The majority of US youth are of healthy weight, but the majority of US adults are overweight or obese. Therefore, a major health challenge for most American children and adolescents is obesity prevention-today, and as they age into adulthood. In this report, we review the most recent evidence regarding many behavioral and practice interventions related to childhood obesity, and we present recommendations to health care providers. Because of the importance, we also suggest approaches that clinicians can use to encourage obesity prevention among children, including specific counseling strategies and practice-based, systems-level interventions. In addition, we suggest how clinicians may interact with and promote local and state policy initiatives designed to prevent obesity in their communities.www.pediatrics.org/cgi
The adoption of healthful lifestyles by individuals and families can result in a reduction in many chronic diseases and conditions of which obesity is the most prevalent. Obesity prevention, in addition to treatment, is an important public health priority. This clinical report describes the rationale for pediatricians to be an integral part of the obesity-prevention effort. In addition, the 2012 Institute of Medicine report “Accelerating Progress in Obesity Prevention” includes health care providers as a crucial component of successful weight control. Research on obesity prevention in the pediatric care setting as well as evidence-informed practical approaches and targets for prevention are reviewed. Pediatricians should use a longitudinal, developmentally appropriate life-course approach to help identify children early on the path to obesity and base prevention efforts on family dynamics and reduction in high-risk dietary and activity behaviors. They should promote a diet free of sugar-sweetened beverages, of fewer foods with high caloric density, and of increased intake of fruits and vegetables. It is also important to promote a lifestyle with reduced sedentary behavior and with 60 minutes of daily moderate to vigorous physical activity. This report also identifies important gaps in evidence that need to be filled by future research.
ABSTRACT. Background. Leptin, the protein product of the ob gene, is produced by the adipocyte and seems to function as a link between adiposity, satiety, and activity. Leptin has also been found to be necessary for pubertal development, conception, and pregnancy in mice, and is increased in prepubertal children, independent of adiposity, suggesting a role in childhood growth and development. This study investigated 100 mother/newborn pairs to determine the role of leptin in neonatal development. Placental tissue was assayed for leptin mRNA to evaluate it as a source of leptin production in utero.Methods. One hundred mother/newborn pairs were enrolled in this study. Radioimmunoassay was performed for leptin on maternal venous and newborn cord blood. Leptin concentrations were measured in 43 children in Tanner stages 1 and 2 as a control group. Placental tissue was obtained from five mothers and assayed for leptin mRNA by reverse transcription/polymerase chain reaction (RT/PCR). Human placental cell lines JAR and JEG-3 were also assayed for leptin mRNA expression.Results. Leptin was present in all newborns studied at a mean concentration of 8.8 ng/mL (؎9.6 standard deviations). Leptin concentrations in cord blood correlated with newborn weight (r ؍ .51), body mass index (BMI) (r ؍ .48), and arm fat (r ؍ .42). There was no correlation between leptin and insulin. When statistically covarying for adiposity for newborns and Tanner stages 1 and 2 children, newborns had greater concentrations of leptin (mean, 10.57 ng/mL) than children (mean, 3.04 ng/mL). Leptin was present in all mothers at a mean value of 28.8 ng/mL (؎22.2 standard deviations). Leptin concentration correlated with prepregnancy BMI (r ؍ .56), BMI at time of delivery (r ؍ .74), and arm fat (r ؍ .73). Maternal leptin correlated with serum insulin (r ؍ .49). There was no correlation between maternal and newborn leptin concentrations. Thirteen percent of newborns had higher leptin concentrations than their mothers. Placental tissue from five separate placentas expressed leptin mRNA at comparable or greater levels than adipose tissue. Two human trophoblastic placental cell lines, JAR and JEG-3, also expressed leptin mRNA. Conclusions.The correlation between leptin and adiposity found in children and adults was also found in newborns. Serum leptin concentrations in newborns were increased more than three-fold compared with children in Tanner stages 1 and 2 when controlling for adiposity, suggesting that leptin concentrations in the newborn are not explained by adiposity alone. Maternal leptin concentrations correlated with measures of adiposity at delivery but did not correlate with newborn adiposity or leptin. Leptin mRNA was expressed both in placental tissue and in two human placental cell lines. These data suggest that leptin has a role in intrauterine and neonatal development and that the placenta provides a source of leptin for the growing fetus. Pediatrics 1997; 100(1). URL: http://www.pediatrics.org/cgi/content/full/ 100/1/e1; leptin, ...
Leptin has recently been shown to be produced by the human placenta and potentially plays a role in fetal and neonatal growth. Many functions of the placenta are replaced by the mammary gland in terms of providing critical growth factors for the newborn. In this study, we show that leptin is produced by human mammary epithelial cells as revealed by RT/PCR analysis of total RNA from mammary gland and immunohistochemical staining of breast tissue, cultured mammary epithelial cells, and secretory epithelial cells present in human milk. We also verify that immunoreactive leptin is present in whole milk at 30- to 150-fold higher concentrations than skim milk. We propose that leptin is secreted by mammary epithelial cells in milk fat globules, which partition into the lipid portion of breast milk.
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