Padres Preparados, Jóvenes Saludables: intervention impact of a randomized controlled trial on Latino father and adolescent energy balance-related behaviors.

BACKGROUND: Studies have shown associations among food and activity behaviors and body weight of Latino fathers and adolescents. However, few Latino father-focused interventions have been designed to improve energy balance-related behaviors (EBRBs) and weight status among early adolescents. Thus, this efficacy study aims to evaluate the Padres Preparados, Jóvenes Saludables (Padres) youth obesity prevention program for positive changes in EBRBs (fruit, vegetable, sugar-sweetened beverage (SSB), sweet/salty snack, and fast-food consumption, physical activity, and screen time) and weight status among low-income Latino fathers and adolescents (10-14 years). METHODS: A two-arm (treatment versus delayed-treatment control group) randomized controlled trial was conducted to evaluate the efficacy of 8 weekly experiential learning sessions (2.5 hours each) based on social cognitive theory. The sessions included food preparation, parenting skills, nutrition, and physical activity. The program was delivered to father-adolescent dyads (mothers were encouraged to attend) in trusted community-based settings in a Midwest metropolitan area between 2017 and 2019. In March 2020, in-person implementation was discontinued due to COVID-19 pandemic restrictions, which limited the sample size. Father/adolescent dyads were randomized to treatment or control group within each site. Surveys and measurements were completed by fathers and adolescents to assess changes in food and activity behaviors from baseline to post-intervention. Adolescents also completed 24-hour dietary recall interviews at baseline and post-intervention. Intervention effects were assessed using linear regression mixed models adjusted for covariates and accounting for clustering of participants within sites. RESULTS: Data from 147 father/adolescent dyads who completed at least the baseline data collection were used. No significant differences were observed for baseline to post-intervention changes in adolescents' and fathers' EBRBs or weight status between treatment and control groups. Fathers' SSB and fast food intakes were not statistically significant (p = 0.067 and p = 0.090, respectively). CONCLUSIONS: The Padres program resulted in no significant improvements in adolescent and father EBRBs and weight status. Additional Latino father-focused interventions are needed to examine intervention effects on EBRBs among Latino adolescents. TRIAL REGISTRATION: The Padres Preparados, Jóvenes Saludables study is registered with the U.S. National Library of Medicine, ClinicalTrials.gov Identifier: NCT03469752 (19/03/2018).

Serving vegetables first: A strategy to increase vegetable consumption in elementary school cafeterias.

Vegetable consumption in the United States is low despite the wealth of evidence that vegetables play an important role in reducing risk of various chronic diseases. Because eating patterns developed in childhood continue through adulthood, we need to form healthy eating habits in children. The objective of this study was to determine if offering vegetables before other meal components would increase the overall consumption of vegetables at school lunch. We served kindergarten through fifth-grade students a small portion (26-33 g) of a raw vegetable (red and yellow bell peppers) while they waited in line to receive the rest of their lunch meal. They then had the options to take more of the bell peppers, a different vegetable, or no vegetable from the lunch line. We measured the amount of each vegetable consumed by each child. Serving vegetables first greatly increased the number of students eating vegetables. On intervention days most of the vegetables consumed came from the vegetables-first portions. Total vegetable intake per student eating lunch was low because most students chose to not eat vegetables, but the intervention significantly increased this value. Serving vegetables first is a viable strategy to increase vegetable consumption in elementary schools. Long-term implementation of this strategy may have an important impact on healthy eating habits, vegetable consumption, and the health consequences of vegetable intake.

Soy induces phase II enzymes but does not inhibit dimethylbenz[a]anthracene-induced carcinogenesis in female rats.

Isoflavones in soy may play a role in the prevention of cancer through their capacity to affect antioxidant or protective phase II enzyme activities. This study evaluated the effects of dietary isoflavone levels on the induction of antioxidant and phase II enzyme activities and inhibition of breast carcinogenesis. Female Sprague-Dawley rats (36 d) were fed one of four purified diets with casein, or with soy containing three levels of isoflavonoids (0.03, 0.4 or 0.81 mg/g diet; low, middle and high level of isoflavones, respectively). After 2 wk, enzyme activity was determined of rats (n = 6-7) from each diet group. Liver glutathione peroxidase and glutathione reductase activities, blood glutathione levels, kidney glutathione S-transferase and colon quinone reductase (QR) activities were greater in rats consuming the high isoflavone diet compared to rats consuming the casein diet. Kidney QR and liver, kidney, small intestine, and colon UDP-glucuronosyltransferase activities were greater in rats fed the high isoflavone diet compared to rats fed the casein and low-isoflavone diets. Liver and blood oxidized glutathione were lower in rats fed the high-isoflavone diet compared to those fed the low-isoflavone diet. A subset of rats (n = 86) was fed the purified diets for 2 wk and intubated with dimethylbenz[a]anthracene or peanut oil and palpated weekly for tumors. At 13 wk, there was an inverse relationship (R(2) = 0.911, P < 0.09) between tumor incidence and increasing isoflavone intake. These data support the mechanism of soy and soy isoflavones as antioxidant and phase II enzyme inducers, but not as tumor inhibitors.

Soy feeding induces phase II enzymes in rat tissues.

The ability of soy to induce phase II detoxification enzymes was evaluated in male Sprague-Dawley rats. Soybeans contain biologically active compounds that are known inducers of phase II enzyme activity. Rats were fed soy flour (SF) or soy protein isolate (SPI) to provide 75% of total protein as soy. Rats were given free access to food for one- and two-week periods before enzyme activity was compared with that of casein control groups (AIN-93G). Hepatic glutathione S-transferase (GST) activity was significantly greater in rats fed SF for one and two weeks and in rats fed SPI for two weeks than in controls. Quinone reductase activity was significantly greater (12- to 14-fold) in the colon of rats fed SF and SPI for two weeks and in serum (1.8- to 2-fold) in the SF group at one and two weeks. Liver, kidney, and small intestine uridine 5'-diphosphate-glucuronosyl transferase activity was significantly increased in the SPI and SF groups at two weeks. A time dependence in induction of phase II enzymes was observed in several tissues. There was no significant difference in total liver glutathione in either diet group compared with controls. The data indicate that dietary soy enhances phase II enzyme activity, especially quinone reductase and uridine 5'-diphosphate-glucuronosyl transferase, which could lead to protection from potentially harmful xenobiotics.

Modulation of rat hepatic cytochrome P-450 activity by garlic organosulfur compounds.

Garlic organosulfur compounds exert chemopreventive effects at several organ sites in rodents after administration of chemical carcinogens, possibly by inhibiting carcinogen activation via cytochrome P-450-mediated oxidative metabolism. It has been suggested that the variability in potency of tumor inhibition by garlic sulfur compounds is due to structural differences, such as the number of allyl and sulfur groups. In this study, diallyl sulfide (DAS), diallyl disulfide (DADS), and allyl methyl sulfide (AMS) were administered to acetone-treated adult male Sprague-Dawley rats by gastric gavage at a dose of 1.75 mmol/kg in cottonseed oil. After 15 hours, hepatic microsomal cytochrome P-450 activity and content were examined. The activity of p-nitrophenol (pNP) hydroxylase (E.C. 1.14.13.29) was significantly decreased by all garlic compounds, whereas benzphetamine N-demethylase and ethoxyresorufin O-deethylase activities were not changed. The activity of pNP hydroxylase was decreased to 31%, 54%, and 65% of control activity, and immunodetectable CYP2E1 protein levels were decreased in a similar manner by DAS, DADS, and AMS, respectively. Additional acetone-treated rats were given 4-methyl pyrazole, a ligand specific for CYP2E1, intraperitoneally five hours after garlic compound administration. Ten hours later, pNP hydroxylase activity was decreased to 73%, 78%, and 67% of control levels by DAS, DADS, and AMS, respectively. Further studies are needed to determine whether the variable potency of inhibition of CYP2E1 enzyme activity is related to chemopreventive efficacy of garlic sulfur compounds.

Coconut oil and sesame oil affect lymphatic absorption of cholesterol and fatty acids in rats.

Five groups of male Wistar rats weighing approximately 200 g consumed 12 or 24% sesame oil or coconut oil diets or a control diet (14% corn oil) ad libitum for 4 wk. The thoracic ducts of these rats were cannulated, and a lipid emulsion containing [3H]cholesterol and [14C]oleic acid was given through a duodenal catheter. Lymph was collected for 24 h and the isotopic tracers for cholesterol and fatty acid were measured. Rats fed the 24% sesame oil diet had significantly lower lymphatic cholesterol and fatty acid compared with the control group. Absorption of oleic acid in rats fed 24% coconut oil was significantly greater than in controls during 0-8 h but was not significantly different during 0-24 h. There were no differences among groups in the distribution of cholesterol and oleic acid either in the lymph lipoproteins or in the lipid classes. The significant reduction in lymph cholesterol and fatty acids due to sesame oil feeding may be an important factor in reducing hypercholesterolemia.

Effects of D-limonene on hepatic microsomal monooxygenase activity and paracetamol-induced glutathione depletion in mouse.

1. D-Limonene, a monoterpenoid constituent of citrus fruit oil, blocks tumour induction by chemical carcinogens in laboratory animals, apparently by preventing bioactivation of procarcinogens and by enhancing conjugation of proximal carcinogenic metabolites. 2. Inhibitory effects of D-limonene were measured in vitro using cytochrome P450 isoform-specific substrates. D-Limonene inhibited p-nitrophenol hydroxylase (pNP) activity in vitro in liver microsomes from acetone-, phenobarbital (PB)- and beta-naphthoflavone (BNF)-treated mouse, and 7-ethoxyresorufin O-deethylase (EROD) activity in microsomes from PB- and BNF-treated mouse. p-Nitrophenol and ethoxyresorufin are substrates for cytochromes P2E1 and P1A1, respectively. No inhibition of benzphetamine (BNZP) or aminopyrine (AP) demethylases by D-limonene was observed. 3. EROD, BNZP and AP activities in liver microsomes were increased 18 h after i.p. administration of D-limonene to acetone-induced mouse, while pNP activity was unchanged. The immunodetectable protein level of cytochrome P2B1 in non-acetone treated mouse was increased 18 h after D-limonene, with no differences in P2E1 or P1A1. 4. Acute D-limonene did not protect against paracetamol (acetaminophen)-induced depletion of liver reduced glutathione (GSH). A prolonged paracetamol challenge (0.6% diet for 10 days) elevated liver cytosolic GSH-S-transferase activity (GST) two-fold and decreased liver GSH to 46% of control values. Dietary D-limonene (1.0% diet for 10 days) maintained liver GSH concentrations at 92% of control values in the paracetamol-challenged mouse without altering GST activity. D-Limonene also increased liver GSH concentration (23%) in mouse fed 1.0% D-limonene alone.

Prolonged acetaminophen ingestion by mice fed a methionine-limited diet does not affect iron-induced liver lipid peroxidation or S-adenosylmethionine.

This study determined whether acetaminophen (ACAP)-induced glutathione depletion was associated with liver lipid peroxide formation, or the concentrations of liver S-adenosylmethionine and S-adenosylhomocysteine in mice fed diets with L-methionine below or at the requirement level (0.25 or 0.5%) for 7 wk. Iron dextran (281 mg/kg body wt) or saline was administered for 2 d before measurement of lipid peroxide formation. Chronic dietary ACAP (0.5%) in mice fed 0.25% methionine caused a failure to maintain body weight even though food intake was similar to intake by all other treatment groups. Liver GSH (measured as nonprotein sulfhydryl concentration) and cysteine concentrations were depleted by ACAP and by ACAP plus iron. Liver lipid peroxide formation was increased by iron but was not altered additionally by ACAP ingestion. Liver glutathione peroxidase activity was increased by methionine in controls, whereas glutathione S-transferase activity was increased by ACAP ingestion in mice fed 0.5% methionine compared with controls. Liver S-adenosylmethionine and nuclear 5-methyldeoxycytidine concentrations were not affected by dietary ACAP or methionine. Liver S-adenosylhomocysteine levels were lower in mice fed ACAP and 0.25% methionine compared with mice fed ACAP and 0.5% methionine. In conclusion, chronic ACAP did not increase the susceptibility of mice to liver lipid peroxidation or alter the availability of methyl groups for methylation reactions.

Effects of dietary tin and copper on rat hepatocellular antioxidant protection.

The effects of dietary tin on copper status and on enzymes and metabolites involved in hepatocellular antioxidant protection were measured in rats fed copper-adequate or copper-deficient diets with glucose or fructose. Rats became copper-depleted after 4 weeks on diets containing less than 0.5 micrograms of copper/g as evidenced by significant decreases in liver copper and serum ceruloplasmin. Signs of copper deficiency occurred in copper-depleted rats fed diets containing 100 micrograms of tin/g. Significant effects of tin on liver glutathione peroxidase and superoxide dismutase activities and on liver iron and total glutathione concentrations were observed. Interactions between copper and tin on liver copper and iron and on liver superoxide dismutase and malondialdehyde production are reported. Adverse effects of feeding diets containing 100 micrograms of tin/g include (i) copper depletion in rats fed copper-adequate diets, (ii) accelerated development of copper deficiency in rats fed copper-deficient diets, and (iii) reduction in hepatocellular antioxidant protection.

Recovery of fish oil-derived fatty acids in lymph of thoracic duct-cannulated Wistar rats.

The absorption of equivalent doses of eicosapentaenoic and docosahexaenoic acids was compared in rats when administered as the ethyl ester concentrate, ethyl ester concentrate plus olive oil, free fatty acid or triacylglycerol (menhaden oil). Lymph was collected from a thoracic duct cannula for 24 hr after dosing via an indwelling duodenal catheter. After 24 hr, the absorption of eicosapentaenoic acid was greater for the free fatty acid and menhaden oil than for the ethyl ester form, but docosahexaenoic acid absorption was comparable for all forms. Other rats had greater plasma levels of eicosapentaenoic and docosahexaenoic acids 5 hr after oral gavage dosing with menhaden oil than did rats dosed with the ethyl ester form.

Prolonged acetaminophen ingestion in mice: effects on the availability of methionine for metabolic functions.

The objective of this study was to determine the effect of prolonged ingestion of acetaminophen (ACAP) on the availability of methionine for its metabolic functions in mice. ACAP was fed to weanling mice at levels of 0.0, 0.3, 0.5 or 0.8% of the diet, with methionine provided at requirement (0.5%) or at twice the requirement (1.0%) level, for 2 wk to assess its effect on the availability of methionine for growth. In another study, ACAP was fed to adult mice at levels of 0.0, 0.4, or 0.6% of the diet, with methionine at 0.5 or 1.0% of the diet, for 2 wk to assess its effect on the availability of methionine for protein synthesis and methylation reactions. The growth rate of weanling mice decreased with increasing dietary ACAP in mice fed 0.5% methionine, but not in those fed 1.0%. Hepatic reduced glutathione (GSH) decreased and plasma glutamic-pyruvic transaminase activity increased in an ACAP dose-dependent manner in weanling mice fed 0.5% methionine. Protein synthesizing ability decreased in adult mice fed 0.5% methionine and 0.6% ACAP. Relative liver weight and liver lipid decreased with increasing dietary ACAP in mice fed methionine at or above requirement. Neither plasma creatinine or muscle creatine was affected by variations in dietary methionine or ACAP. Ingestion of ACAP for a prolonged period of time increased the methionine requirement for growth, maintenance of hepatic GSH level and protein synthesis, but did not affect the methionine requirement for methylation reactions.

Alterations in colonic thymidine kinase enzyme activity induced by consumption of various dietary fibers.

Dietary fibers may tend to enhance or inhibit chemically induced experimental colon cancer, depending on the particular fiber consumed. This study examined the relationship between colonic thymidine kinase enzyme activity and mucin histochemistry and the reported effects of various dietary fibers on chemically induced colon carcinogenesis. Fiber-supplemented diets containing fibers reported to inhibit (wheat bran) or enhance (guar gum, carrageenan) chemically induced colon carcinogenesis in the rat were selected. Four groups of male Fischer 344 rats consumed 10% wheat bran, 5% guar gum, 5% carrageenan, or fiber-free diets ad libitum for 4 weeks. At the completion of the treatment period, the distal 12 cm of colonic mucosa was scraped off and homogenized for determination of thymidine kinase activity, and a 0.5-cm section of midcolon was processed by the high-iron diamine/Alcian blue method for mucin histochemistry. Final animal weights did not differ significantly among groups. Thymidine kinase enzyme specific activity (mumole thymidine phosphate formed x 10(6)/min/mg protein, means +/- SEMs) was not significantly different in the fiber-free, wheat bran, and guar gum groups (10.98 +/- 1.50, 7.41 +/- 1.09, and 9.11 +/- 2.04, respectively) but was markedly elevated at 41.84 +/- 4.65 in the carrageenan group (alpha less than 0.001). Mucin histochemistry failed to reveal any significant differences among dietary groups.

Effects of prolonged acetaminophen ingestion and dietary methionine on mouse liver glutathione.

Acetaminophen (ACAP) was fed to adult Swiss-Webster mice for 4 weeks to examine the effect of prolonged ACAP ingestion on hepatic reduced glutathione (GSH) concentrations. In the first experiment, male and female mice were pair-fed diets containing ACAP at levels of 0.0 (control), 0.3, 0.6, and 1.0% of diet on a dry weight basis with the total sulfur-amino acids provided at 0.5% of the diet. Hepatic GSH was depleted, and the percentage of dose excreted as the urinary ACAP-GSH-derived conjugate increased in a dose-dependent manner with increasing ACAP. Serum glutamic-pyruvic transaminase activity, relative liver weight, and hepatic microsomal protein content increased in the group given 1.0% ACAP, but microsomal aniline hydroxylation decreased. In the second experiment, adult male mice were fed ad libitum diets containing 0.0 or 0.6% ACAP with total L-methionine provided at 0.25, 0.5 (requirement level), or 1.0%. Hepatic GSH was markedly depleted 1 week after initiation of ACAP treatment in all groups except those receiving 1.0% methionine. This reduction persisted throughout the 4-week treatment period. After 4 weeks, liver cysteine was also reduced as a result of ACAP ingestion and methionine deficiency, whereas serum inorganic sulfate concentration was not changed. Reduction in hepatic cysteine levels was also prevented by 1.0% dietary methionine. The dose-dependent depletion of GSH, the trend toward an increase in ACAP-GSH-derived conjugate excretion, and the prevention of GSH depletion by providing dietary methionine in excess of requirement indicate that prolonged ingestion of ACAP may increase the requirement for sulfur-containing amino acids and limit the availability of methionine and cysteine for protein synthesis, methylation reactions, and drug detoxification.

Effects of methionine deficiency and ethanol ingestion on acetaminophen metabolism in mice.

The interaction of the effect of dietary methionine on the availability of hepatic glutathione (GSH) and the effect of chronic ethanol (EtOH) consumption on the activity of the hepatic oxidation system was studied in relation to acetaminophen (ACAP) metabolism in mice. Adult male Swiss-Webster mice were pair-fed for 4 wk an EtOH-containing liquid diet that provided 50 or 100% of the methionine requirement in a 2 X 2 factorial design. Hepatic microsomal protein, relative liver weight and microsomal aniline hydroxylase activity were higher in EtOH-fed groups than in non-EtOH-fed groups. After an ACAP dose of 300 mg/kg body wt i.p., serum inorganic sulfate, endogenous hepatic methionine and GSH concentrations were lower, whereas uridine diphosphoglucuronosyltransferase activity was not changed compared to controls. GSH levels were lowered to a greater extent in the methionine-deficient groups than in methionine-sufficient groups. Incorporation of [35S]methionine into hepatic proteins was lower in all treatment groups after ACAP administration than in controls. The distribution of ACAP into the urinary sulfate conjugates was lower in methionine-deficient than in methionine-sufficient groups, and the percentage of sulfate and mercapturic acid conjugates formed as determined by high-performance liquid chromatographic analysis was higher in mice fed EtOH than in controls. Methionine deficiency compromises the normal pathways of ACAP disposition in the mouse, and chronic EtOH ingestion may potentiate this effect by increasing the amount of activated ACAP formed.

Effects of dietary methionine and ethanol on acetaminophen hepatotoxicity in mice.

The possible interactive relationship between nutritional compromise of acetaminophen detoxification and ethanol enhancement of acetaminophen hepatotoxicity was studied in mice by using a 2-X-2 factorial design. Ethanol was administered to adult male mice at 0 or 15% solution in the drinking water, and dietary methionine levels were at 54 or 100% of the requirement. After 4 weeks, a significant reduction in the median lethal time (LT50) following a high dose of acetaminophen was seen in the methionine-deficient groups. Methionine deficiency also caused a reduction in hepatic glutathione levels in the control group and in mice receiving sublethal doses of acetaminophen. PGOT levels were increased significantly by methionine deficiency but were markedly increased by the interaction of ethanol treatment and methionine deficiency. Glutathione-S-transferase activity was not affected by any treatment combinations, and p-nitroanisole O-demethylase activity and relative liver weights were not increased because of chronic ethanol ingestion. These findings indicate that methionine deficiency causes glutathione reduction, which predisposes the mouse to increased acetaminophen hepatotoxicity. Ethanol consumption did not seem to potentiate the increased hepatotoxic effects caused by methionine deficiency, except as indicated by PGOT activity.