Abstract

BackgroundIn 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.AimTo study the body temperature daily rhythm of diabetic animals and the effects of insulin and/or melatonin treatment on its structure.MethodsWe 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.ResultsDiabetes 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.ConclusionsTaken 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.Electronic supplementary materialThe online version of this article (doi:10.1186/s13098-015-0035-2) contains supplementary material, which is available to authorized users.

Highlights

  • In mammals, the temperature rhythm is regulated by the circadian pacemaker located in the suprachiasmatic nuclei, and is considered a “marker rhythm”

  • 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

  • Since body temperature (BT) rhythm is considered a marker rhythm for the circadian system, we evaluated the effects of long-term diabetes (33 days after STZ injection) on the BT rhythmical structure and on its rhythmic parameters

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Summary

Introduction

The temperature rhythm is regulated by the circadian pacemaker located in the suprachiasmatic nuclei, and is considered a “marker rhythm”. Previous studies show that both experimental animals as well as patients with metabolic pathologies, such as obesity and type 2 diabetes mellitus present circadian abnormalities [14,15]. In spite of being a well-structured rhythm, body temperature is susceptible to chronic shifts in mealtime resulting in pathological changes of carbohydrate and lipid metabolisms daily rhythms [18]. These effects could be due to a misalignment of the body temperature, melatonin, and sleeping rhythms [19]

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