Metformin normalizes insulin binding to monocytes from obese nondiabetic subjects and obese type II diabetic patients

V. Trischitta, D. Gullo, V. Pezzino, R. Vigneri

Research output: Contribution to journalArticle

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Abstract

In order to evaluate the in vivo effects of biguanides on the insulin receptor, we have studied insulin binding to circulating monocytes of six normal controls, eight obese nonidiabetic subjects, and six obese type II diabetic patients, both before and after 4 days of treatment with the biguanide metformin (850 mg twice daily orally). Before drug administration, 125I-insulin binding to monocytes was decreased in obese subjects and diabetic patients. After metformin administration, an increase in insulin binding to peripheral monocytes was observed in seven of eight obese nondiabetic subjects (3.57 ± 0.43 to 4.69 ± 0.59% bound at 107 monocytes, mean ± SEM, P <0.01) and in all diabetic patients (3.21 ± 0.21 to 5.22 ± 0.34, P <0.01). Scatchard plots indicated that the increased binding was due to an increase in the receptor number. In contrast, no significant change in insulin binding was found in normal controls after metformin administration (5.31 ± 0.14 and 4.70 ± 0.12). It is suggested, therefore, that the action of metformin on the insulin receptor may be one of the mechanisms of the antidiabetic effect of this drug.

Original languageEnglish
Pages (from-to)713-718
Number of pages6
JournalJournal of Clinical Endocrinology and Metabolism
Volume57
Issue number4
Publication statusPublished - 1983

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Metformin
Monocytes
Insulin
Biguanides
Insulin Receptor
Hypoglycemic Agents
Pharmaceutical Preparations
Scanning electron microscopy
Therapeutics

ASJC Scopus subject areas

  • Biochemistry
  • Endocrinology, Diabetes and Metabolism

Cite this

Metformin normalizes insulin binding to monocytes from obese nondiabetic subjects and obese type II diabetic patients. / Trischitta, V.; Gullo, D.; Pezzino, V.; Vigneri, R.

In: Journal of Clinical Endocrinology and Metabolism, Vol. 57, No. 4, 1983, p. 713-718.

Research output: Contribution to journalArticle

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