Reduced Carbohydrate Content Research Articles

Carbohydrates of influenza virus. I. Glycopeptides derived from viral glycoproteins after labeling with radioactive sugars.

The carbohydrate moiety of the influenza glycoproteins NA, HA(1), and HA(2) were analyzed by labeling with radioactive sugars. Analysis of glycopeptides obtained after digestion with Pronase indicated that there are at least two different types of carbohydrate side chains. The side chain of type I is composed of glucosamine, mannose, galactose, and fucose. It is found on NA, HA(1), and HA(2). The side chain of type II contains a high amount of mannose and is found only on NA and HA(2). The molecular weights of the corresponding glycopeptides obtained from virus grown in chicken embryo cells are 2,600 for type I and 2,000 for type II. The glycoproteins of virus grown in MDBK cells have a higher molecular weight than those of virus grown in chicken embryo cells, and there is a corresponding difference in the molecular weights of the glycopeptides. Under conditions of partial inhibition of glycosylation, virus particles were isolated that contained hemagglutinin with reduced carbohydrate content. Glycopeptide analysis indicated that this reduction is due to the lack of whole carbohydrate side chains and not to the incorporation of incomplete ones. This observation suggests that glycosylation of the viral glycoproteins involves en bloc transfer of the core sugars to the polypeptide chains.

Effects of 2-deoxyglucose, glucosamine, and mannose on cell fusion and the glycoproteins of herpes simplex virus

2-Deoxyglucose and glucosamine were found to inhibit cell fusion caused by a syncytial mutant of herpes simplex virus and to inhibit the glycosylation of viral glycoproteins in the infected cells. The inhibition of fusion and the inhibition of glycosylation caused by 2-deoxyglucose were substantially prevented when mannose was also present during infection. When glycosylation was inhibited, three new bands were found in major glycoprotein region on sodium dodecyl sulfate-polyacrylamide gels. These bands may be precursors to the normal glycoproteins. The correlation between fusion and glycosylation in the presence of 2-deoxyglucose, glucosamine, and mannose suggests that the cells cannot fuse if their glycoproteins have a considerably reduced carbohydrate content.

Effects of carbohydrate restriction on glucose tolerance of normal men and reactive hypoglycemic patients

Normal individuals ingesting a low carbohydrate diet frequently develop an impairment of glucose tolerance as measured by the oral glucose tolerance test; most of these diets, however, have been high in fat content. Our present studies demonstrate that a low carbohydrate diet (57 g/day) did not impair the glucose tolerance of normal men if the fat content was similar to values on a standard (301 g/day) carbohydrate diet. However, a low carbohydrate diet did lead to impaired glucose tolerance when the fat content was 16 per cent higher than on the control diet. Thus our present and previous studies demonstrate that normal men maintain normal glucose tolerance on low carbohydrate diets and suggest that the deterioration of the glucose tolerance observed on high fat diets is related to the increased fat content rather than to the reduced carbohydrate content of these diets. Seven patients with reactive hypoglycemia were exquisitely sensitive to carbohydrate deprivation. Whereas the glucose tolerance tests of normal men were not altered by a low carbohydrate, high protein diet, a significant deterioration of glucose tolerance occurred when reactive hypoglycemic patients were changed from control diets to low carbohydrate, high protein diets. These hypoglycemic patients also showed an exaggerated deterioration of the glucose tolerance after a 48-hour fast when compared tothe response of normal men. Our observations suggest that a low carbohydrate, high protein diet is not the best therapeutic diet for certain patients with reactive hypoglycemia because this diet does not provide symptomatic improvement and, in addition, leads to impaired glucose tolerance.

GLUCOSE‐GALACTOSE MALABSORPTION

SummaryThe histories of 6 cases, 2 male and 4 female, with glucose‐galactose malabsorption (GGM) are presented. Of these, 4 have survived and are in good general health on a diet with a reduced carbohydrate content. One case died at 2 months of age with severe malnutrition due to intractible diarrhoea before a diagnosis was made. The other patient who died, was diagnosed and treated from the neonatal period, and he was progressing until infection occurred by a Candida albicans, followed by death at 3 months of age in a picture of agam‐maglobulinaemia. One patient is now a woman of 41. The main symptoms are diarrhoea from birth, dehydration and malnutrition. Glucose is found in the watery stools and there is also a slight glucosuria. Hyperosmolar serum is often seen. Two patients, not those treated at an early stage, developed renal concrements probably owing to the long lasting water loss with the stools. Treatment during the first months consisted of replacement of the ordinary dietary carbohydrates by fructose. Although the basic biochemical disorder lasts throughout life, limited amounts of starch and milk could be introduced later in infancy. Some absorption of glucose could be demonstrated, tentatively due to a second pathway for intestinal glucose absorption which is apparently not shared by galactose. Hydrolysis of disac‐charides occurred in the small intestine of GGM patients but the released glucose was absorbed no better than when administered as a monosaccharide. This implies that the site of disaccharidase activity is located more superficially at the luminal side of the epithelial cell membrane than the disturbed step of glucose and galactose transport.