Interactions of dietary fat and 2,5-anhydro-D-mannitol on energy metabolism in isolated rat hepatocytes.
Interactions of dietary fat and 2,5-anhydro-D-mannitol on energy metabolism in isolated rat hepatocytes.
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膳食脂肪和 2,5-脱水-D-甘露醇对离体大鼠肝细胞能量代谢的相互作用。
DOI：
10.1152/ajpregu.00159.2001
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发表时间：
2002
期刊：
影响因子：
--
通讯作者：
Friedman,MarkI
中科院分区：
文献类型：
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作者：
Ji,Hong;Graczyk-Milbrandt,Grazyna;Osbakken,MaryD;Friedman,MarkI
果糖类似物 2,5-脱水-d-甘露醇 (2,5-AM) 通过减少肝脏中的 ATP 含量来刺激大鼠进食。这些行为和代谢影响发生在喂食高碳水化合物/低脂肪（HC/LF）饮食的老鼠身上，但当动物吃高脂肪/低碳水化合物（HF/LC）食物时，这些行为和代谢影响会被预防或减弱。为了检查饮食这种影响的代谢基础，我们评估了 2,5-AM 对喂食两种饮食之一的大鼠分离肝细胞中 ATP 含量、耗氧量和底物氧化的作用。与喂食 HC/LF 饮食的大鼠细胞（“HC/LF”细胞）相比，喂食 HF/LC 饮食的大鼠细胞（“HF/LC”细胞）具有相似的 ATP 含量，但耗氧量较低，果糖减少，棕榈酸氧化增加。 2,5-AM 不会像在 HC/LF 肝细胞中那样降低 HF/LC 细胞中的 ATP 含量或耗氧量，并且仅影响 HC/LF 细胞中的果糖和棕榈酸酯氧化。 31 P-NMR 光谱表明，磷酸盐捕获的差异导致了 2,5-AM 消耗 ATP 的差异。这些结果表明，摄入 HF/LC 饮食可以通过改变肝细胞代谢以脂肪而非碳水化合物作为能量产生底物来防止进食反应并减轻肝脏 ATP 的下降。
The fructose analog 2,5-anhydro-d-mannitol (2,5-AM) stimulates feeding in rats by reducing ATP content in the liver. These behavioral and metabolic effects occur with rats fed a high-carbohydrate/low-fat (HC/LF) diet, but they are prevented or attenuated when the animals eat high-fat/low-carbohydrate (HF/LC) food. To examine the metabolic bases for this effect of diet, we assessed the actions of 2,5-AM on ATP content, oxygen consumption, and substrate oxidation in isolated hepatocytes from rats fed one of the two diets. Compared with cells from rats fed the HC/LF diet (“HC/LF” cells), cells from rats fed the HF/LC diet (“HF/LC” cells) had similar ATP contents but lower oxygen consumption, decreased fructose, and increased palmitate oxidation. 2,5-AM did not decrease ATP content or oxygen consumption in HF/LC cells as much as it did in HC/LF hepatocytes, and it only affected fructose and palmitate oxidation in HC/LF cells.31P-NMR spectroscopy indicated that differences in phosphate trapping accounted for differences in depletion of ATP by 2,5-AM. These results suggest that intake of the HF/LC diet prevents the eating response and attenuates the decline in liver ATP by shifting hepatocyte metabolism to favor fat over carbohydrate as an energy-yielding substrate.