产前地塞米松和产后高脂肪饮食编程导致肥胖，导致内脏脂肪组织中营养感觉信号和昼夜节律基因的明显改变。
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.
机构信息
Department of Obstetrics and Gynecology, Kaohsiung Chang Gung Memorial Hospital, Chang Gung University, College of Medicine, Kaohsiung, 83301, Taiwan.
Graduate Institute of Clinical Medicine, Kaohsiung Medical University, Kaohsiung, 80708, Taiwan.
出版信息
Lipids Health Dis. 2019 Jan 18;18(1):19. doi: 10.1186/s12944-019-0963-1.
BACKGROUND
Prenatal dexamethasone treatment has been shown to enhance the susceptibility of offspring to postnatal high-fat (HF) diet-induced programmed obesity. We investigated the metabolic phenotypes, nutrient-sensing signal and circadian-clock genes in adipose tissue that are programmed by prenatal dexamethasone exposure and postnatal HF diet.
METHODS
Male offspring of Sprague-Dawley rats were divided into four experimental groups: normal diet, prenatal dexamethasone exposure, postnatal HF diet, and prenatal dexamethasone plus postnatal HF diet. Postnatal HF diet was prescribed from weaning to 6 months of age.
RESULTS
Prenatal dexamethasone and postnatal HF diet exerted synergistic effects on body weight and visceral adiposity, whereas prenatal dexamethasone and postnatal HF diet altered the metabolic profile and caused leptin dysregulation. Prenatal dexamethasone and postnatal HF diet distinctly influenced nutrient-sensing molecules and circadian-clock genes in adipose tissue. The mRNA expression of mTOR, AMPK-α2, PPAR-α, and PPAR-γ was suppressed by prenatal dexamethasone but enhanced by postnatal HF diet.
CONCLUSION
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.
背景
产前地塞米松处理已被证明可增强后代对产后高脂肪（HF）饮食诱导的程序化肥胖的易感性。我们研究了由产前地塞米松暴露和产后 HF 饮食编程的脂肪组织中的代谢表型、营养感应信号和昼夜节律基因。
方法
雄性 Sprague-Dawley 大鼠的后代分为四组实验：正常饮食、产前地塞米松暴露、产后 HF 饮食和产前地塞米松加产后 HF 饮食。产后 HF 饮食从断奶到 6 个月大时服用。
结果
产前地塞米松和产后 HF 饮食对体重和内脏脂肪有协同作用，而产前地塞米松和产后 HF 饮食改变了代谢特征并导致瘦素失调。产前地塞米松和产后 HF 饮食明显影响脂肪组织中的营养感应分子和昼夜节律基因。mTOR、AMPK-α2、PPAR-α 和 PPAR-γ 的 mRNA 表达被产前地塞米松抑制，但被产后 HF 饮食增强。
结论
产前地塞米松和产后 HF 处理导致内脏脂肪中营养感应分子和昼夜节律基因的失调。改变的营养感应分子和昼夜节律基因具有治疗意义，与产前应激和产后 HF 饮食相关代谢紊乱的发病机制和治疗有关。
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