Abstract

SummaryAimMelatonin supplementation reduces insulin resistance and protects the heart in obese rats. However, its role in myocardial glucose uptake remains unknown. This study investigated the effect of short-term melatonin treatment on glucose uptake by cardiomyocytes isolated from obese and insulin-resistant rats.MethodsCardiomyocytes were isolated from obese rats fed a high-calorie diet for 16 to 23 weeks, their age-matched controls, as well as young control rats aged four to eight weeks. After incubation with melatonin with or without insulin, glucose uptake was initiated by the addition of 2-deoxy-D-[3H] glucose and measured after 30 minutes. Additional control and obese rats received melatonin in the drinking water (4 mg/kg/day) for the last six weeks of feeding (20 weeks) and glucose uptake was determined in isolated cardiomyocytes after incubation with insulin. Intraperitoneal glucose tolerance and biometric parameters were also measured.ResultsObese rats (fed for more than 20 weeks) developed glucose intolerance. Cardiomyocytes isolated from these obese rats had a reduced response to insulin-stimulated glucose uptake (ISGU) (p < 0.05). Melatonin administration in vitro had no effect on glucose uptake per se. However, it increased ISGU by cardiomyocytes from the young rats (p < 0.05), while having no effect on ISGU by cardiomyocytes from the older control and obese groups. Melatonin in vivo had no significant effect on glucose tolerance, but it increased basal (p < 0.05) and ISGU by cardiomyocytes from the obese rats (50.1 ± 1.7 vs 32.1 ± 5.1 pmol/mg protein/30 min, p < 0.01).ConclusionThese data suggest that short-term melatonin treatment in vivo but not in vitro improved glucose uptake and insulin responsiveness of cardiomyocytes in obesity and insulin-resistance states.

Highlights

  • ObjectivesMelatonin supplementation reduces insulin resistance and protects the heart in obese rats

  • Melatonin treatment (10 and 100 nM, 10 and 50 μM) had no significant effect on glucose uptake by the cardiomyocytes isolated from normal rats (Fig. 1A)

  • When insulin was added to cells treated with melatonin (100 nM), there was a further stimulation of glucose uptake (3.4 ± 0.5- vs 2.5 ± 0.2-fold increase, p < 0.05) (Fig. 1B)

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Summary

Objectives

Melatonin supplementation reduces insulin resistance and protects the heart in obese rats. The aim of this study was to investigate the effect of melatonin treatment on myocardial glucose uptake using cardiomyocytes isolated from insulin-resistant rats and their aged-matched controls. Our aim was to investigate the effect of melatonin treatment on basal glucose uptake and insulin responsiveness as indicated by glucose uptake, using cardiomyocytes isolated from young control rats, age-matched controls and obese, insulin-resistant rats

Methods
Results
Discussion
Conclusion

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