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Low-grade metabolic acidosis as a driver of insulin resistance
Open Heart ( IF 2.8 ) Pub Date : 2021-09-01 , DOI: 10.1136/openhrt-2021-001788
James J DiNicolantonio 1 , James H O'Keefe 2
Affiliation  

Metabolic acidosis occurs when there is retention of acid in the body which leads to a drop in the acid buffering capacity of the body. However, acid retention can occur even when serum bicarbonate is normal.1 There are four mechanisms through which the body can develop metabolic acidosis: (1) increased ingestion of dietary acid, (2) increased production of fixed acid such as in diabetic ketoacidosis, alcoholic ketoacidosis or prolonged fasting, (3) increased loss of base (ie, diarrhoea) and (4) reduced kidney excretion of acid. Additionally, specific medications can cause or contribute to metabolic acidosis. There are two major types of acid in the body, carbonic acid and non-carbonic acid. Carbonic acid is formed when a bicarbonate molecule combines with a hydrogen ion. Eventually carbonic acid is turned into water and carbon dioxide. Thus, if we create bicarbonate in the body from alkalinity supplied by the diet then we can breathe out the acid without depleting our own bicarbonate levels. Non-carbonic acids are fixed acids and cannot be exhaled via the lungs. They include lactic acid, phosphoric acid, sulfuric acid, uric acid and the ketoacids acetoacetic acid and beta-hydroxybutyric acid. Some of these fixed acids can be excreted in the urine in their free form, however, the urine pH can only drop to around 4.4 and hence only negligible quantities of strong acids, like sulfuric acid, can be eliminated in its free titratable form.2 So, 99% of the time sulfuric acid must be turned into hydrogen ions and sulfate and then it can be eliminated by the body. When we eat animal protein high in sulfur-containing amino acids such as methionine, cysteine and taurine, we form sulfuric acid, which gets broken down into two hydrogen ions and one sulfate molecule. If we consume a large amount of animal protein, …

中文翻译:

低度代谢性酸中毒是胰岛素抵抗的驱动因素

当体内酸滞留导致身体酸缓冲能力下降时,就会发生代谢性酸中毒。然而,即使血清碳酸氢盐正常,也会发生酸潴留。 1 身体发生代谢性酸中毒的机制有四种:(1) 摄入膳食酸增加,(2) 固定酸的产生增加,例如糖尿病酮症酸中毒,酒精性酮症酸中毒或长期禁食,(3) 碱损失增加(即腹泻)和 (4) 肾脏排泄酸减少。此外,特定药物可导致或促成代谢性酸中毒。人体内有两种主要的酸,碳酸和非碳酸。当碳酸氢盐分子与氢离子结合时形成碳酸。最终碳酸变成水和二氧化碳。因此,如果我们通过饮食提供的碱度在体内产生碳酸氢盐,那么我们可以呼出酸而不会消耗我们自己的碳酸氢盐水平。非碳酸是固定酸,不能通过肺部呼出。它们包括乳酸、磷酸、硫酸、尿酸和酮酸乙酰乙酸和β-羟基丁酸。其中一些固定酸可以以游离形式从尿液中排出,然而,尿液的 pH 值只能降至 4.4 左右,因此只有微量的强酸(如硫酸)可以以游离形式排出体外。 2所以,99%的时候硫酸必须转化为氢离子和硫酸盐,然后才能被人体排出。当我们食用蛋氨酸、半胱氨酸和牛磺酸等含硫氨基酸含量高的动物蛋白时,会形成硫酸,它被分解成两个氢离子和一个硫酸盐分子。如果我们摄入大量动物蛋白,...
更新日期:2021-09-09
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