Nutrition and metabolism最新文献

Biotin deficiency induced in the rat, with a biotin-deficient diet but with added avidin involves clinical symptoms of deficiency as well as an important drop (80%) in propionyl-CoA carboxylase activity in the liver, heart and kidneys. But major biochemical anomalies (ketoacidosis and increased urinary elimination of propionic acid), characteristic of propionic acidaemia due to propionyl-CoA carboxylase deficiency in man, are not observed in the rat. Nevertheless, abnormal urinary elimination of methylcitrate and tiglylglycine reflects an appreciable decrease in the metabolism of propionyl-CoA in these animals. The propionyl-CoA load caused by the administration of metabolic precursors of this substance, mainly L-isoleucine, does not induce important biochemical variations except for excretion of propionylglycine.

Pregnant guinea pigs were fed on one of three diets: a commercial low-fat diet or a high-fat diet containing either maize oil or beef dripping. The young were killed at birth, the brain removed and dissected into three regions; the cerebellum, cerebrum and stem. The fatty acid composition of the major phospholipid classes, phosphatidylcholine and phosphatidylethanolamine was determined using gas chromatography. Compared with those fed the commercial or beef dripping diet the brain of the young of mothers fed maize oil during pregnancy had an increased percentage of linoleic acid and of its long-chain derivatives arachidonic acid and docosapentaenoic acid and a lower percentage of docosahexaenoic acid. These changes occurred in both lipid classes and in all regions of the brain. The results demonstrate that the fatty acid composition of the brain lipids of newborn guinea pigs can be influenced by the nature of the maternal dietary fat consumed during the last weeks of pregnancy.

High-density lipoproteins (HDL) are macromolecular complexes of lipids and proteins which float in the ultracentrifuge between densities of 1.063 and 1.21 g/l. A major division of HDL into two subclasses according to their specific density as been proposed: HDL2 (d = 1.063-1.125) and HDL3 (d = 1.125-1.21). The division is supported by the different proportions of lipids and apoproteins in the two subclasses and by evidence suggesting that the protective effect of HDL lies mostly in the HDL2 subclasses. Recent epidemiological, experimental and clinical data have supported a probable role or HDL as an anti-risk factor due to their negative correlation with the prevalence of ischaemic heart disease. Some of these data are presented and discussed in this paper.

Low density potassium intake, particularly among black hypertensive patients, appears to contribute significantly to this disease and its major sequellae. The high sodium intake of industrialized societies and the epidemic prevalence of hypertension must be considered in the light of a relatively greater urinary potassium excretion as compared to a low-sodium diet with a lower urinary potassium excretion. There is no reason to assume that weight reduction per se is the major contributor to lowering of elevated blood pressure levels although claims to this effect have been made. In general, a high-caloric diet is loaded with sodium while a low-energy diet has a drastically reduced sodium content. The hypothesis that a higher dietary linoleic acid intake via increased prostaglandin synthesis may lead to natriuresis and a drop in blood pressure levels is an interesting development which needs more testing.

In vitro data suggest that low-density lipoprotein (LDL) is bound to specific receptors located in pits on the surface of fibroblasts by a high-affinity process and subsequently undergoes catabolism in lysosomes. This binding seems to be mediated by ionic interaction between LDL and its receptor, the latter being totally or partially absent from the fibroblasts of patients with familial hypercholesterolaemia (FH). In vivo data suggest that LDL is also catabolised by a concentration-dependent, low-affinity pathway which is probably mainly located in the liver. LDL catabolism is reduced in FH and after saturated fat feeding, whereas polyunsaturated fat has the reverse effect. Hypocatabolism of LDL alters LDL composition, accelerates atherosclerosis and may lead to premature death from coronary heart disease.

Rats were undernourished by being given half their normal diet from the 10th day of pregnancy, 10-, 15- and 30-day-old rats were studied. Incorporation of labelled precursors into brain DNA and RNA was carried out in vitro with slices from cerebral cortex, brain stem and cerebellum. Neuronal and glial cells were subsequently isolated and analyzed for specific radioactivity. The proliferation and differentiation of all brain cells were affected by undernutrition. Glial cells in particular and the small neuronal cells appeared most vulnerable probably because of their intense postnatal development.

The effects of low protein diet on lipid and carbohydrate metabolism in uremia were investigated in 22 patients treated during a period of 3--18 months (mean 9.5 months). Before treatment, the patients showed elevated serum triglycerides, low alpha-lipoprotein cholesterol and reduced glucose elimination rate. There were no major changes in mean serum lipid or carbohydrate metabolism variables during treatment. The arachidonic acid content of lecithin decreased while linoleic acid increased during treatment. While the dietary treatment was effective in ameliorating uremic symptoms, it did evidently not influence the deranged lipid/carbohydrate metabolism.