Gene expression analysis of diet induced obesity model zebrafish
Ontology highlight
ABSTRACT:
ORGANISM(S): Danio rerio
SUBMITTER: oka takehiko
PROVIDER: E-GEOD-18566 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:The effect of a year-long 10 reduction in water temperature on global gene expression in tail skeletal muscle from adult, male zebrafish was determined using a long oligonucleotide probe set (16,399 65mers from Compugen) spotted onto glass slides. Outbred male zebrafish were obtained from a commercial supplier (Liles Tropical Fish, FL) at 6 months of age. Fish were maintained at 28 until 10 months of age. (see Gerhard et al., Exp Gerontol 37,1055-68, 2002) For temperature reduction, water temperature was decreased by 2.5 per week for 4 weeks. Fish were maintained until 22 months of age. Fish were fed fish flakes (Wardely Corp. Secaucus, NJ) twice per day. Each feeding was a discrete event in which a small measured amount of granular food was sprinkled on the water surface. A second small aliquot was offered if the first has been eaten within a few minutes. The feeding stopped when food from the previous aliquot has not been eaten and feeding behavior has ceased. By providing a consecutive series of small aliquots until food is no longer accepted, every member of the tank has an opportunity to eat until satiety, yet the amount of uneaten food is minimized. At 22 months of age, fish were euthanized by decapitation. Total RNA was harvested from a pool of tail muscle samples from 5 fish. Two independent pools of 5 fish per pool were collected from fish maintained at 18 and 28. Flip-dye hybridizations were performed on each pool for a total of 4 hybridizations in this study. Experiments DAR011d0001 and DAR011d0002 are flip-dye hybridizations from Pool 1. Experiments DAR011d0003 and DAR011d004 are flip-dye hybridizations from Pool 2.
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Project description:An intrinsic property of the heart is an ability to rapidly and coordinately adjust flux through metabolic pathways in response to physiologic stimuli (termed metabolic flexibility). Cardiac metabolism also fluctuates across the 24-hr day, in association with diurnal sleep-wake and fasting-feeding cycles. Although loss of metabolic flexibility has been proposed to play a causal role in the pathogenesis of cardiac disease, it is currently unknown whether day-night variations in cardiac metabolism are altered during disease states. Here, we tested the hypothesis that diet-induced obesity disrupts cardiac “diurnal metabolic flexibility”, which is normalized by time-of-day-restricted feeding. Chronic high fat feeding (20-wk) induced obesity in mice, abolished diurnal rhythms in whole body metabolic flexibility, and increased markers of adverse cardiac remodeling (hypertrophy, fibrosis, and steatosis). RNAseq analysis revealed that 24-hr rhythms in the cardiac transcriptome were dramatically altered during obesity; only 22% of rhythmic transcripts in control hearts were unaffected by obesity. However, day-night differences in cardiac substrate oxidation were essentially identical in control and high fat fed mice. In contrast, day-night differences in both cardiac triglyceride synthesis and lipidome were abolished during obesity. Next, a subset of obese mice (induced by 18-wks ad libitum high fat feeding) were allowed access to the high fat diet only during the 12-hr dark (active) phase, for a 2-wk period. Dark phase restricted feeding partially restored whole body metabolic flexibility, as well as day-night differences in cardiac triglyceride synthesis and lipidome. Moreover, this intervention partially reversed adverse cardiac remodeling in obese mice. Collectively, these studies reveal diurnal metabolic inflexibility of the heart during obesity specifically for non-oxidative lipid metabolism (but not for substrate oxidation), and that restricting food intake to the active period partially reverses obesity-induced cardiac lipid metabolism abnormalities and adverse remodeling of the heart.
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