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A Luyckx

Publications and source records attributed to A Luyckx.

At least 73 records · Page 4Linked to original sources
PubMed1975

Naturally labeled 13C-glucose. Metabolic studies in human diabetes and obesity.

The 13C/12C ratio in most commercial preparations of glucose used in clinical investigation is much higher than that of expired air. Variations in expired air 13C, after glucose load, are indicative of the catabolism of this exogenous glucose. The changes in the 13C/12C ratio of CO2 in expired air after oral administration of glucose were determined by mass spectrometry. Results in eleven healthy volunteers and seven obese subjects with normal oral glucose tolerance tests (OGTT) are reported. In all cases, the administration of glucose resulted in a marked rise in the 13C/12C ration of expired CO2, reaching its maximum at the fourth hour and then declining progressively. In seven obese patients with chemical diabetes and in five insulin-dependent diabetics, the 13C/12C ratio of expired CO2 during OGTT was significantly reduced, in comparison with the results obtained from the control groups. This study demonstrates the potential of this procedure using "naturally labeled" 13C glucose for the metabolic studies in man as anticipated from previous studies of Duchesne and his coworkers.

Adolescent↗
PubMed1975

[The role of glucagon in hyperglycemia. A review (author's transl)].

Glucagon is secreted not only by A2-cells of the pancreatic islets but also by A cells in the gastric fundus and duodenum. Several reports have demonstrated that the glucagon plasma concentration is increased in genetic diabetes as well as in many conditions associated with a decreased glucose tolerance such as hepatic cirrhosis, myocardial infarction, infectious diseases, burns, taumatic shock, glucagonomas, acute pancreatitis, acromegaly, pheochromacytoma and Cushing's syndrome. Hyperglucagonemia is particularly important in diabetic ketoacidosis and in non-ketotic hyperosmolar coma. The mechanisms responsible for the diabetic's hyperglucagonemia remain controversial. According to several authors, the increased glucagon secretion is, for its main part, secondary to a prolonged defect in insulin secretion and thus relatively insensitive to an acute insulin administration. According to others, the A cell abnormality is of primary origin, independant from insulin deficiency and its effects are cumulative with those of the insulin lack. Several reports dealing with induced or spontaneous experimental diabetes are in favor of the first or the second hypothesis. It appears likely that glucagon plays a role in the metabolic derangments of diabetes. Indeed, hepatic glucose production is closely related to the ratio of molar concentrations of insulin and glucagon. Finally, in insulin-dependant diabetics, somatostatin infusion reduces plasma glucagon concentration and blood glucose and prevents the development of ketosis after withdrawal of insulin therapy. These results illustrate the contribution of glucagon in the pathogenesis of hyperglycemia and ketosis. Several arguments have been accumulated in favor of the following concept: diabetes hyperglycemia results both from glucose under-utilization secondary to insulin lack and from hepatic glucose over-production due to glucagon excess. Although controversial, the role of glucagon in ketogenesis appears likely.

Acromegaly↗