in male Wistar rats: three-month-old male Wistar rats were divided into the following groups: control (daily s.c. injections of vehicle were administered), 25 μg 3,5-diiodothyronine (3,5-T2) (daily s.c. injections of 25 μg 3,5-T2/100 g body weight (BW)), 50 μg 3,5-T2 (daily s.c. injections of 50 μg 3,5-T2/100 g BW), and 75 μg 3,5-T2 (daily s.c. injections of 75 μg 3,5-T2/100 g BW). The experiments were conducted for 3 month. After 3 months of 3,5-T2 administration, body mass and retroperitoneal fat pad mass were significantly reduced, whereas the heart rate and mass were unchanged. Thus, 3,5-T2 acts as a direct stimulator of energy expenditure and reduces body mass gain; however, TSH suppression may develop secondary to 3,5-T2 administration.

It was evaluated 3,5-diiodo-L-thyronine (T2) 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.