Time-restricted feeding restores muscle function in Drosophila models of obesity and circadian-rhythm disruption.
Jesús E VillanuevaChristopher LiveloAdriana S TrujilloSahaana ChandranBrendon WoodworthLeo AndradeHiep D LeUri ManorSatchidananda PandaGirish C MelkaniPublished in: Nature communications (2019)
Pathological obesity can result from genetic predisposition, obesogenic diet, and circadian rhythm disruption. Obesity compromises function of muscle, which accounts for a majority of body mass. Behavioral intervention that can counteract obesity arising from genetic, diet or circadian disruption and can improve muscle function holds untapped potential to combat the obesity epidemic. Here we show that Drosophila melanogaster (fruit fly) subject to obesogenic challenges exhibits metabolic disease phenotypes in skeletal muscle; sarcomere disorganization, mitochondrial deformation, upregulation of Phospho-AKT level, aberrant intramuscular lipid infiltration, and insulin resistance. Imposing time-restricted feeding (TRF) paradigm in which flies were fed for 12 h during the day counteracts obesity-induced dysmetabolism and improves muscle performance by suppressing intramuscular fat deposits, Phospho-AKT level, mitochondrial aberrations, and markers of insulin resistance. Importantly, TRF was effective even in an irregular lighting schedule mimicking shiftwork. Hence, TRF is an effective dietary intervention for combating metabolic dysfunction arising from multiple causes.
Keyphrases
- insulin resistance
- skeletal muscle
- high fat diet induced
- weight loss
- metabolic syndrome
- adipose tissue
- type diabetes
- high fat diet
- polycystic ovary syndrome
- drosophila melanogaster
- weight gain
- oxidative stress
- signaling pathway
- randomized controlled trial
- glycemic control
- atrial fibrillation
- poor prognosis
- genome wide
- risk assessment
- endothelial cells
- gene expression
- high glucose
- diabetic rats
- human health
- drug induced
- dna methylation