Nutrition Intervention to Hispanic Groups: Pilot Studies with Children and Caregivers.

Childhood obesity is a pressing public health issue, especially in the Hispanic community. Two pilot studies were performed; Study 1 was performed to assess the effect of a nutrition education intervention on the nutrition-related knowledge, attitudes, and behaviors of Hispanic children in an after-school program. Nutrition educational lessons were administered 1 h per week. Evaluation was conducted as a baseline Pre-test, a Post-test (following the last session) and a 4-month follow-up. Children showed a significant decrease in the consumption of less-healthy foods from the time of the Pre-test to the Post-test measure (P < .05) and could identify healthy foods. Study 2 was performed to assess the effect of a nutrition education intervention on Hispanic children's caregivers' willingness to engage in healthy behaviors. Caregivers increased their willingness to engage in healthy behaviors (P < .05). This indicates that knowledge and attitudes about foods can be altered, and that caregiver education is needed so to ensure that healthy foods are available in a child's diet and to reinforce positive attitudes about foods.

Nutrition Education Intervention to Improve Nutrition-Related Knowledge, Attitudes, and Behaviors for Hispanic Children.

This study was performed to assess the effect of a nutrition education intervention on the nutrition-related knowledge, attitudes, and behaviors of Hispanic children, ages 6-10 years, in a local after-school program. The intervention included seven weekly lessons that lasted an average of 30 minutes each. Pre- and post-tests were used to evaluate the program. There was a statistically significant difference, p < .04, observed for the intervention group (n = 7) between the pre- and posttest scores for knowledge. In addition, the posttest scores for the intervention group were significantly higher, p < .04, than for the control group (n = 3). Changes in nutrition-related attitudes and behavior were not significant. The only measure that showed significant improvement was knowledge about the differences between healthy and unhealthy food choices after the intervention, which is crucial in the development of healthy behaviors.

Bone quality and strength are greater in growing male rats fed fructose compared with glucose.

Optimization of peak bone mass during adolescence is important for osteoporosis prevention. Studies in rodents and humans have demonstrated the harmful effects of sugar intake on bone health. With the high levels of sucrose in the diets of adolescents, it is necessary to understand the influence of glucose and fructose on growing bones. This study compared the effects of dietary glucose and fructose on bone formation, microarchitecture, and strength. Because of the different metabolic effects of glucose and fructose, we hypothesized that their individual effects on bone would be different. Eighteen male Sprague-Dawley rats (age, 60 days) were randomly assigned to high-fructose (n = 9; 40% fructose, 10% glucose) or high-glucose diet (n = 9; 50% glucose) for 12 weeks. Bone measurements included histology and histomorphometry of trabecular bone in the distal femur and a 3-point bending test of the whole tibia. Whole liver mass and postprandial serum glucose, insulin, and triglycerides were used to assess differences in energy metabolism between the diets. There were no differences in food intake, body weight, or visceral adiposity between groups, but fructose consumption led to heavier livers (P = .001) and elevated serum triglycerides (P = .00). The distal femurs of fructose-fed rats had greater bone volume (bone volume/total volume; P = .03), lower bone surface (bone surface/bone volume; P = .02), and thicker trabeculae (trabecular thickness; P = .01). The tibias of the fructose-fed rats also withstood a greater maximum flexure load (P = .032). These results indicate that consumption of the high-fructose diet resulted in stronger bones with enhanced microarchitecture than consumption of the high-glucose diet.

Maternal high fat feeding and gestational dietary restriction: effects on offspring body weight, food intake and hypothalamic gene expression over three generations in mice.

Excessive gestational weight gain and maternal obesity have both been associated with increased incidence of obesity and metabolic disorder in offspring in both humans and animal models. The objectives of this study were to determine (1) whether mild gestational food restriction during the third trimester (GFR) would alter food intake and growth parameters of offspring, (2) whether effects of GFR depended on diet (high fat [HF] vs chow), (3) whether effects of excessive gestational weight gain (WG) would become magnified across generations, and (4) whether diet and GFR would alter hypothalamic gene expression in adult offspring. Three generations of female C57BL/6 mice were fed chow or HF diet, mated at 11 weeks of age and assigned to ad libitum feeding or 25% GFR. Offspring were fed the same diet as their mothers. Results showed (1) maternal gestational WG was positively correlated with offspring WG. (2) HF offspring weighed less (p<0.01) at weaning (WWT) but gained more during the 8 weeks after weaning than chow-fed offspring (p<0.05), resulting in higher final body weights (BW) (p<0.01). (3) HF males from GFR mothers had higher WWT (p<0.05), but subsequent WG and final BW were less (p<0.05) compared to males from ad lib mothers. (4) In the HF group, GFR also resulted in decreased FI (p<0.05) and FE (p<0.07) in offspring, compared to offspring from ad lib mothers. (5) In generation 3, hypothalamic expression of tyrosine hydroxylase was lower in HF males from GFR mothers compared to HF males from ad lib mothers (p<0.05). In conclusion, gender and maternal GFR had independent effects on growth and FI, and hypothalamic gene expression was dependent on both gender and maternal GFR in HF offspring. Even mild food restriction of obese mothers during pregnancy may have beneficial effects in reducing the risk or degree of obesity in offspring.

Direct effects of nutrients, acetylcholine, CCK, and insulin on ghrelin release from the isolated stomachs of rats.

Ghrelin is a powerful orexigenic peptide predominantly secreted by the stomach. Blood concentration of ghrelin increases before meals and fall postprandial. Its regulation appears to be influenced by the type of macronutrient ingested, the vagus nerve stimulation and by other post-meal stimulated hormonal factors. However, the direct role of nutrients (amino acids or lipids), neuronal (vagal neurotransmitter acetylcholine) and satiety-inducing factor such as CCK are not known. To study this we applied amino acids, lipids, acetylcholine and CCK via vascular perfusion to the isolated stomachs and found that amino acids significantly reduced ghrelin release from the isolated stomach by approximately approximately 30% vs. the control while lipids (10% intralipid) had no affect. Acetylcholine (1 microM) increased ghrelin release from the stomach by approximately 37% whereas insulin (10nM) decreased it by approximately 30% vs. the control. Interestingly, CCK (100 nM) potently increased ghrelin release by approximately 200% vs. the control. Therefore it appears that ghrelin secretion from the stomach is under direct influence of amino acids, neurotransmitter acetylcholine and hormones such as insulin and CCK.

Role of AgRP on Ghrelin-induced feeding in the hypothalamic paraventricular nucleus.

MT II, agonist for MC3/4-Rs, inhibited Ghrelin's orexigenic effect in the paraventricular nucleus of the hypothalamus (PVN). To further investigate the role of the melanocortin system as mediator of ghrelin's orexigenic actions, we explored the involvement of AgRP in Ghrelin's orexigenic effect by testing the effect on food intake after their co-administration in the PVN, during the light and dark phases of feeding in rats. During both the phases of feeding, co-administration of Ghrelin with either AgRP 50 or AgRP 100 pmol into the PVN did not produce a synergistic effect on the food intake, suggesting that ghrelin induction of feeding occurs by recruiting Agrp as one of the obligatory mediators of its orexigenic effect.

Action of MT-II on ghrelin-induced feeding in the paraventricular nucleus of the hypothalamus.

Ghrelin is a 28 amino-acid peptide that has been shown to induce positive energy balance when administered both peripherally and centrally. This effect appears to occur by increasing food intake and by reducing fat utilization. Ghrelin injected into the PVN increases food intake dose-dependently. The NPY receptor has been implicated in the orexigenic effect of ghrelin, but until now, the role of melanocortins on the effect of ghrelin in the PVN has not been reported. Sprague-Dawley rats were stimulated to eat by PVN ghrelin. Pre-injection of 10 pmol of MT II into the PVN caused a significant decrease in ghrelin-induced feeding in both 0-1 h and 0-4 h food intake studies. This finding indicates that MC 3/4-R signaling appears to be recruited by ghrelin, in the PVN, in its role to induce feeding.

Interrelationships between mu opioid and melanocortin receptors in mediating food intake in rats.

The present study examined the interrelationships between feeding responses produced by mu opioid receptor agonists and melanocortin-3 or 4 (MC-3/4) receptor antagonists. Feeding induced by the mu-sensitive opioid peptide, beta-endorphin (betaEND, 10 microg, i.c.v.) was significantly and dose-dependently reduced by pretreatment with the MC-3/4 receptor agonist, melanotan-II (MTII: 0.01-10 nmol, i.c.v.). Moreover, the selective mu opioid antagonist, beta-funaltrexamine (betaFNA: 2-20 mug, i.c.v.), significantly and dose-dependently reduced feeding and weight gain elicited by the potent MC-3/4 receptor antagonist, SHU-9119 (0.5 nmol, i.c.v.), especially at those intake periods (24-48 h) when SHU-9119 produced maximal ingestive effects. These data extend previous findings demonstrating interactions between opioid and melanocortin receptors in the mediation of food intake.

Agouti-related protein: appetite or reward?

Agouti-related protein (AgRP) is an orexigenic peptide that acts as an antagonist of the melanocortin-3 and -4 receptors in the hypothalamus. Studies suggest that the melanocortin and opioid systems interact in the control of ingestive behavior. Also, AgRP has been shown to especially increase intake of a palatable diet. Given these observations, we wished to examine whether the effects of AgRP on ingestive behavior resemble those of opioids. AgRP was injected into the hypothalamic paraventricular nucleus in animals given a choice between a palatable sucrose solution and calorically dense chow. As a result of AgRP injection, animals increased intake of chow but not sucrose relative to controls, in contrast to what has been seen with opioid agonists. These results together with prior findings suggest that the primary effect of AgRP is to cause an increase in food intake to satisfy energy needs, though AgRP also has opioid-like effects, possibly due to melanocortin-opioid interactions.

Effect of Agouti-related protein on development of conditioned taste aversion and oxytocin neuronal activation.

Agouti-related protein (Agrp) is an orexigenic peptide that acts as an antagonist of the melanocortin-3 and -4 receptors. Initial studies suggest similarities between the effects of Agrp and opioid peptides on ingestive behavior. Given these observations, we examined whether Agrp, similarly to opioids, alleviates conditioned taste aversion (CTA) generated by peripheral injection of LiCl. Agrp (1 nmol) delivered to the lateral cerebral ventricle, a dose known to cause orexigenic effects, was shown to partially block acquisition of LiCl-induced CTA. Agrp also decreased the percentage of c-Fos-positive oxytocin neurons induced by LiCl in the hypothalamic paraventricular and supraoptic nuclei. Inhibitory effects of Agrp on acquisition of CTA and aversion-associated activation of oxytocin neurons parallel what has previously been shown with opioid receptor agonists.