PUYAU, MAURICE R., ANNE L. ADOLPH, FIROZ A. VOHRA, AND NANCY F. BUTTE. Validation and calibration of physical activity monitors in children. Obes Res. 2002;10:150 -157. Objective: This study was designed to validate accelerometer-based activity monitors against energy expenditure (EE) in children; to compare monitor placement sites; to field-test the monitors; and to establish sedentary, light, moderate, and vigorous threshold counts. Research Methods and Procedures:Computer Science and Applications Actigraph (CSA) and Mini-Mitter Actiwatch (MM) monitors, on the hip or lower leg, were validated and calibrated against 6-hour EE measurements by room respiration calorimetry, activity by microwave detector, and heart rate by telemetry in 26 children, 6 to 16 years old. During the 6 hours, the children performed structured activities, including resting metabolic rate (RMR), Nintendo, arts and crafts, aerobic warm-up, Tae Bo, treadmill walking and running, and games. Activity energy expenditure (AEE) computed as EE Ϫ RMR was regressed against counts to derive threshold counts. Results: The mean correlations between EE or AEE and counts were slightly higher for MM-hip (r ϭ 0.78 Ϯ 0.06) and MM-leg (r ϭ 0.80 Ϯ 0.05) than CSA-hip (r ϭ 0.66 Ϯ 0.08) and CSA-leg (r ϭ 0.73 Ϯ 0.07). CSA and MM performed similarly on the hip (inter-instrument r ϭ 0.88) and on the lower leg (inter-instrument r ϭ 0.89). Threshold counts for the CSA-hip were Ͻ800, Ͻ3200, Ͻ8200, and Ն8200 for sedentary, light, moderate, and vigorous categories, respectively. For the MM-hip, the threshold counts were Ͻ100, Ͻ900, Ͻ2200, and Ն2200, respectively. Discussion: The validation of the CSA and MM monitors against AEE and their calibration for sedentary, light, moderate, and vigorous thresholds certify these monitors as valid, useful devices for the assessment of physical activity in children.

SUMMARY Hepatic glucose release into the circulation is vital for brain function and survival during periods of fasting and is modulated by an array of hormones that precisely regulate plasma glucose levels. We have identified a fasting-induced protein hormone that modulates hepatic glucose release. It is the C-terminal cleavage product of profibrillin, and we name it Asprosin. Asprosin is secreted by white adipose, circulates at nanomolar levels, and is recruited to the liver, where it activates the G protein-cAMP-PKA pathway, resulting in rapid glucose release into the circulation. Humans and mice with insulin resistance show pathologically elevated plasma asprosin, and its loss of function via immunologic or genetic means has a profound glucose- and insulin-lowering effect secondary to reduced hepatic glucose release. Asprosin represents a glucogenic protein hormone, and therapeutically targeting it may be beneficial in type II diabetes and metabolic syndrome.

This article reviews maternal metabolic strategies for accommodating fetal nutrient requirements in normal pregnancy and in gestational diabetes mellitus (GDM). Pregnancy is characterized by a progressive increase in nutrient-stimulated insulin responses despite an only minor deterioration in glucose tolerance, consistent with progressive insulin resistance. The hyperinsulinemic-euglycemic glucose clamp technique and intravenous-glucose-tolerance test have indicated that insulin action in late normal pregnancy is 50-70% lower than in nonpregnant women. Metabolic adaptations do not fully compensate in GDM and glucose intolerance ensues. GDM may reflect a predisposition to type 2 diabetes or may be an extreme manifestation of metabolic alterations that normally occur in pregnancy. In normal pregnant women, basal endogenous hepatic glucose production (R(a)) was shown to increase by 16-30% to meet the increasing needs of the placenta and fetus. Total gluconeogenesis is increased in late gestation, although the fractional contribution of total gluconeogenesis to R(a), quantified from (2)H enrichment on carbon 5 of glucose (65-85%), does not differ in pregnant women after a 16-h fast. Endogenous hepatic glucose production was shown to remain sensitive to increased insulin concentration in normal pregnancy (96% suppression), but is less sensitive in GDM (80%). Commensurate with the increased rate of glucose appearance, an increased contribution of carbohydrate to oxidative metabolism has been observed in late pregnancy compared with pregravid states. The 24-h respiratory quotient is significantly higher in late pregnancy than postpartum. Recent advances in carbohydrate metabolism during pregnancy suggest that preventive measures should be aimed at improving insulin sensitivity in women predisposed to GDM. Further research is needed to elucidate the mechanisms and consequences of alterations in lipid metabolism during pregnancy.