Obesity alters circadian expressions of molecular clock genes in the brainstem.

摘要: Abstract Major components of energy homeostasis, including feeding behavior and glucose lipid metabolism, are subject to circadian rhythms. Recent studies have suggested that dysfunctions molecular clock genes involved in the development obesity diabetes. To examine whether metabolic states per se alter central nervous system (CNS), we analyzed daily mRNA expression profiles core caudal brainstem nucleus solitary tract (NTS). In lean C57BL/6 mice, transcript levels (Npas2, Bmal1, Per1, Per2 Rev-erbα) clearly showed 24-h rhythmicity. On other hand, Bmal1 Rev-erbα were attenuated mice with high fat diet-induced as well genetically obese KK-Ay ob/ob mice. Clock increased Cry1 decreased addition, peroxisome proliferator-activated receptor α (PPARα), which reportedly increases BMAL1 transcriptional level, was up-regulated NTS these murine models insulin resistance, suggesting involvement PPARα attenuation rhythms states. Furthermore, a profile of a downstream target genes, large conductance Ca2+-activated K+channel, disturbed models. These perturbations might contribute neuronal dysfunction This is first report showing perturbs expressions CNS.