Continued glucose output after re-feeding contributes to glucose intolerance in hyperthyroidism.
The effects of hyperthyroidism to elicit glucose intolerance after glucose administration were decreased under conditions where hepatic glucose output was suppressed. It is concluded that continued hepatic glucose output contributes to abnormal glucose tolerance in hyperthyroidism.
Department of Chemical Pathology, London Hospital Medical College, U.K.
M J
MJ
Holness
M C
MC
Sugden
D000818:Animals; D001786:Blood Glucose / Q000378:metabolism*; D005260:Female; D005943:Gluconeogenesis / Q000187:drug effects; D005947:Glucose / Q000378:metabolism* / Q000494:pharmacology; D006980:Hyperthyroidism / Q000378:metabolism*; D008099:Liver / Q000187:drug effects / Q000378:metabolism*; D008112:Liver Glycogen / Q000378:metabolism; D010764:Phosphorylase Kinase / Q000172:deficiency; D010848:Picolinic Acids / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D013217:Starvation / Q000378:metabolism
D001786:Blood Glucose; D008112:Liver Glycogen; D010848:Picolinic Acids; C008363:3-mercaptopicolinic acid; D010764:Phosphorylase Kinase; D005947:Glucose