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Objectives: To develop and validate a prediction model for fat mass in infants ≤12 kg using easily accessible measurements such as weight and length., Study Design: We used data from a pooled cohort of 359 infants age 1-24 months and weighing 3-12 kg from 3 studies across Southern California and New York City. The training data set (75% of the cohort) included 269 infants and the testing data set (25% of the cohort) included 90 infants age 1-24 months. Quantitative magnetic resonance was used as the standard measure for fat mass. We used multivariable linear regression analysis, with backwards selection of predictor variables and fractional polynomials for nonlinear relationships to predict infant fat mass (from which lean mass can be estimated by subtracting resulting estimates from total mass) in the training data set. We used 5-fold cross-validation to examine overfitting and generalizability of the model's predictive performance. Finally, we tested the adjusted model on the testing data set., Results: The final model included weight, length, sex, and age, and had high predictive ability for fat mass with good calibration of observed and predicted values in the training data set (optimism-adjusted R 2 : 92.1%). Performance on the test dataset showed promising generalizability (adjusted R 2 : 85.4%). The mean difference between observed and predicted values in the testing dataset was 0.015 kg (-0.043 to -0.072 kg; 0.7% of the mean)., Conclusions: Our model accurately predicted infant fat mass and could be used to improve the accuracy of assessments of infant body composition for effective early identification, surveillance, prevention, and management of obesity and future chronic disease risk., (Copyright © 2022 Elsevier Inc. All rights reserved.)

Scope: Glucose intolerance during pregnancy is associated with short- and long-term maternal and offspring health consequences. In young male mice, knockout of the major pro-inflammatory mediator interleukin-1-receptor-1 (IL1R1) protects against high-fat diet (HFD)-induced glucose intolerance and metabolic dysfunction. This phenotype has not been examined during pregnancy. The hypothesis that IL1R1 depletion will protect females against HFD-induced glucose intolerance and metabolic dysfunction before, during, and post pregnancy is tested., Methods and Results: C57BL/6J control and IL1R1 knockout (IL1R1 -/- ) mice are randomized to either a control diet (10% kcal from fat) or HFD (45% kcal from fat), and three distinct cohorts are established: nulliparous, pregnant, and postpartum females. Contrary to the authors' hypothesis, it is found that IL1R1 -/- does not protect against glucose intolerance in nulliparous or pregnant females, and while control HFD animals see a resolution of glucose tolerance postpartum, IL-1R1 -/- mice remain impaired. These effects are accompanied by adipocyte hypertrophy, hyperleptinemia, and increased adipose tissue inflammatory gene expression. Maternal genotype differentially affects fetal growth in male and female fetuses, demonstrating sexual dimorphism in this genotype prior to birth., Conclusions: These findings suggest that IL1R1 signaling is important for normal metabolic functioning in females, during and outside of pregnancy., (© 2019 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.)

Background: Sugar-sweetened beverage consumption is associated with metabolic dysfunction. Artificially sweetened beverages (ASBs) are often promoted as an alternative. However, evidence for the safety of ASB consumption during pregnancy is lacking., Objectives: The effects of sugar-sweetened beverage and ASB consumption during pregnancy in mice were examined, and we hypothesized that both sugar-sweetened beverages and ASBs would impair maternal metabolic function., Methods: Pregnant female C57BL/6J mice received control drinking water (CD), high-fructose corn syrup (Fr; 20% kcal intake; 335 mM), or the artificial sweetener acesulfame potassium (AS; 12.5 mM) in their drinking water, from gestational day (GD) 0.5 (n = 8/group). Body weights and food and water intakes were assessed every second day, an oral-glucose-tolerance test (OGTT) was performed at GD 16.5, and mice were culled at GD 18.5. RT-PCR was carried out on adipose tissue, liver, and gut. Adipose tissue morphology was assessed using histological methods. In a separate cohort of animals, pregnancy length was assessed. Repeated-measures ANOVA was performed for the OGTT and weight gain data. All other data were analyzed by 1-way ANOVA., Results: Fr and AS significantly impaired glucose tolerance, as demonstrated by OGTT (21% and 24% increase in AUC, respectively; P = 0.0006). Fr and AS reduced expression of insulin receptor (39.5% and 33% reduction, respectively; P = 0.02) and peroxisome proliferator-activated receptor γ (45.2% and 47%, respectively; P = 0.039), whereas Fr alone reduced expression of protein kinase B (36.9% reduction; P = 0.048) and resulted in an increase in adipocyte size and leptin concentrations (40% increase; P = 0.03). AS, but not Fr, reduced male fetal weight (16.5% reduction; P = 0.04) and female fetal fasting blood glucose concentration at cull (20% reduction; P = 0.02) compared with CD. AS significantly reduced the length of pregnancy compared with the CD and Fr groups (1.25 d shorter; P = 0.02)., Conclusions: Fr and AS consumption were associated with maternal metabolic dysfunction in mice. AS was also associated with reduced fetal growth and fetal hypoglycemia. Therefore, ASBs may not be a beneficial alternative to sugar-sweetened beverages during pregnancy., (Copyright © The Author(s) on behalf of the American Society for Nutrition 2020.)