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.
3,5-diiodo-L-thyronine (T-2), a naturally existing iodothyronine, has biological effects on humans, but no information is available on its action on pancreatic (beta-cells. We evaluated its effect vs triiodothyronine (T-3), on glucose -induced insulin secretion in INS -le cells, a rat insulinoma line, and on human islets. INS le were incubated in the presence/absence of T-2 or T-3 (0.1 nmol/L-10 mu mol/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< 0.01) stimulated by 1-100 nmol/L T-2 and 0.1 nmoUL-1.0 mu mol/L T-3, and inhibited with higher concentrations of both (1-10 gmoUL T-2 and 10 mu mol/L T-3). Human islets were incubated with 3.3 mmol/L glucose in presence/absence of T-3 or T-2 (0.1 nmol/L, 0.1 mu mol/L, and 1 mu mol/L). T-2 (0.1 nmol/L-0.1 mu mol/L) significantly (p< 0.01) stimulated insulin secretion, while higher concentrations (1 mu mol/L) inhibited it. A modest increase in insulin secretion was evidenced with 1 mu mol/L T-3. In conclusion, T-2 and T-3 have a direct regulatory role in insulin secretion, depending on their concentrations and the glucose level itself. At concentrations near the physiological range, T-2 enhances glucose-induced insulin secretion in both rat beta-cells and human islets.
BOTH 3,5-DIIODO-L-THYRONINE (T-2) AND T-3 MODULATE GLUCOSE-INDUCED INSULIN SECRETION
Goglia, F;Lanni, A;
2017
Abstract
3,5-diiodo-L-thyronine (T-2), a naturally existing iodothyronine, has biological effects on humans, but no information is available on its action on pancreatic (beta-cells. We evaluated its effect vs triiodothyronine (T-3), on glucose -induced insulin secretion in INS -le cells, a rat insulinoma line, and on human islets. INS le were incubated in the presence/absence of T-2 or T-3 (0.1 nmol/L-10 mu mol/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< 0.01) stimulated by 1-100 nmol/L T-2 and 0.1 nmoUL-1.0 mu mol/L T-3, and inhibited with higher concentrations of both (1-10 gmoUL T-2 and 10 mu mol/L T-3). Human islets were incubated with 3.3 mmol/L glucose in presence/absence of T-3 or T-2 (0.1 nmol/L, 0.1 mu mol/L, and 1 mu mol/L). T-2 (0.1 nmol/L-0.1 mu mol/L) significantly (p< 0.01) stimulated insulin secretion, while higher concentrations (1 mu mol/L) inhibited it. A modest increase in insulin secretion was evidenced with 1 mu mol/L T-3. In conclusion, T-2 and T-3 have a direct regulatory role in insulin secretion, depending on their concentrations and the glucose level itself. At concentrations near the physiological range, T-2 enhances glucose-induced insulin secretion in both rat beta-cells and human islets.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
