Abstract
Circadian phenomena rule many activities of life on earth. Disruptions in circadian rhythmicity and rhythms have been recognized as a contributing factor for diseased states, for instance metabolic disruptions like diabetes. Diabetes develops as a consequence of faulty insulin pathway signaling, either by lack of insulin production (diabetes type I), or by loss of responsiveness in target tissues (diabetes type 2). In this work we use the model organism Drosophila melanogaster with three different mutant hypomorphic conditions at different levels of the insulin pathway. The insulin pathway is a very evolutionarily conserved pathway. We study these different diabetic conditions as a source of circadian rhythm abnormalities and circadian-related co-morbidities. We do so by studying circadian rhythmicity, activity, sleep and sleep structure, and feeding behavior. Results show that flies with impaired insulin signaling show circadian rhythm and rhythmic-related co-morbidities, especially female flies, as a consequence of the diabetic state. The most extreme disruptions occur in flies with impaired insulin receptor signaling, which stands at the beginning of the insulin pathway, in principle affecting most if not all aspects of this pathway. Our work shows that defective insulin signaling is a source of circadian rhythm and rhythmic related co-morbidities.
