Family Dinner and Adolescent Overweight

Objective: The purpose of this study was to examine both cross‐sectional and longitudinal associations between frequency of family dinner and overweight status in a large sample of 9‐ to 14‐year‐old children. Research Methods and Procedures: We studied a cohort of 7784 girls and 6647 boys, 9 to 14 years of age at baseline in 1996, participating in the Growing Up Today Study. From annual mailed surveys, we calculated BMI from self‐reported height and weight and assessed frequency of family dinner over the previous year. We defined “overweight” as age‐ and sex‐specific BMI >85th percentile. We performed multiple logistic regression analyses; the longitudinal analyses assessed the association of previous year family dinner consumption with 1‐year incidence of becoming overweight, using prospective data from 1996 through 1999. Results: At baseline in 1996, 16% of participants had family dinner “never or some days,” 40% on “most days,” and 44% “every day.” Across these categories, overweight prevalence for girls was 19.4%, 16.6%, and 16.7% and for boys was 24.6%, 23.3%, and 22.7%, respectively. In cross‐sectional analyses, adjusting for potential confounders, the odds of being overweight was 0.85 [95% confidence interval (CI): 0.76, 0.96] among children who ate family dinner on “most days” or “every day” compared with those who ate family dinner “never or some days.” In longitudinal multivariate models, the odds ratios between previous year frequency of eating family dinner and 1‐year incidence of becoming overweight were 0.95 (95% CI: 0.78, 1.16) and 1.04 (95% CI: 0.85, 1.27) for children who ate family dinner on “most days” and “every day,” respectively, compared with those who ate family dinner “never or some days.” Discussion: The frequency of eating family dinner was inversely associated with overweight prevalence at baseline but not with likelihood of becoming overweight in longitudinal analyses.     

Increased activity of rat liver N2-guanine tRNA methyltransferase II in response to liver damage

Alterations in rat liver transfer RNA (tRNA) methyltransferase activities have been observed after liver damage by various chemicals or by partial hepatectomy. The qualitative and quantitative nature of these activity changes and the time course for their induction have been studied. Since homologous tRNAs are essentially fully modified in vivo, E. coli tRNAs were used as in vitro substrates for the rat liver enzymes in these studies. Each of the liver-damaging agents tested rapidly caused increases in activities of the enzyme(s) catalyzing methyl group transfer to tRNAs that have an unmodified guanine at position 26 from the 5′ end of the molecule. This group of tRNAs includes E. coli tRNA^Nfmet, tRNA^Ala₁, tRNA^Leu₁, or ^Leu₂, and tRNA^Ser₃ (Group 1). In each case N²-methylguanine and N²,N²-dimethylguanine represented 90% or more of the products of these in vitro methylations. The product and substrate specificity observed are characteristic of N²-guanine methyltransferase II ($\text{S-}\text{adenosyl}\text{-}\text{L}\text{-}\text{methionine:tRNA}$ (guanine-2)-methyltransferase, EC 2.1.1.32). In crude and partially purified preparations derived from livers of both control and treated animals this enzyme activity was not diminished significantly by exposure to 50°C for 10 min. The same liver-damaging agents induced little or no change in the activities of enzymes that catalyze methyl group transfer to various other E. coli tRNAs that do not have guanine at position 26 (Group 2). The results of mixing experiments appear to rule out the likelihood that the observed enzyme activity changes are due to stimulatory or inhibitory materials present in the enzyme preperations from control or treated animals. Thus, our experiments indicate that liver damage by each of several different methods, including surgery or administration of chemicals that are strong carcinogens, hepatotoxins, or cancer-promoting substances, all produce changes in liver tRNA methyltransferase activity that represent a selective increase in activity of N²-guanine tRNA methyltransferase II. It is proposed that the specificity of this change is not fortuitous, but is the manifestation of an as yet unidentified regulatory process.