Search

Background: The sensitivity of commercially available devices to detect changes in skin carotenoids is not known., Objectives: We aimed to determine the sensitivity of pressure-mediated reflection spectroscopy (RS) to detect changes in skin carotenoids in response to increasing carotenoid intake., Methods: Nonobese adults were randomly assigned to a control (water; n = 20; females = 15 (75%); mean age: 31 ± 3 (SE) y; mean BMI: 26 ± 1 kg/m 2 ) or one of 3 carotenoid intake levels: 1) LOW - 13.1 mg; n = 22; females = 18(82%); age: 33 ± 3 y; BMI: 25 ± 1 kg/m 2 ; 2) MED - 23.9 mg; n = 22; females = 17 (77%); age: 30 ± 2 y; BMI: 26 ± 1 kg/m 2 ); or 3) HIGH - 31.0 mg; n = 19; females = 9 (47%); age: 33 ± 3 y; BMI: 24 ± 1 kg/m 2 . A commercial vegetable juice was provided daily to ensure that the additional carotenoid intake was achieved. Skin carotenoids (RS intensity [RSI]) were measured weekly. Plasma carotenoid concentrations were assessed at wk 0, 4, and 8. Mixed models were used to test the effect of treatment, time, and their interaction. Correlation matrices from mixed models were used to determine the correlation between plasma and skin carotenoids., Results: A correlation was observed between skin and plasma carotenoids (r = 0.65; P < 0.001). Skin carotenoids were greater than baseline starting at week 1 in the HIGH (290 ± 20 vs. 321 ± 24 RSI; P ≤ 0.01), week 2 in the MED (274 ± 18 vs. 290 ± 23 RSI; P ≤ 0.03), and week 3 in the LOW (261 ± 18 vs. 288 ± 15 RSI; P ≤ 0.03). Compared with control, differences in skin carotenoids were observed starting at week 2 in the HIGH ([268 ± 16 vs. 338 ± 26 RSI; P ≤ 0.01] except for week 3 [287 ± 20 vs. 335 ± 26 RSI; P = 0.08]) and week 6 in the MED (303 ± 26 vs. 363 ± 27 RSI; P ≤ 0.03). No differences were observed between the control and LOW., Conclusions: These findings demonstrate that RS can detect changes in skin carotenoids in adults without obesity when daily carotenoid intake is increased by 13.1 mg for a minimum of 3 wk. However, a minimum difference in intake of 23.9 mg of carotenoids is needed to detect group differences. This trial was registered at ClinicalTrials.gov as NCT03202043., (Published by Elsevier Inc.)

Background: Food reinforcement, or the motivation to obtain food, can predict choice and consumption. Vegetable consumption is well below recommended amounts for adults, so understanding how to increase vegetable reinforcement could provide valuable insight into how to increase consumption., Objectives: We sought to determine whether daily consumption of the Dietary Guidelines for Americans (DGA) recommendations for vegetable intake induces sensitization of vegetable reinforcement in adults with overweight and obesity., Methods: Healthy adults with a BMI ≥ 25 kg/m2 who consumed ≤1 cup-equivalent of vegetables/day were randomly assigned to a vegetable intervention (VI; n = 55) or an attention control (AC; n = 55) group. The VI consisted of the daily provision of vegetables in the amounts and types recommended by the DGA (∼270 g/day) for 8 weeks. Participants were followed for an additional 8 weeks to assess sustained consumption. Compliance was measured weekly by resonance Raman light-scattering spectroscopy (RRS). Vegetable reinforcement was tested at weeks 0, 8, 12, and 16 using a computer choice paradigm., Results: In the VI group, RRS intensity increased from week 0 to 8 (from 22,990 to 37,220), returning to baseline by week 16 (27,300). No change was observed in the AC group. There was no main effect of treatment (P = 0.974) or time (P = 0.14) and no treatment x time interaction (P = 0.44) on vegetable reinforcement. There was no moderating effect of sex (P = 0.07), age (P = 0.60), BMI (P = 0.46), delay discounting (P = 0.24), 6-n-propylthiouracil taster status (P = 0.15), or dietary disinhibition (P = 0.82) on the change in vegetable reinforcement., Conclusions: These findings suggest no effects of the provision of a variety of vegetables to meet DGA recommendations for 8 weeks on vegetable reinforcement and highlight the difficulty in increasing vegetable consumption in adults. This trial was registered at clinicaltrials.gov as NCT02585102., (Published by Oxford University Press on behalf of the American Society for Nutrition 2021.)

We sought to determine the impact of breed and finishing ration that reduces the saturated fat (SFA) content of beef on SFA intake (%E) in adults. Using National Health and Nutrition Examination Surveys (2001-2016), we replaced the current fatty acid profile of beef with that from two breeds (Angus, Wagyu) and three finishing rations (pasture, 15% flaxseed supplementation, 35% wet distiller's grain (WDG) supplementation). Dietary replacement levels in the model were 10%, 25%, 50%, 100%. Overall, men consumed more beef fat than women (12.0 g (11.6-12.4 g, 95%CI) and 6.6 g (6.4-6.9 g, 95%CI), respectively). The contribution of beef fat to SFA intake was 2.1%E (2.1-2.2%E, 95%CI) in men and 1.6%E (1.6-1.7%E, 95%CI) in women. SFA intake decreased with each increased replacement level for all beef types. At 100% replacement, SFA intake decreased 0.5% (Angus), 2.8% (Wagyu), 1.9% (pasture), 4.1% (flaxseed), 2.6% (WDG). Our findings demonstrate that breed and finishing ration that reduces the SFA content of beef can decrease population-level SFA intake., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Published by Elsevier Ltd.)

Background: Diet quality among federal food assistance program participants remains low, and little research has assessed the diet quality of food insecure non-participants. Further research is needed to assess the extent to which food substitutions can improve the nutritional status of these vulnerable populations. Substituting egg dishes for other commonly consumed dishes at certain eating occasions may be an effective strategy for improving the daily nutrient intake among these groups. Eggs are rich in many important nutrients, and are low-cost and part of a wide range of cultural food menus, which are important considerations for low-income and ethnically diverse populations. To help guide the focus of targeted nutrition interventions and education campaigns for vulnerable populations, the present work begins by 1) estimating the prevalence of nutrient inadequacy among these groups, and then models the effect of consuming egg dishes instead of commonly consumed dishes at each eating occasion on 2) the prevalence of nutrient inadequacy, and 3) the mean intake of nutrients., Methods: Dietary data from 34,741 adults ≥ 20 y were acquired from the National Health and Nutrition Examination Survey, 2001-2014. Diet pattern modeling was used to substitute commonly consumed egg dishes for commonly consumed main dishes at breakfast, lunch, and dinner. National Cancer Institute usual intake methods were used to estimate the prevalence of inadequate intake of 31 nutrients pre- and post-substitution, and a novel index was used to estimate change in intake of all nutrients collectively., Results: Substituting eggs for commonly consumed main dishes at lunch or dinner did not change total daily nutrient intake for each group (P > 0.05), but decreased the prevalence of vitamin D inadequacy by 1-4 percentage points (P < 0.01). Substituting eggs for commonly consumed foods at breakfast increased the prevalence of folate inadequacy by 8-12 percentage points among each group (P < 0.01)., Conclusions: When making food substitutions to increase nutrient intake, eating occasion should be an important consideration. Further research is needed to better understand how food substitutions affect diet costs, which may be an important driver of food purchasing decisions among low income individuals with limited food budgets.

Eggs have the potential to contribute essential nutrients to nutritionally vulnerable populations on limited food budgets. Further research is needed to better understand patterns of egg consumption across diverse sociodemographic groups in order to inform clinical practice to improve nutrient adequacy. Data on demographics and egg intake of 29,694 U.S. adults were obtained from the National Health and Nutrition Examination Survey, 2001-2012. The National Cancer Institute's usual intake methodology was used to estimate the distribution of egg intake. Linear and logistic regression models were used to test for time trends in egg consumption and for differences between sociodemographic groups. The proportion of the U.S. population, overall (21%-22%; p = 0.311) and by sociodemographic group ( p > 0.05 for all groups), that reported consuming eggs remained unchanged from 2001 to 2012. Mean egg consumption increased overall from 23.0 (95% CI, 20.8-25.2) g/day in 2001-2002 to 25.5 (22.7-28.4) g/day in 2011-2012 ( p = 0.012), but not among food insecure individuals ( p = 0.816) and Supplemental Nutrition Assistance Program (SNAP) participants ( p = 0.399). No differences in the odds of egg consumption were observed by income level, food security status, or SNAP participation status ( p > 0.05 for all groups). Given the nutritional benefits of eggs, as well as their low cost and culinary versatility, the results presented here have important implications for reducing disparities in health outcomes and diet quality, in particular among food insecure individuals and SNAP participants. Further research is needed to examine factors that influence egg consumption and associated nutrient intake, and to identify potential barriers to increasing egg consumption, such as egg price changes, across diverse sociodemographic groups.

Greater food variety is related to increased energy intake, and one approach to reduce food intake is to reduce food variety. The effects of varying the variety of foods at the dinner meal to reduce energy intake was assessed in laboratory and field experiments. Experiment 1 randomly assigned 31 overweight children to one of three conditions that provided one laboratory meal per day over a week. Conditions were the SAME macaroni and cheese, SIMILAR types of macaroni and cheese, or a VARIETY of high-energy-dense foods. On days 1 and 5 all children consumed the same macaroni and cheese meal. Results showed significant differences in energy consumed between SAME and SIMILAR versus VARIETY from day 1 to 5, with SAME and SIMILAR decreasing and VARIETY increasing energy intake. Trials to habituation, a potential mechanism for the variety effect, showed the same pattern of between group differences as energy intake. Experiment 2 randomly assigned 30 overweight children to conditions that provided the SAME, SIMILAR or VARIETY of high-energy-dense entrees along with a variety of low-energy-dense dinner entrees to eat in their homes for 4 weeks. Results showed significant between group differences in energy intake across weeks, with significant decreases over weeks for the SAME and SIMILAR versus VARIETY groups. The pattern of results across the experiments shows the same pattern of reduction in energy intake if children eat the same or similar characteristics of foods (types of macaroni and cheese), which may provide ideas about how to develop dietary variety prescriptions that can reduce intake and be tested in clinical trials., (Copyright © 2012 Elsevier Ltd. All rights reserved.)

Objective: To determine whether dietary restraint modifies stress-induced eating in youth., Research Methods and Procedures: Snacking was measured in boys (9.5 +/- 0.3 years) and girls (9.0 +/- 0.3 years), with and without dietary restraint, across a control day after reading children's magazines and/or coloring, and on a stress day after giving a videotaped speech, with order of conditions counterbalanced. Children were divided into four groups based on dietary restraint and changes in perceived stress: low-restraint/low-reactive (n = 9), low-restraint/high-reactive (n = 13), high-restraint/low-reactive (n = 10), and high-restraint/high-reactive (n = 8). Body composition was estimated by skinfolds., Results: Energy intake of snack foods was influenced differently by dietary restraint and stress reactivity in the stress and control conditions (p < 0.01). After being stressed, low-restraint/low-reactive children ate fewer snacks and high-restraint/high-reactive children ate more snacks compared with the control condition. After covarying for percentage of body fat, the interactions remained (p < 0.01). Girls ate less than boys (p < 0.001), but sex did not influence eating in control and stress conditions., Discussion: Dietary restraint occurs in children and may influence the effect of stress on eating. Interpersonal stress decreases snacking in low dietary restrained youth but increases snacking in high dietary restrained children, perhaps because of stress-induced disinhibition.

Abstract Objective Methods and measures Results Conclusion The purpose of the present study was to examine how information source (control—no source, U.S. Department of Agriculture (USDA), fictitious hospital, or fictitious social media) impacts perceptions of diet information.Participants (N = 537) completed an online survey in which they viewed one flyer containing dietary information and guidance on consuming pulses. The purported source of the flyer information was manipulated to create the 4 conditions. Participants rated the flyer in terms of perceived accuracy, trustworthiness, reliability, desirability for learning more from the source, and likelihood of following the advice. Attitudes, perceived control and norms, and past behavior were used to measure components of the Theory of Planned Behavior (TPB).ANOVA results indicated that the USDA and hospital sources were perceived as more accurate, trustworthy, reliable, and more desirable to learn more from relative to control and social media. There were no differences in likelihood of following guidance depending on source. Multiple regression showed that measures of the TPB were predictors of likelihood of following advice.Overall, these findings suggest that trust in the source of information does not influence perceived likelihood of following dietary recommendations for pulses. [ABSTRACT FROM AUTHOR]

Background: Controlled intervention trials are needed to confirm a positive association from epidemiological studies between vegetable consumption and bone health.Objective: We investigated whether providing vegetables at the Dietary Guidelines for Americans (DGA) recommended amount affects excretion of acid and calcium in urine and bone turnover markers in serum in adults with low vegetable intake.Methods: In total, 102 adults (19 males and 83 females, age 18-65 y, BMI ≥25 kg/m2) consuming ≤1 serving of vegetables (128 g raw leafy or 64 g cooked vegetables) per d were recruited in a 2-arm, parallel, randomized, controlled, and community-based 8-wk feeding intervention trial. The 2 arms included a vegetable intervention (VI) during which participants received extra vegetables (∼270 g/d) and an attention control (CON) group that conducted only the testing visits. Measurements included nutrient intake, plasma carotenoids, and bone-related markers in serum and urine. Differences between CON and VI at week 8 were tested using the ANCOVA with baseline values as a covariate.Results: Compared with CON, carotenoid intake (mean ± SD) was higher (6.4 ± 3.4 compared with 2.0 ± 1.2 mg/d) (P < 0.01) and dietary potential renal acid load was lower (20 ± 13 compared with 3.4 ± 14 mEq/d) (P < 0.01) in VI. Compared with CON at week 8, urine titratable acid and Mg were 24 and 26% lower, respectively, while urine pH was 3% greater (P < 0.05) and serum C-terminal telopeptide of type I collagen (CTX) was 19% lower in VI. There were no group differences in serum concentrations of propeptide of type 1 procollagen and tartrate-resistant acid phosphatase or urinary excretion of deoxypyridinoline and CTX.Conclusions: Consumption of vegetables at the DGA-recommended amount by adults with low vegetable intake potentially benefits bone health. This trial was registered at clinicaltrials.gov as NCT02585102. [ABSTRACT FROM AUTHOR]

Adipose tissue macrophages (ATM) are implicated in adipose tissue inflammation and obesity-related insulin resistance. Maternal low protein models result in fetal programming of obesity. The study aims to answer whether maternal undernutrition by protein restriction affects the ATM M1 or M2 phenotype under postnatal high fat diet in F1 offspring. Using a rat model of prenatal low protein (LP, 8% protein) diet followed by a postnatal high fat energy diet (HE, 45% fat) or low fat normal energy diet (NE, 10% fat) for 12 weeks, we investigated the effects of these diets on adiposity, programming of the offspring ATM phenotype, and the associated inflammatory response in adipose tissue. Fat mass in newborn and 12-week old LP fed offspring was lower than that of normal protein (20%; NP) fed offspring; however, the adipose tissue growth rate was higher compared to the NP fed offspring. While LP did not affect the number of CD68+ or CD206+ cells in adipose tissue of NE offspring, it attenuated the number of these cells in offspring fed HE. In offspring fed HE, LP offspring had a lower percentage of CD11c+CD206+ ATMs, whose abundancy was correlated with the size of the adipocytes. Noteworthy, similar to HE treatment, LP increased gene expression of IL-6 within ATMs. Two-way ANOVA showed an interaction of prenatal LP and postnatal HE on IL-6 and IL-1β transcription. Overall, both LP and HE diets impact ATM phenotype by affecting the ratio of CD11c+CD206+ ATMs and the expression of IL-6. [ABSTRACT FROM AUTHOR]

OBJECTIVE: To test in the primary care setting the short- and long-term efficacy of a behavioral intervention that simultaneously targeted an overweight child and parent versus an information control (IC) targeting weight control only in the child. METHODS: Two- to 5-year-old children who had BMI ≥85th percentile and an overweight parent (BMI >25 kg/m2) were randomized to Intervention or IC, both receiving diet and activity education over 12 months (13 sessions) followed by 12-month follow-up (3 sessions). Parents in the Intervention group were also targeted for weight control and received behavioral intervention. Pediatricians in 4 practices enrolled their patients with the assistance of embedded recruiters (Practice Enhancement Assistants) who assisted with treatment too. RESULTS: A total of 96 of the 105 children randomized (Intervention n = 46; IC n = 50) started the program and had data at baseline. Children in the Intervention experienced greater reductions in percent over BMI (group × months; P = .002) and z-BMI (group × months; P < 0.001) compared with IC throughout treatment and follow-up. Greater BMI reduction was observed over time for parents in the Intervention compared with IC (P < .001) throughout treatment and follow-up. Child weight changes were correlated with parent weight changes at 12 and 24 months (r = 0.38 and 0.26; P < .001 and P = .03). CONCLUSIONS: Concurrently targeting preschool-aged overweight and obese youth and their parents in primary care with behavioral intervention results in greater decreases in child percent over BMI, z-BMI, and parent BMI compared with IC. The difference between Intervention and IC persists after 12 months of follow-up. [ABSTRACT FROM AUTHOR]

Objective: Family-based treatments for pediatric obesity were developed over 25 years ago. Over that time, youth have become more obese and the environment more obesiogenic, which may influence efficacy of pediatric weight control. Mixed-effects regression models were used to compare the efficacy of programs initiated 20 to 25 years ago to current programs through 24-month follow-up, as well as to reanalyze 10-year outcomes of previous research using contemporary measures and analytic strategies. Main outcome measures: z-BMI and percent overweight. Results: Results showed significant reductions over time, with no differences in z-BMI change for older versus contemporary studies. Age was a predictor of z-BMI up to 24 months, with younger children showing larger change. Mixed-effects regression models replicated previous long-term effects of family-based interventions. Gender was a predictor of long-term z-BMI change, with girls benefiting more over time than did boys. Conclusion: The efficacy of the family-based behavioral approach to treating pediatric obesity replicates over a 25-year period. Challenges in evaluating treatment effects over time are discussed. Ideas for studying choice of treatments that vary in effect size and for strengthening family-based behavioral treatments are noted. [ABSTRACT FROM AUTHOR]

OBJECTIVE- Magnesium deficiency has been associated with insulin resistance (IR) and increased risk for type 2 diabetes in adults. This study was designed to determine whether obese children exhibit serum or dietary magnesium deficiency and its potential association with IR. RESEARCH DESIGN AND METHODS -- We studied 24 obese nondiabetic children (BMI ≥85th percentile) and 24 sex- and puberty-matched lean control subjects (BMI <85th percentile). We measured serum magnesium, indexes of insulin sensitivity, dietary magnesium intake (using a food frequency questionnaire), and body composition (by air displacement plethysmography). RESULTS -- Serum magnesium was significantly lower in obese children (0.748 + 0.015 mmol/l, means ± SE) compared with lean children (0.801 ± 0.012 mmol/l) (P = 0.009). Serum magnesium was inversely correlated with fasting insulin (rs = - 0.36 [95 % CI - 0.59 to - 0.08]; P = 0.011) and positively correlated with quantitative insulin sensitivity check index (QUICKI) (0.35 [0.06-0.58]; P = 0.015). Dietary magnesium intake was significantly lower in obese children (obese: 0.12 ± 0.004 vs. lean: 0.14 ± 0.004 mg/kcal; P = 0.003). Dietary magnesium intake was inversely associated with fasting insulin (-0.43 [-0.64 to 0.16]; P = 0.002) and directly correlated with QUICKI (0.43 [0.16-0.64]; P = 0.002). CONCLUSIONS -- The association between magnesium deficiency and IR is present during childhood. Serum magnesium deficiency in obese children may be secondary to decreased dietary magnesium intake. Magnesium supplementation or increased intake of magnesium-rich foods may be an important tool in the prevention of type 2 diabetes in obese children. [ABSTRACT FROM AUTHOR]

Background: At any given time, a majority of women are engaged in some type of weight loss diet; however, these efforts are difficult to sustain for long-term weight control. Because women are more likely to develop obesity and suffer a greater severity of obesity-related health and economic consequences, we sought to identify the key factors that make adhering to a weight loss diet difficult for overweight/obese women. Methods: Ten nominal group technique (NGT) sessions aimed at identifying perceived barriers to adherence to a weight loss diet were conducted as part of a weight loss study for overweight/obese women (n = 33) during the controlled feeding weight loss phase. Results: Individual-level barriers to emerge from the sessions included knowing when to stop eating, being able to control cravings and emotional eating, and sustaining healthier dietary habits. Environmental-level barriers included family/social events that bring people together, especially those centered around food and drink, eating out, cost, and busy schedules. Conclusions: These findings offer a deeper understanding of barriers women find most salient to adhering to a weight loss diet, providing direction for the clinical application of weight loss programs. [ABSTRACT FROM AUTHOR]

We previously have shown that male offspring (F1) of fathers (F0) fed a high-fat (HF) diet and that exercised had greater skeletal muscle insulin signaling and reduced type 2 diabetes mellitus (T2DM) risk compared to fathers fed HF diet and that remained sedentary. The current study extends this work by hypothesizing that F0 HF diet and exercise regulate F1 T2DM risk by alterations in placental tissue growth via changes in sperm miRNA expression. To test these hypotheses, 3-week-old male C57BL/6 mice were fed a normal-fat diet (16% fat) or an HF diet (45% fat) and assigned to either voluntary wheel running exercise or cage activity for 3 months. Results showed that F0 sperm miRNA 193b expression was decreased while miRNA 204 was increased by paternal exercise. Protein expression of dimethylated histone 3 lysine 9 was decreased with F0 HF diet. Placental and fetal tissue weights were decreased by F0 HF diet in F1 males. Placental interleukin-1β and tumor necrosis factor (TNF)-α mRNA expression was reduced by paternal exercise, while nutrient transporter mRNA expression was decreased by paternal HF diet only in the placentae of F1 females. Treatment of primary placental cell with miRNA 193b inhibited TNF-α mRNA expression, and treatment of TNF-α decreased SLC38a2 mRNA expression. Moreover, paternal exercise increased body weight at weaning in a female offspring. These results demonstrate that placental tissue weight, placental nutrient transporter gene expression and fetal weights are altered by paternal exercise, while placental inflammatory gene expression is influenced by paternal exercise in offspring in a sex-specific manner. [ABSTRACT FROM AUTHOR]

We have shown that prenatal low-protein (LP) followed by postnatal high-fat (HF) diets result in a rapid increase in subcutaneous adipose tissue (subc-AT) mass in the offspring, contributing to development of obesity and insulin resistance. Studies have shown that a key transcription factor, PR domain containing 16 (PRDM16), and fibroblast growth factor 21 (FGF21) are involved in conversion of precursor cells into mitochondria (mt)-enriched beige adipocytes (BA). Our hypothesis is that a maternal LP and postnatal HF diets increase the risk of obesity and insulin resistance in offspring, in part, by reducing the conversion of precursor cell into BA in the subc-AT of offspring. Using obese-prone Sprague-Dawley rats fed 8% LP or 20% normal-protein (NP) diets for 3 weeks prior to conception and throughout pregnancy and lactation followed by 12 weeks of 10% normal-fat (NF) or 45% HF diet feeding, we investigated whether prenatal LP and postnatal HF diets affect BA number and oxidative respiratory function in subc-AT. Results showed that subc-AT and liver FGF21, PRDM16 and BA marker CD137 mRNA increase with postnatal HF diet in maternal NP group rats. In contrast, rats fed maternal LP and postnatal HF diets showed no increase in subc-AT mt copy number, oxygen consumption rate, FGF21, PRDM16 and CD137 mRNA, whereas protein expression of an inhibitor for FGF21 transcription (histone methyltransferase, G9a) increased. These findings suggest that LPHF diets cause offspring metabolic alterations by reduced BA and FGF21 mRNA and increased G9a protein expression in subc-AT. [ABSTRACT FROM AUTHOR]

Maternal dietary conditions play a major role in fetal growth and brain development. The primary aim of this study was to determine the effects of 5% of energy substitution by vegetables in a maternal dietary fat on placental and fetal weight and on fetal brain gene expression. Two-month-old female C57BL/6 mice were fed 16% (normal-fat, NF), 45% fat (HF), or HF substituted with vegetables (5% energy, HF+VS) diets for 12 weeks. Dams were then bred with NF diet-fed male mice. Placenta and fetal weights were measured at gestational age 19 (D19). RNA was isolated from fetal whole brains and sequenced using Illumina HiSeq. HF+VS diet prevented maternal HF diet-induced decreases in placental weight at D19. Feeding of a maternal HF diet was associated with 79 differentially expressed genes (DEGs), while maternal vegetable substitution was associated with 131 DEGs. The vegetable substitution diet decreased Apold1 (P=.0319), Spata2l (P=.0404), and Celsr1 (P<.03) expression compared to HF diet. Enrichment analysis of HF vs. HF+VS DEGs identified that synapse organization and regulation of embryonic development were significantly represented. KEGG enrichment analysis identified a significant representation of DEGs in the ubiquitin mediated proteolysis pathway in HF vs. HF+VS, and chemokine signaling pathway in NF vs. HF. These findings suggest that at D19, in a rodent model, a maternal HF diet alters placental and fetal growth, and that vegetable supplementation renders a protective effect against these changes. [ABSTRACT FROM AUTHOR]

Maternal low-protein and postnatal high-fat (HF) diets program offspring obesity and type 2 diabetes mellitus (T2DM) risk by epigenetically reducing beige adipocytes (BAs) via increased G9a protein expression (Histone3 Lysine9 dimethyl transferase), an inhibitor of the BA marker fibroblast growth factor 21 (FGF21). Conversely, offspring exercise reduces fat mass and white adipocytes, but the mechanisms are not yet understood. This work investigated whether exercise reduces offspring obesity and T2DM risk caused by a maternal HF diet via regulation of G9a and FGF21 expression that would convert white to BA. Two-month-old female C57Bl/6J mice (F0) were fed a 16% (normal fat; NF) or a 45% HF diet for 3 months prior to breeding, and subsequent gestation and lactation. Male offspring (F1) were fed the same NF and HF diets and further divided into either sedentary (S) or voluntary wheel running (Ex) groups for an additional 3 months yielding eight groups: NF (maternal treatment condition)-NF-S (postweaning treatment conditions), NF-HF-S, NF-NF-Ex, NF-HF-Ex, HF-NF-S, HF-HF-S, HF-NF-Ex, and HF-HF-Ex. Subcutaneous adipose tissue was collected for protein and mRNA analysis of FGF21, peroxisome proliferator-activated receptor-gamma coactivator (PGC-1 alpha, inducer of FGF21), G9a, E4BP4 (G9a coactivator), and protein expression of H3K9 demethylases (KDM4C). Postnatal HF diet decreased FGF21 positive BA numbers regardless of maternal diets and postnatal exercise. Under sedentary conditions, postnatal HF diet increased protein expression of FGF21 transcription inhibitors G9a and E4BP4 compared to NF diet resulting in decreased FGF21 expression. In contrast, postnatal HF diet and exercise decreased G9a and E4BP4 protein expression while decreasing FGF21 expression compared to NF diet. Under exercised condition, postnatal HF diet-induced KDM4C protein expression while no changes in KDM4C protein expression were induced by postnatal HF diet under sedentary conditions. These findings suggest that the postnatal diet exerts a greater impact on offspring adiposity and BA numbers than maternal diets. These data also suggest that offspring exercise induces KDM4C to counter the increase in G9a that was triggered by maternal and postnatal HF diets. Future studies need to determine whether KDM4C induces methylation status of G9a to alter thermogenic function of BA. [ABSTRACT FROM AUTHOR]