Fonteles M C, Cohen J J, Black A J, Wertheim S J
Am J Physiol. 1983 Mar;244(3):F235-46. doi: 10.1152/ajprenal.1983.244.3.F235.
To determine whether the oxidation of long-chain fatty acids (LCFA) derived from renal tissue lipids can support renal function, we perfused isolated rat kidneys with a substrate-free Krebs-Ringer bicarbonate solution containing 6 g/100 ml substrate-free (defatted) albumin. We measured GFR, TNa+, and Qo2 at 7-min intervals from 15 to 99 min after cannulation of the renal artery. Two groups (A and B) of 12 perfusions each were done. During substrate-free perfusion mean %TNa+ was low (A = 45 +/- 2%, B = 62 +/- 5%). When 10(-4) M 2-tetradecylglycidic acid (2-TDGA), a specific and irreversible inhibitor of long-chain acylcarnitine transferase-I, was added to the substrate-free perfusate, significant decreases in %TNa+ (A to approximately 25%; B to approximately 35%) and in Qo2 (delta = -25%) occurred. During perfusion with either 5 mM lactate or 5 mM alpha-ketoglutarate (alpha-KG) %TNa+ increased to approximately 80%. When 2-TDGA was added in the presence of lactate or of alpha-KG no decrease in %TNa+ or Qo2 occurred. Thus, 2-TDGA does not inhibit net renal Na+ transport or O2 uptake in the presence of high concentrations of lactate or alpha-KG, substrates not requiring long-chain acylcarnitine transferase for their utilization. We conclude that oxidation of LCFA released from renal tissue lipids can support a significant portion of Na+ reabsorption.
为了确定源自肾组织脂质的长链脂肪酸（LCFA）氧化是否能维持肾功能，我们用含有6 g/100 ml无底物（脱脂）白蛋白的无底物 Krebs-Ringer 碳酸氢盐溶液灌注离体大鼠肾脏。在肾动脉插管后15至99分钟内，每隔7分钟测量一次肾小球滤过率（GFR）、总钠排泄分数（TNa+）和氧耗量（Qo2）。每组进行12次灌注，共两组（A组和B组）。在无底物灌注期间，平均总钠排泄分数较低（A组 = 45 ± 2%，B组 = 62 ± 5%）。当向无底物灌注液中加入10⁻⁴ M 2-十四烷基甘油酸（2-TDGA，一种长链酰基肉碱转移酶-I的特异性不可逆抑制剂）时，总钠排泄分数显著降低（A组降至约25%；B组降至约35%），氧耗量也降低（下降 = -25%）。在用5 mM乳酸或5 mMα-酮戊二酸（α-KG）灌注期间，总钠排泄分数增加至约80%。当在乳酸或α-KG存在的情况下加入2-TDGA时，总钠排泄分数或氧耗量没有降低。因此，在高浓度乳酸或α-KG存在时，2-TDGA不抑制肾脏净钠转运或氧摄取，乳酸和α-KG这些底物的利用不需要长链酰基肉碱转移酶。我们得出结论，肾组织脂质释放的LCFA氧化可维持相当一部分钠重吸收。
