Both 3,5-diiodo-L-thyronine (T2) and T3 modulate glucose-induced insulin secretion

P Fallahi, S M Ferrari, E Santini, S Camastra, G Frenzilli, M Puccini, F Goglia, A Lanni, P Marchetti, A Antonelli

Article ID: 4349
Vol 31, Issue 2, 2017
DOI: https://doi.org/10.54517/jbrha4349
Received: 6 June 2022; Accepted: 6 June 2022; Available online: 6 June 2022; Issue release: 6 June 2022

Abstract

3,5-diiodo-L-thyronine (T2), a naturally existing iodothyronine, has biological effects on humans, but no information is available on its action on pancreatic b-cells. We evaluated its effect vs triiodothyronine (T3), on glucose-induced insulin secretion in INS-1e cells, a rat insulinoma line, and on human islets. INS-1e were incubated in the presence/absence of T2 or T3 (0.1 nmol/L-10 μmol/L), and glucose (3.3, 7.5, 11.0, and 20 mmol/L). Insulin release and content (at 11.0 and 20 mmol/L glucose) were significantly (p less than 0.01) stimulated by 1-100 nmol/L T2 and 0.1 nmol/L-1.0 μmol/L T3, and inhibited with higher concentrations of both (110 μmol/L T2 and 10 μmol/L T3). Human islets were incubated with 3.3 mmol/L glucose in presence/absence of T3 or T2 (0.1 nmol/L, 0.1 μmol/L, and 1 μmol/L). T2 (0.1 nmol/L-0.1 μmol/L) significantly (p less than0.01) stimulated insulin secretion, while higher concentrations (1 μmol/L) inhibited it. A modest increase in insulin secretion was evidenced with 1 μmol/L T3. In conclusion, T2 and T3 have a direct regulatory role in insulin secretion, depending on their concentrations and the glucose level itself. At concentrations near the physiological range, T2 enhances glucose-induced insulin secretion in both rat b-cells and human islets.


Keywords

diiodothyronine;triiodothyronine;islets;b-cells;INS-1e;insulin secretion


References

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