BACKGROUND: The purpose of this research was to investigate the relationship of unbalanced diet habits and eating behaviors between school age children and their mothers. METHODS: From the Wonju area of Gangwon-do, 232 children and their mothers were recruited for this study. General characteristics, degree of unbalanced diet, eating behaviors, factors associated with food preferences, food preferences, and food intake frequencies were obtained through a questionnaire. RESULTS: The degree of unbalanced diet habits were significantly correlated between school age children and their mothers. Children's eating behaviors were also highly affected by their mother's eating behaviors. Especially, the frequency of eating breakfast showed a significant correlation between children and mothers. Among the factors associated with food preferences, family eating habits, appetite, and emotions showed significant associations between girls and mothers. As for food preferences, preference for meat in children was not significantly associated with that in their mothers, whereas preference for perilla oil and butter was significantly associated with preference in their mothers. The relationship of food preferences between children and mothers differed according to the sex of the children. Further, the intake frequencies for most foods were highly correlated between children and mothers. CONCLUSIONS: Our study showed that the unbalanced diet habits and eating behaviors of mothers can affect those in their children. Moreover, the correlations of food preferences between children and their mothers were different depending on the sex of the children. Our data suggest that educating mothers about their diet and eating behaviors could improve the eating practices of their children.
Appetite ; Breakfast ; Butter ; Child* ; Diet* ; Eating ; Feeding Behavior* ; Female ; Food Habits ; Food Preferences ; Gangwon-do ; Humans ; Meat ; Mothers* ; Perilla ; Surveys and Questionnaires

BACKGROUND/OBJECTIVES: Iron deficiency in early life is associated with developmental problems, which may persist until later in life. The question of whether iron repletion after developmental iron deficiency could restore iron homeostasis is not well characterized. In the present study, we investigated the changes of iron transporters after iron depletion during the gestational-neonatal period and iron repletion during the post-weaning period. MATERIALS/METHODS: Pregnant rats were provided iron-deficient (< 6 ppm Fe) or control (36 ppm Fe) diets from gestational day 2. At weaning, pups from iron-deficient dams were fed either iron-deficient (ID group) or control (IDR group) diets for 4 week. Pups from control dams were continued to be fed with the control diet throughout the study period (CON). RESULTS: Compared to the CON, ID rats had significantly lower hemoglobin and hematocrits in the blood and significantly lower tissue iron in the liver and spleen. Hepatic hepcidin and BMP6 mRNA levels were also strongly down-regulated in the ID group. Developmental iron deficiency significantly increased iron transporters divalent metal transporter 1 (DMT1) and ferroportin (FPN) in the duodenum, but decreased DMT1 in the liver. Dietary iron repletion restored the levels of hemoglobin and hematocrit to a normal range, but the tissue iron levels and hepatic hepcidin mRNA levels were significantly lower than those in the CON group. Both FPN and DMT1 protein levels in the liver and in the duodenum were not different between the IDR and the CON. By contrast, DMT1 in the spleen was significantly lower in the IDR, compared to the CON. The splenic FPN was also decreased in the IDR more than in the CON, although the difference did not reach statistical significance. CONCLUSIONS: Our findings demonstrate that iron transporter proteins in the duodenum, liver and spleen are differentially regulated during developmental iron deficiency. Also, post-weaning iron repletion efficiently restores iron transporters in the duodenum and the liver but not in the spleen, which suggests that early-life iron deficiency may cause long term abnormalities in iron recycling from the spleen.
Animals ; Diet ; Duodenum ; Hematocrit ; Hepcidins ; Homeostasis ; Iron* ; Iron, Dietary ; Liver ; Rats* ; Recycling ; Reference Values ; RNA, Messenger ; Spleen ; Weaning