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Hypothalamic Noradrenergic Hyperactivity and Detrimental Bone Status in an Animal Model of Nutritional Growth Retardation

机译:营养生长迟缓动物模型中的下丘脑去甲肾上腺素能亢进和有害骨状态。

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We have studied hypothalamic noradrenergic activity in relation with bone status in a nutritional growth retardationmodel (ND). Control rats (C) were fed ad libitum. ND received 80% of the diet consumed by C for 4 weeks andlater refed ad libitum for 8 weeks. Food restriction induced detrimental effects on body and femur weight and length(P<0.05) and bone biomechanical properties (P<0.001). Thickness of proliferative and hypertrophic zone (μm) of growthplate cartilage and bone volume (%, mean±SE) were 225.96±5.70 v. 280.70±12.52, 95.16±5.81 v. 134.60±9.30,17.64±3.23 v. 26.80±2.03, respectively (P<0.05); anterior and posterior hypothalamus norepinephrine uptake and releaseand tyrosine hydroxylase activity (% of control) were 79.05±3.56, 67.00±10.00, 164.26±16.58 and 80.65±5.92,147.00±1.00, 152.42±9.30, respectively (P<0.05). Thus, impaired biomechanical bone performance in ND could be due,in part, to the increased hypothalamic noradrenergic activity in response to restriction. Normalization of parameters withrefeeding suggests no long-term side-effects in undernourished rats.
机译:我们已经研究了在营养生长迟缓模型(ND)中下丘脑的去甲肾上腺素能活性与骨骼状态的关系。随意喂养对照大鼠(C)。 ND接受C消耗的饮食的80%,持续4周,后来拒绝随意饮食8周。食物限制对人体和股骨的重量和长度(P <0.05)和骨骼生物力学特性(P <0.001)有不利影响。生长板软骨增生和肥厚区的厚度(μm)和骨体积(%,平均值±标准误差)为225.96±5.70 v.280.70±12.52,95.16±5.81 v.134.60±9.30,17.64±3.23 v.26.80±2.03,分别为(P <0.05);下丘脑前部和后部去甲肾上腺素的摄取和释放以及酪氨酸羟化酶活性(对照的百分比)分别为79.05±3.56、67.00±10.00、164.26±16.58和80.65±5.92、147.00±1.00、152.42±9.30(P <0.05)。因此,ND的生物力学骨性能受损可能部分归因于响应于限制而增加的下丘脑去甲肾上腺素能活性。再喂养参数的正常化表明在营养不良的大鼠中没有长期的副作用。

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