Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In 10 healthy men, we have compared the respective effects of an intravenous injection of glucagon (1 mg) and an oral glucose load (75 G) in eliciting the release of C-peptide and insulin from the pancreas. Serum C-peptide and insulin concentrations increased respectively to median values of 190% and 500% at 6 minutes after glucagon injection, and 344% and 794% at 30 minutes and 268% and 278% at 60 minutes following glucose ingestion. The oral glucose load was as effective as glucagon injection in testing beta cell function and was free from the unpleasant side effects (nausea, vomiting, syncope) commonly associated with glucagon. We conclude that oral glucose loading is probably the test of choice to elicit C-peptide release when screening populations of normal subjects for adequacy of beta cell function.
 ...
PMID:Comparison of oral glucose loading and intravenous glucagon injection as stimuli to C-peptide secretion in normal men. 295 15

A young, diabetic woman suffering from fainting spells, vomiting, and diarrhea is described. Extensive investigations showed total cardiac denervation, orthostatic hypotension, and disturbances in the the pupillary and sudomotor functions, as well as impairment of glucagon secretion during hypoglycemia. These disturbances were found to be caused by autonomic neuropathy. No signs of peripheral neuropathy could be detected. To the best of our knowledge this is the second case of total cardiac denervation due to diabetic neuropathy described in the literature.
 ...
PMID:Cardiac denervation and other multisystem manifestations caused by isolated autonomic neuropathy in a young diabetic patient. 743 22

A major problem in the insulin therapy of patients with diabetes type 2 (T2DM) is the increased occurrence of hypoglycemic events which, if left untreated, may cause confusion or fainting and in severe cases seizures, coma, and even death. To elucidate the potential contribution of the liver to hypoglycemia in T2DM we applied a detailed kinetic model of human hepatic glucose metabolism to simulate changes in glycolysis, gluconeogenesis, and glycogen metabolism induced by deviations of the hormones insulin, glucagon, and epinephrine from their normal plasma profiles. Our simulations reveal in line with experimental and clinical data from a multitude of studies in T2DM, (i) significant changes in the relative contribution of glycolysis, gluconeogenesis, and glycogen metabolism to hepatic glucose production and hepatic glucose utilization; (ii) decreased postprandial glycogen storage as well as increased glycogen depletion in overnight fasting and short term fasting; and (iii) a shift of the set point defining the switch between hepatic glucose production and hepatic glucose utilization to elevated plasma glucose levels, respectively, in T2DM relative to normal, healthy subjects. Intriguingly, our model simulations predict a restricted gluconeogenic response of the liver under impaired hormonal signals observed in T2DM, resulting in an increased risk of hypoglycemia. The inability of hepatic glucose metabolism to effectively counterbalance a decline of the blood glucose level becomes even more pronounced in case of tightly controlled insulin treatment. Given this Janus face mode of action of insulin, our model simulations underline the great potential that normalization of the plasma glucagon profile may have for the treatment of T2DM.
 ...
PMID:Kinetic modeling of human hepatic glucose metabolism in type 2 diabetes mellitus predicts higher risk of hypoglycemic events in rigorous insulin therapy. 2297 53