INFLUENCE OF EXOGENOUS FAT AND GLUCONEOGENIC SUBSTRATES ON GLUCOSE HOMEOSTASIS IN NEWBORN RAT
INFLUENCE OF EXOGENOUS FAT AND GLUCONEOGENIC SUBSTRATES ON GLUCOSE HOMEOSTASIS IN NEWBORN RAT
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DOI：
10.1152/ajpendo.1978.234.2.e129
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发表时间：
1978-01-01
影响因子：
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通讯作者：
GIRARD, JR
中科院分区：
文献类型：
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作者：
FERRE, P;PEGORIER, JP;GIRARD, JR
题名/责任者：The Firry，P.新生大鼠外源性FNT和葡萄糖异生作用的研究上午好。J.Physiol.234(2)：E129-E136,1978年或上午生理内分泌：内分泌。美多宝+胃动素试验。物理。3(Z)：E129-E136,1978。-研究了新生大鼠在出生后16小时的禁食期间发生严重低血糖的机制。口服甘油三酯或注射糖异生底物(乳酸、丙酮酸、甘油、丙氨酸、谷氨酰胺、丝氨酸乙酯)可以部分逆转这种空腹低血糖，当这两种治疗联合使用时，这种低血糖完全逆转。甘油三酯喂养引起的血糖升高并不是葡萄糖利用率下降的次要原因，因为禁食和甘油三酯喂养的新生儿在腹腔注射葡萄糖后葡萄糖消失率相似。甘油三酯饲喂与提供脂肪酸刺激糖异生有关：i)甘油三酯饲喂后血糖的升高完全被糖异生抑制剂(3-巯基匹配酸)抑制；2)甘油三酯饲喂后体内标记乳酸或丙氨酸转化为葡萄糖的能力增加了三倍；以及？7)同时抑制肝脏脂肪酸氧化的Pent+enoate可消除与甘油三酯饲喂相关的血糖升高。这些数据表明，缺乏糖异生底物不是限制禁食新生大鼠糖异生活性的主要因素。相反，充足的游离脂肪酸供应对于维持葡萄糖异生代谢底物向葡萄糖的高比率转化所需的能量是必不可少的。因此，在其他状态下，体内脂肪储备的缺乏(如新生大鼠)或耗尽可能通过这种机制与低血糖有因果关系。禁食；甘油三酯喂养；糖异生；葡萄糖利用；酮生成
FERRY, P., JP PEGORIOR, E. B. MARLISS, AND JR GIRARD. Iflfkerlce of exogenous fnt and gluconeogenic S&I-stmtes OII glucose homemtmis in the newborn rat. Am. J. Physiol. 234 (2): E129-E136, 1978 or Am. J. Physiol.: Endocrinol. Metab+ Gastrointest. Physiol. 3 (Z): E129-E136, 1978.-The mechanism of the profound hypoglycemia that develops in newborn rats during a fast of 16 h beginning at birth has been investigated. This fasting hypoglycemia was partially reversed by giving oral triglycerides or an injection of gluconeogenic substrates (lactate, pyruvate, glycerol, alanine, glutamine, serinel, and completely reversed when these two treatments were combined. The rise in blood glucose induced by triglyceride feeding was not secondary to a decreased glucose utilization because the rate of glucose disappearance after intraperitoneal glucose injection was similar in fasted and triglyceride-fed newborns. That triglyceride feeding was associated with stimulation of gluconeogenesis by provision of fatty acids is inferred from the following: I) the rise in blood glucose after triglyceride feeding was totally suppressed by an inhibitor of gluconeogenesis(3-mercaptopicolinate); 2) a threefold increase in the conversion of labeled lactate or alanine into glucose was observed in vivo after triglyceride feeding; and? 7) concurrent inhibition of hepatic fatty acid oxidation by sodium pent+ enoate abolished the glycemic rise related to triglyceride feeding. These data suggest that lack of gluconeogenic substrate was not the primary factor limiting the activity of gluconeogenesis in fasted newborn rats. Rather, adequate free fatty acid availability appears essential to supply the energy required to sustain a high rate of gluconeogenie substrate conversion to glucose. Absence (as in newborn rats) or depletion of body fat stores could thus be causally associated with hypoglycemia by such a mechanism in other states. fasting; triglyceride feeding; gluconeogenesis; glucose utilization; ketogenesis