Endocrine Abstracts

Diabetes mellitus (DM) is a disease that results from impairment of insulin synthesis/secretion or signaling. The glycemia of type 1 DM (DM1) patients is controlled by insulin replacement therapy, which chronically results in insulin resistance. We have shown that alloxan-induced diabetic rats present hypothyroidism, and that T3 treatment reduced the inflammatory state and hepatic glucose production and increased insulin sensitivity, improving glycemia control. Considering that insulin replacement is the unique treatment for DM1 and that T3 was shown to increase insulin sensitivity in DM1 rats, this study aimed at investigating whether T3 could act as an adjuvant of insulin for DM1 treatment. Male Wistar rats (250 g) were made diabetic with alloxan injection (150 mg/kg, ip), and assorted in different groups that were subjected to insulin treatment (3 or 6 U) associated or not with T3 (1.5 μg/100 g de PC), for 4 weeks. Non-diabetic rats were subjected to the same procedures, but treated with saline instead of T3 and/or insulin. They were weekly weighted, and subjected to the evaluation of fasting glycemia. The insulin sensitivity was evaluated by the constant rate for the Insulin Tolerance Test (kITT). It was shown that DM rats treated or not with T3 presented lower body weight (BW) than control group and insulin treated group. kITT returned to control levels when DM rats were treated with 3 or 6U of insulin or with 3U of insulin plus T3. However, the kITT was reduced when DM rats were treated with 6U of insulin plus T3. The fasting glycemia of DM rats was higher than those observed in all groups studied. The fasting glycemia of DM rats treated with insulin (both doses) and/or T3, was lower than non-treated DM rats. Our findings reinforce that T3 treatment improves insulin sensitivity and fasting glycemia of DM rats, and show that the association of T3 with insulin in the lower dose (3U) ameliorates glucose homeostasis, since it reduces the fasting glycemia and increases the kITT to the levels of the control group, restoring the insulin sensitivity. We conclude that T3 could act as an adjuvant of insulin (3U) in the DM treatment. The implication of this data is that with this association lower doses of insulin could be used for the DM treatment, which would postpone the development of insulin resistance that classically occurs in patients under insulin chronic treatment.