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Insulin resistance in Graves' disease: a quantitative in‐vivo evaluation
Author(s) -
CAVALLOPERIN P.,
BRUNO A.,
BOINE LAURA,
CASSADER M.,
LENTI G.,
PAGANO G.
Publication year - 1988
Publication title -
european journal of clinical investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 107
eISSN - 1365-2362
pISSN - 0014-2972
DOI - 10.1111/j.1365-2362.1988.tb01275.x
Subject(s) - insulin resistance , in vivo , medicine , insulin , biology , microbiology and biotechnology
. Hyperthyroidism is considered to be an insulin‐resistant state, but a quantitative evaluation of some action of insulin is still lacking. We performed euglycaemic clamp at about 350 and 7000 pmol l ‐1 plasma insulin concentration in combination with the 3H‐glucose infusion in 12 patients with Graves' disease and in 12 matched controls. Fasting plasma insulin (126±6·5 vs. 77·5±5·7 pmol l ‐1 ; P <0·001), C‐peptide (502±36 vs. 363±41 pmol l ‐1 ; P <0·001) and glucagon (47±3·3 vs. 33·3±3 pmol l ‐1 ; P >0·01) were significantly higher in hyperthyroids than in euthyroids. Basal hepatic glucose production was significantly higher in hyperthyroids than in euthyroids (18·3±1·4 vs. 9·2±0·5 μmol l ‐1 ; P <0·0001), and its suppression during physiological hyperinsulinaemia was only 50% in hyperthyroids. Glucose utilization and suppression of lipolysis were normally stimulated by insulin. All parameters altered during hyperthyroidism were normalized during methimazole‐induced euthyroidism. We conclude that insulin resistance involves mainly glucose rather than lipid and is selective at the hepatic level.