Obesity programmed by prenatal dexamethasone and postnatal high-fat diet leads to distinct alterations in nutrition sensory signals and circadian-clock genes in visceral adipose tissue.
Ching-Chou TsaiMao-Meng TiaoJiunn-Ming SheenLi-Tung HuangYou-Lin TainI-Chun LinYu-Ju LinYun-Ju LaiChih-Cheng ChenKow-Aung ChangHong-Ren YuPublished in: Lipids in health and disease (2019)
Prenatal dexamethasone and postnatal HF treatment cause dysregulation of nutrient-sensing molecules and circadian-clock genes in visceral adipose tissue. Characterizing altered nutrient-sensing molecules and circadian-clock genes has potential therapeutic relevance with respect to the pathogenesis and treatment of prenatal stress and postnatal HF diet-related metabolic disorders.
Keyphrases
- insulin resistance
- high fat diet
- adipose tissue
- pregnant women
- preterm infants
- genome wide
- metabolic syndrome
- type diabetes
- skeletal muscle
- physical activity
- low dose
- weight loss
- high fat diet induced
- high dose
- genome wide identification
- bioinformatics analysis
- heart failure
- dna methylation
- combination therapy
- replacement therapy
- genome wide analysis
- body mass index