Description
Obesity is associated with elevated risk for cardiovascular and other metabolic diseases along with skeletal muscle dysfunctions. The disruption of the metabolic clock may play a role in worsening obesity and many who have late night working conditions and erratic eating patterns are at risk. Our study explores how the restoration of the metabolic clock can attenuate skeletal muscle dysfunction in obesity. We have established the effects of a metabolically homeostatic clock in obesity through the development of novel Drosophila melanogaster (fruit flies) models, which delay age-associated muscle dysfunction with Time-Restricted Feeding (TRF). We subjected wild type adult flies along with diet and genetically obese flies to 24-hour ad libitum feeding (ALF) or 12-hour time-restricted feeding (TRF) whereby food access is limited exclusively to daytime. We tested the muscle performance of TRF and ALF flies using a flight and geotactic assay, which tests the flies’ ability to fly and climb. RNA sequencing was done with flys’ indirect flight muscle (IFM) to compare gene expression profiles of ALF and TRF flies. TRF obese flies showed a significant improvement in flight and climbing ability and showed significant differences in ALF vs. TRF expressed genes. Transcriptomic data showed ALF obese flies had different gene expression levels of immune, serine pepsidases, transferases and zinc ion protein binding genes. We found a significant reduction in oxidative stress mRNA, lipases and DNA regulatory genes in our TRF flies. Obesity-induced cardiomyopathy and other metabolic syndromes, including skeletal muscle dysfunction, are alarming public health problems due to their negative health effects. Healthy meal timing has potential to attenuate obesity and skeletal muscle dysfunction safely as an avenue of therapy, which may reduce global obesity.
