This study represents the first attempt to evaluate the American Medical Association Nutrition Advisory Group (NAG) recommendations for intravenous vitamin A, D, and E dosages for infants and children. Patients studied included 18 preterm infants (group 1) and 26 term infants and children (group 2A) receiving total parenteral nutrition for 2 to 4 weeks and eight infants and children receiving total parenteral nutrition for 3 to 6 months (group 2B). Term gestation infants and children up to 11 years of age all received the same dosages (those that were recommended by the NAG for children weighing more than 10 kg). Preterm infants received 65% of these doses. In group 1, cord blood α-tocopherol levels were <0.22 mg/dL in seven preterm infants (reference value = 0.29 ± 0.04), but mean levels increased to 1.65 ± 0.17 mg/dL after four days of treatment. Eight infants consistently received additional vitamin E orally (80 to 150 mg daily), and their levels increased to 2.18 ± 0.26 mg/dL by four days of study and to 3.49 ± 0.57 mg/dL after 3 weeks. Oral supplementation in the preterm infants appeared to be unnecessary because intravenous vitamins alone maintained levels above 1.1 mg/dL. In group 2, α-tocopherol levels were maintained within the reference range. Patients receiving lipid emulsions containing substantial quantities of α-tocopherol had significantly higher blood levels than patients receiving lipid emulsions containing little α-tocopherol (P < .01). Mean 25-OH vitamin D levels were mintained above or within the reference range in groups 2A and 2B. Although only seven patients in group 1 had measurements performed after beginning total parenteral nutrition, their 25-OH vitamin D levels increased during total parenteral nutrition and were maintained within the reference range. Mean vitamin A levels in group 2 were maintained within the reference range of 23.5 ± 1.8 µg/dL, although three of eight patients in group 2A who had levels 2 SD less than the reference mean levels initially did not increase their levels during the 2-week period of treatment. Patients on home total parenteral nutrition (group 2B) showed a mean increase in retinol, from 29.2 ± 3.0 µg/dL to 37.4 ± 7.1 µg/dL. There was also good correlation between retinol-binding protein and retinol in all patients in group 2. Premature infant (group 1) levels were 13.9 ± 1.3 µg/dL initially (reference value = 15.7 µg/dL) and did not change after 28 days of treatment (13.5 ± 2.5 µg/dL). In addition, there was poor correlation with retinol-binding protein. The failure of retinol to increase with treatment may be secondary to losses of retinol in the delivery system. Further studies are needed to better define vitamin A and D needs during parenteral feeding of premature infants, although the dosage levels in term infants appear to maintain mean blood levels of all of the vitamins within the reference range.
Summary ― Insulin and glucagon levels, the mass of glucose presented to the liver and the portal signal are important regulators of the liver's response to glucose delivery. The portal signal not only serves to direct glucose into the liver but also appears to stimulate its deposition in glycogen. Moreover, the portal signal impacts on tissues other than the liver: intraportal glucose delivery is associated with changes in glucose uptake by nonhepatic tissues and neurally-mediated enhancement of pancreatic insulin secretion. Our current understanding of the neural control of hepatic glucose metabolism includes a tonic block to the entry of glucose into the liver, probably mediated both by sympathetic neural activity and by a low insulin:glucagon ratio. An increase in the portal vein glucose level is detected by sensors in the portal region, which cause a decrease in the firing rate in the afferent fibers in the hepatic branch of the vagus nerve. The change in the afferent firing rate is processed in the hypothalamus and instigates a change in the efferent firing rate in the hepatic and pancreatic branches of the vagus (with corresponding increases in insulin secretion and net hepatic glucose uptake). The
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