood diets indicate greater incorporation of C4 foods (millets), particularly for males.DiscussionChildhood diets included greater amounts of C3 foods than expected, suggesting that grains such as wheat may have been adopted in these communities as foods for children. Nevertheless, dietary differentiation between females and males began in childhood, with boys eating more millets (C4 foods) than girls. The findings suggest that feeding children was a significant aspect of socialization and cultural gendering of individuals in ancient China.

Child nutrition process and habits of a food doctrine for a lifetime

Food defines, helps and influences our quality of life as well as our longevity. A Poor nutrition in childhood can reflect in problems later in adulthood with consequences in old age, just as a poor diet in adulthood can reflect in problems in old age, an adequate nutrition can increase longevity as well as quality of life. Taking into account the increase in the age group of the elderly, the need for adequate nutrition to prevent and combat age limitations, deficiencies and typical diseases of aging also increases.&#x0D; The objective of this work is not to create an idea that we have to live a whole life since childhood as machines that feed in an indoctrinated way to have a better old age, but to present types of diets as options, where nutrition is favorable and fun. It is the habits that we introduce since breastfeeding and childcare that educate the child to become an adult with good eating habits.&#x0D; Based on the knowledge of neuroscience, neuropsychology, psychoanalysis and clinical nutrition, present diets, preventions, examples and explanations that favor the understanding of the need and results of good nutrition. Some key points will assist us in this nutritional summary in this work:&#x0D; &#x0D; Child nutrition options to help in a good childhood.&#x0D; Habits and techniques for a fun and enjoyable nutrition.&#x0D; How nutrition helps in mood and learning.&#x0D;

Gestational oxidative stress protects against adult obesity and insulin resistance

Pregnancy complications such as preeclampsia cause increased fetal oxidative stress and fetal growth restriction, and associate with a higher incidence of adult metabolic syndrome. However, the pathophysiological contribution of oxidative stress per se is experimentally difficult to discern and has not been investigated. This study determined, if increased intrauterine oxidative stress (IUOx) affects adiposity, glucose and cholesterol metabolism in adult Ldlr−/−xSod2+/+ offspring from crossing male Ldlr−/−xSod2+/+ mice with Ldlr−/−xSod2 +/- dams (IUOx) or Ldlr−/−xSod2 +/- males with Ldlr−/−xSod2+/+ dams (control). At 12 weeks of age mice received Western diet for an additional 12 weeks. Adult male IUOx offspring displayed lower body weight and reduced adiposity associated with improved glucose tolerance compared to controls. Reduced weight gain in IUOx was conceivably due to increased energy dissipation in white adipose tissue conveyed by higher expression of Ucp1 and an accompanying decrease in DNA methylation in the Ucp1 enhancer region. Female offspring did not show comparable phenotypes. These results demonstrate that fetal oxidative stress protects against the obesogenic effects of Western diet in adulthood by programming energy dissipation in white adipose tissue at the level of Ucp1.

Perinatal iron deficiency combined with a high salt diet in adulthood causes sex-dependent vascular dysfunction in rats.

Perinatal iron deficiency causes changes in offspring mesenteric artery function in adulthood, particularly in males, which can be exacerbated by chronic intake of a high salt diet. Perinatal iron deficient male offspring exhibit enhanced conversion of big endothelin-1 to active endothelin-1, coinciding with decreased nitric oxide levels. Perinatal iron deficient male offspring have reduced nitric oxide-mediated endothelial-dependent vasodilatation coincident with increased vascular superoxide levels following consumption of a high salt diet. Perinatal iron deficiency has no apparent effects on vascular function in female offspring, even when fed a high salt diet. These results help us better understand underlying vascular mechanisms contributing to increased cardiovascular risk from perinatal stressors such as iron deficiency. Pre- and immediate postnatal stressors, such as iron deficiency, can alter developmental trajectories and predispose offspring to long-term cardiovascular dysfunction. Here, we investigated the impact of perinatal iron deficiency on vascular function in the adult offspring, and whether these long-term effects were exacerbated by prolonged consumption of a high salt diet in adulthood. Female Sprague Dawley rats were fed either an iron-restricted or -replete diet prior to and throughout pregnancy. Six weeks prior to experimentation at 6months of age, adult offspring were fed either a normal or high salt diet. Mesenteric artery responses to vasodilators and vasoconstrictors were assessed ex vivo by wire myography. Male perinatal iron deficient offspring exhibited decreased reliance on nitric oxide with methacholine-induced vasodilatation (interaction P=0.03), coincident with increased superoxide levels when fed the high salt diet (P=0.01). Male perinatal iron deficient offspring exhibit enhanced big endothelin-1 conversion to active endothelin-1 (P=0.02) concomitant with decreased nitric oxide levels (P=0.005). Female offspring vascular function was unaffected by perinatal iron deficiency, albeit the high salt diet was associated with impaired vasodilation and decreased nitric oxide production (P=0.02), particularly in the perinatal iron deficient offspring. These findings implicate vascular dysfunction in the sex-specific programming of cardiovascular dysfunction in the offspring by perinatal iron deficiency.

Developmental origins of ovarian disorder: impact of maternal lean gestational diabetes on the offspring ovarian proteome in mice†.

Gestational diabetes mellitus (GDM) is an obstetric disorder affecting approximately 10% of pregnancies. The four high-fat, high-sucrose (HFHS) mouse model emulates GDM in lean women. Dams are fed a HFHS diet 1 week prior to mating and throughout gestation resulting in inadequate insulin response to glucose in mid-late pregnancy. The offspring of HFHS dams have increased adiposity, thus, we hypothesized that maternal metabolic alterations during lean GDM would compromise ovarian function in offspring both basally and in response to a control or HFHS diet in adulthood. Briefly, DLPL were lean dams and control diet pups; DLPH were lean dams and HFHS pups; DHPL were HFHS dams and control diet pups; and DHPH were HFHS dams and HFHS pups. A HFHS challenge in the absence of maternal GDM (DLPL vs. DLPH) increased 3 and decreased 30 ovarian proteins. Maternal GDM in the absence of a dietary stress (DLPL vs. DHPL) increased abundance of 4 proteins and decreased abundance of 85 proteins in the offspring ovary. Finally, 87 proteins increased, and 4 proteins decreased in offspring ovaries due to dietary challenge and exposure to maternal GDM in utero (DLPL vs. DHPH). Canopy FGF signaling regulator 2, deleted in azoospermia-associated protein 1, septin 7, and serine/arginine-rich splicing factor 2 were altered across multiple offspring groups. Together, these findings suggest a possible impact on fertility and oocyte quality in relation to GDM exposure in utero as well as in response to a western diet in later life.