[Preliminary results of comparative trials of oral contraceptives].
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Biomedical subjects
Publications and source records attributed to M Arnold.
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To investigate meal-induced changes in hepatic fat and carbohydrate metabolism in rats, hepatic venous, portal venous, and aortal plasma levels of several metabolites as well as changes in hepatic glycogen and lactate content were measured during and after the first nocturnal meal following a 12-h fast. The rats were fed a diet with about 46%, 41%, and 13% of the total energy (approximately 16.5 kJ/g) derived from carbohydrates, fats, and protein, respectively. During the later part of the meal and thereafter, plasma triglyceride level increased in all blood vessels. After a transient initial decrease, portal venous and aortal nonesterified fatty acid (NEFA) levels, net hepatic NEFA uptake, and hepatic beta-hydroxybutyrate (BHB) production increased and reached fasting (meal onset) values by 30 min after the meal. Although liver glycogen did not change significantly, the liver released glucose continuously. The liver initially accumulated lactate and maintained a high lactate concentration despite switching from lactate uptake to net release of lactate around 10 min into the meal. Taken together, these data indicate that hepatic glycolysis, gluconeogenesis, and considerable fatty acid oxidation occur concurrently in rat liver during and after a fat- and carbohydrate-rich meal. The findings are relevant to contemporary hypotheses of the metabolic control of eating and, in particular, to hypotheses linking hepatic fatty acid oxidation to postprandial satiety.
To determine whether depletion of liver glycogen or accumulation of liver fat (steatosis) was associated with the development of hypoglycaemia in children with fatal diarrhoeal illnesses, a case-control study was carried out comparing 17 children who had blood sugars less than or equal to 30 mg/dl with 17 age matched control children who had blood sugars greater than or equal to 59 mg/dl. The most common causes of diarrhoea in the hypoglycaemic children were Shigella sp. and Vibrio cholerae. The mean duration of diarrhoea before admission for the hypoglycaemic children, 7.8 d, was shorter than the 20.7 d for the controls (P less than 0.01). Most children in both groups showed signs of malnutrition, metabolic acidosis, and pneumonia. Liver specimens were obtained at post-mortem examination and stained with haematoxylin and eosin for general assessment and with periodic acid-Schiff stain for glycogen. Glycogen depletion was detected in 9 hypoglycaemic children and in only 3 control children (P less than 0.05). Hepatic steatosis, on the other hand, occurred with equal frequency in both groups but was associated with severe malnutrition in the hypoglycaemic patients (P less than 0.05). This result suggested that hypoglycaemia develops during acute diarrhoeal illnesses because gluconeogenesis fails to maintain the blood sugar concentration after depletion of liver glycogen. Frequent feeding of children with diarrhoea might help to prevent this complication.
Cocaine and multiple drug abuse among young adults has spawned research interest in fetal exposure and the sequela of that exposure during the formative developmental years. Previous study of the language development of exposed children has not specifically addressed phonological acquisition. In the present study, the speech of 25 children prenatally exposed to cocaine and multiple drugs was analyzed and compared to that of 25 children who were not prenatally exposed to determine if differences were evident in their phonological patterns. The children ranged in age from 22 months to 51 months. The number and type of phonological processes produced, number of utterances needed to produce a 50-word sample, number of unintelligible words produced, and Home Observation for Measurement of the Environment (HOME) scores were recorded and analyzed. The use of cocaine and multiple drugs during pregnancy was associated with an increase in the use of phonological processes.
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