Glucocorticoid activity and metabolism with NaCl-induced low-grade metabolic acidosis and oral alkalization: results of two randomized controlled trials
Glucocorticoid activity and metabolism with NaCl-induced low-grade metabolic acidosis and oral alkalization: results of two randomized controlled trials
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DOI：
10.1007/s12020-015-0730-7
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发表时间：
2016-04-01
期刊：
影响因子：
3.7
通讯作者：
Heer, Martina
中科院分区：
文献类型：
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作者：
Buehlmeier, Judith;Remer, Thomas;Heer, Martina
由高膳食酸负荷或氯化钠（NaCl）摄入引起的低度代谢性酸中毒（LGMA）已被证明会增加骨和蛋白质的催化活性。潜在的机制尚未完全了解，但从临床代谢性酸中毒的酸碱平衡与糖皮质激素（GC）代谢的相互作用是已知的。我们的目的是研究GC活性/代谢碱性补充和NaCl诱导的LGMA。八名年轻、健康、体重正常的男性参与了两项交叉设计的干预性研究。在研究A中，进行了两个为期10天的高NaCl饮食（32 g/d）阶段，一个阶段补充90 mmol KHCO 3/d。在研究B中，参与者接受高和低NaCl饮食（31 g/天vs. 3 g/天），各持续14天。在低NaCl期间，通过用非碱化饮用水替换富含碳酸氢盐的矿泉水（在高NaCl期间消耗）来适度酸化饮食。在重复收集的24小时尿液样本中，分析了潜在的无生物活性GC（尿液游离皮质醇+游离可的松）以及四氢皮质醇（THF）、5 α-THF和四氢可的松（THE）。补充90 mmol KHCO 3后，总肾上腺GC分泌标志物（THF + 5 α-THF + THE）下降（p = 0.047），潜在无生物活性GC减少（p = 0.003）。然而，在研究B中，GC分泌和潜在的无生物活性GC未表现出预期的NaCl减少下降，因为净酸排泄增加了30 mEq/d。饮食诱导的酸化/碱化影响GC活性和代谢，如果长期摄入习惯性酸化的西方饮食，可能构成骨降解和心脏代谢疾病的独立风险因素。
Low-grade metabolic acidosis (LGMA), as induced by high dietary acid load or sodium chloride (NaCl) intake, has been shown to increase bone and protein catabolism. Underlying mechanisms are not fully understood, but from clinical metabolic acidosis interactions of acid-base balance with glucocorticoid (GC) metabolism are known. We aimed to investigate GC activity/metabolism under alkaline supplementation and NaCl-induced LGMA. Eight young, healthy, normal-weight men participated in two crossover designed interventional studies. In Study A, two 10-day high NaCl diet (32 g/d) periods were conducted, one supplemented with 90 mmol KHCO3/day. In Study B, participants received a high and a low NaCl diet (31 vs. 3 g/day), each for 14 days. During low NaCl, the diet was moderately acidified by replacement of a bicarbonate-rich mineral water (consumed during high NaCl) with a non-alkalizing drinking water. In repeatedly collected 24-h urine samples, potentially bioactive-free GCs (urinary-free cortisol + free cortisone) were analyzed, as well as tetrahydrocortisol (THF), 5 alpha-THF, and tetrahydrocortisone (THE). With supplementation of 90 mmol KHCO3, the marker of total adrenal GC secretion (THF + 5 alpha-THF + THE) dropped (p = 0.047) and potentially bioactive-free GCs were reduced (p = 0.003). In Study B, however, GC secretion and potentially bioactive-free GCs did not exhibit the expected fall with NaCl-reduction as net acid excretion was raised by 30 mEq/d. Diet-induced acidification/alkalization affects GC activity and metabolism, which in case of long-term ingestion of habitually acidifying western diets may constitute an independent risk factor for bone degradation and cardiometabolic diseases.