Related Experiment Video
Updated: Apr 12, 2026
A Protocol for Constructing a Rat Wound Model of Type 1 Diabetes
Published on: February 17, 2023
Streptozotocin-induced diabetes disrupts the body temperature daily rhythm in rats
Angela M Ramos-Lobo1, Daniella C Buonfiglio1, José Cipolla-Neto1
1Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of São Paulo, Av. Lineu Prestes, 1524, São Paulo, SP 05508-000 Brazil.
Background:
In mammals, the temperature rhythm is regulated by the circadian pacemaker located in the suprachiasmatic nuclei, and is considered a "marker rhythm". Melatonin, the pineal gland hormone, is a major regulator of the endogenous rhythms including body temperature. Its production is influenced by many factors, such as type 1 diabetes mellitus. In rats, diabetes leads to hypothermia and reduced melatonin synthesis; insulin treatment reestablishes both.
Aim:
To study the body temperature daily rhythm of diabetic animals and the effects of insulin and/or melatonin treatment on its structure.
Methods:
We studied the effects of streptozotocin-induced diabetes (60 mg/kg) on the body temperature rhythm of Wistar rats and the possible modifications resulting from early and late treatments with insulin (6U/day) and/or melatonin (daily 0.5 mg/kg). We monitored the daily body temperature rhythm, its rhythmic parameters (MESOR, amplitude and acrophase), glycemia and body weight for 55 days. Data were classified by groups and expressed as mean ± SEM. One-way ANOVA analysis was performed followed by Bonferroni posttest. Statistical significance was set at p < 0.05.
Results:
Diabetes led to complete disruption of the temperature rhythm and hypothermia, which were accentuated over time. All early treatments (insulin or/and melatonin) prevented the temperature rhythm disruption and hypothermia. Insulin plus melatonin restored the body temperature rhythm whereas insulin alone resulted less efficient; melatonin alone did not restore any of the parameters studied; however, when supplemented close to diabetes onset, it maintained the temperature rhythmicity. All these corrective effects of the early treatments were dependent on the continuous maintenance of the treatment.
Conclusions:
Taken together, our findings show the disruption of the body temperature daily rhythm, a new consequence of insulin-dependent diabetes, as well as the beneficial effect of the complementary action of melatonin and insulin restoring the normal rhythmicity.
