本文适合进阶补剂爱好者
内容标签：GOBHB®
审查：朱倩妮 译稿：华珏琴
责编：过凌洋 校对：过红兴
β-羟基丁酸(BHB) 是一种酮体，您的细胞可以利用它来获取能量，尤其是在葡萄糖无法利用时。它们在生酮饮食讨论中得到了认可，您可以将酮视为继蛋白质、脂肪和碳水化合物之后的第四种常量营养素。
当身体缺乏膳食碳水化合物时，就会进入酮症状态，此时身体会燃烧脂肪（包括膳食脂肪和体内储存的脂肪）来产生高能分子，即酮体。
在这种状态下，身体很容易利用酮作为主要能量来源——它们是葡萄糖的有力替代品。旨在产生酮并长期维持这种状态的饮食通常称为生酮饮食，简称“生酮饮食”。[1]
与标准美国饮食 (SAD) 相比，研究表明生酮饮食具有多种潜在的健康益处，尤其是对于代谢困难的人群。
这些益处包括减肥、[2-13]更好的血糖控制、[5,6,10-14]改善代谢和脂质生物标志物、[7-9]减少肝脏疾病、[10]增强认知能力、[15,16]改善食欲、[17]甚至改善皮肤质量。[18]
然而，并不是每个人都能（或愿意）坚持传统上用来产生酮体和维持酮症状态的高脂肪、低碳水化合物、中等蛋白质饮食。那么，我们能否在不严格遵循生酮饮食的情况下获得酮体的一些好处呢？
酮体适合所有人，不只适合生酮饮食者
虽然在碳水化合物限制期间，您的细胞可以自行产生 BHB，但由于现代科学的进步，我们现在可以将酮体作为膳食补充剂外源性地服用。
看到节食者从 SAD 饮食转换为生酮饮食时获得的好处，面临的主要问题是：“这些好处是来自酮体，还是来自葡萄糖和胰岛素的减少？
”答案是两者兼而有之，但对于偶尔享受进入酮症状态的健康人和运动员来说，主要是前者——外源性BHB 补充剂具有多种益处。
我们可以在不彻底改变饮食的情况下获得 BHB 的好处吗？当然可以。
在本文中，我们详细介绍了外源性酮补充剂的益处，特别关注BHB 盐和BHB 游离酸，它们由 Ketone Labs 以goBHB 的名称销售。我们还讨论了市场上各种酮补充剂之间的一些差异，以及需要注意的一些陷阱。
BHB 补充剂的好处
我们首先应该讨论一下 BHB 最显著、可能最重要的作用，这些作用发生在大脑中。在“正常”条件下（即标准美国饮食的混合宏观喂养模式），大脑对血糖水平的波动高度敏感，因为神经元依靠葡萄糖来获取能量。
预防血糖波动
任何使用过连续血糖监测仪(CGM) 的人可能都会告诉你，血糖下降通常与紧张或焦虑的感觉有关。许多使用 CGM 的人报告说，BHB 补充剂可以大大减少这些周期，通常被称为“血糖过山车”。
多项动物研究支持了这一观点，表明补充 BHB 有助于降低焦虑行为的严重程度。[19,20]针对人类和动物的研究一致表明，外源性 BHB 可以降低血糖水平，[21-26]稳定血糖波动。
对大脑健康的益处
一项针对小鼠的临床前研究表明，BHB 实际上可以预防动物患上神经退行性疾病。更具体地说，这项研究是在3xTgAD小鼠身上进行的，这些小鼠是经过培育的，容易产生淀粉样蛋白和 tau 蛋白，而这些蛋白会聚集并形成神经毒性斑块。[19]
在这项研究中，一组去除牙菌斑的小鼠被喂以碳水化合物为主的饮食，而另一组则通过摄入酮体来提高其血清 BHB 水平。在整个研究期间，酮体组在一系列认知测试中的表现明显优于碳水化合物组。[19]
根据研究作者的说法，对此最可能的解释是较高的血清 BHB 水平对小鼠的神经元线粒体功能产生有益影响，并具有抗炎作用。
随着文献的进展，最近两篇研究评论的作者分别指出：
“人们普遍认为，酮症（血液中酮体水平升高，例如 β-羟基丁酸）可以产生神经保护作用” [27] 服用外源性酮类补充剂（如酮盐）“可产生快速而持续的营养性酮症和代谢变化，这可能对中枢神经系统 (CNS) 疾病（包括精神疾病）产生潜在的治疗效果。” [28]
减轻创伤性脑损伤 (TBI) 和脑震荡损伤
所有头部创伤，无论多么轻微，都有可能引发神经代谢级联反应，损害神经元的健康和功能。[29]
神经精神方面的益处
尽管人们对精神疾病的了解仍不完全，但最前沿的研究表明，神经炎症在抑郁症综合征和症状中起着重要作用。
与此相关，值得一提的是，BHB 可以降低炎症调节剂的表达，例如白细胞介素-1β (IL-1β) 和肿瘤坏死因子-α (TNF-α)，这些调节剂与抑郁症的病理生理学有关。
因此，补充 BHB 可以显著降低抑郁相关行为的严重程度也就不足为奇了。[33]
在一项研究中，被施用外源性 BHB 的啮齿动物在心理和身体抗压力测试中表现明显更好，例如强迫游泳测试 (FST) 和旷场测试 (OFT)。[34]
食欲调节
摄入外源性 BHB 带来的代谢益处也会产生连锁反应。例如，2017 年的一项研究表明，补充 BHB 可显著降低食欲、胰岛素和生长素释放肽[35]，后者本质上是一种刺激饥饿的激素。一般来说，血液中的生长素释放肽越多，你的食欲就越强烈。[36]
心脏保护
2017 年发表的一项人体研究发现，外源性 BHB 给药可显著降低血糖、游离脂肪酸和甘油三酯水平。[21]这三者都是心血管疾病风险的生物标志物，表明 BHB 可能支持心血管系统的健康和功能。
另一项研究证实了这一点，该研究表明，六周的外源性 BHB 补充可显著降低 18 至 35 岁受试者的血压。[38]
减少内脏脂肪
在另一项 2017 年的研究中，BHB 补充剂改善了大鼠的血脂并减少了内脏脂肪。[40]这是一项重要发现，因为内脏脂肪量与胰岛素抵抗和代谢综合征密切相关。这些疾病的发展会对心血管健康产生毁灭性的影响。
研究报告显示，HDL 胆固醇水平较高，LDL 胆固醇水平较低，甘油三酯水平较低，这是心血管健康的圣杯。[40]大量经同行评议的证据表明，HDL 与甘油三酯比率低与胰岛素抵抗有关。[41-46]
我们认为高密度脂蛋白胆固醇是您的“代谢报告单”，尽管制药行业擅长降低低密度脂蛋白胆固醇，但在安全提高高密度脂蛋白胆固醇方面却表现不佳。因此，当我们发现一种可以安全提高高密度脂蛋白胆固醇水平的膳食补充剂时，我们会留意。
提高代谢灵活性
可以说，外源性 BHB最酷的地方在于，它将酮症的好处与生酮生活方式区分开来——无论你是否处于营养性酮症状态，外源性酮体都会起作用。[47]
无论您吃了多少碳水化合物、吃了多少、或何时进食，外源性 BHB 给药都可以为您带来内源性酮生成的好处。
（A）D-BHB、D+L BHB 和 MCT 的血浆酮 iAUC（μM*h）和（B）每卡路里消耗产生的酮量（iAUC/kcal）。[39]
这并不奇怪，因为乳酸（又称乳酸盐）是无氧葡萄糖代谢的副产品，已知乳酸积累后会引起肌肉疲劳。即使在有氧运动（定义为低于个人乳酸盐阈值的强度水平）期间，也会发生一些无氧代谢。通过鼓励身体燃烧脂肪而不是葡萄糖，外源性 BHB 可以减少乳酸的形成并增加有氧活动期间的耐力。[49]
运动员体内的 BHB
虽然关于这个主题的研究很少，但看来，在人类运动员中施用 BHB确实可以通过节省葡萄糖来改善有氧运动表现。[50]然而，高强度（无氧）运动似乎相对不受影响。[51,52]对于运动员来说，BHB 的一个有趣好处是它有潜力减轻或预防剧烈运动后通常出现的暂时性认知能力下降。[52]
支持生酮或间歇性禁食生活方式
如果您仍坚持间歇性禁食和/或生酮生活方式，您可能不得不面对能量下降的问题——尤其是在最初的适应阶段。这使得外源性 BHB 补充剂成为一种很好的权宜之计。通过为您的身体和大脑提供酮体，您可以保持它们的能量，而不会破坏您的禁食或对酮症的适应。
增肌
早在 1988 年[54]就有研究证明 BHB 也能促进肌肉生长。它通过两种方式实现这一目标：它不仅可以增加肌肉蛋白质合成 (MPS)，还可以减少现有肌肉组织的分解和亮氨酸等氨基酸的氧化，使它们保持完整以刺激 MPS。[55,56]
换句话说，BHB 既能保护蛋白质，又能保护肌肉。
由于具有如此多的益处，我们很高兴看到 BHB 补充剂重新成为主流——它们显然不仅适用于生酮饮食者。
但是不同形式的 BHB 补充剂之间有什么区别？您应该考虑服用哪种呢？
BHB 的不同形式（盐、游离酸、酯）
并非所有 BHB 都一样。虽然所有形式的 BHB 都能提高血液中的 BHB 水平，但有些形式比其他形式更有效，而其他形式则不幸地给肝脏带来了灾难。
D-BHB 与 D/L-BHB
丁羟酸 D/L-BHB（D-BHB 和 L-BHB 的混合物），以及 MCT（中链甘油三酯）。
D-BHB 比 MCT 更能提高血酮水平
测量方法很重要：D/L-BHB 增加
当同时测量血浆中的 D-BHB 和 L-BHB 时，D/L-BHB 的总 BHB 浓度明显较大。[21]那么，关于 D-BHB 的“优越性”的传统观点仅仅是由于测量方法吗？
L-BHB（有时也称为S -BHB）“不会大量代谢成能量中间体”。[21,39,57] L-BHB 作为一种益智成分显示出巨大的潜力，科学家们开始对这些关于能量代谢的说法提出质疑——还有很多东西有待探索。
但它的意义远不止左撇子或右撇子这么简单：
游离酸 BHB、BHB 盐和酮酯
市场上有三种主要形式的 BHB 补充剂：
BHB 盐
BHB 盐是由 β-羟基丁酸与钠、镁、钙和钾等矿物质离子结合而形成的。这些盐是广受欢迎的外源性酮补充剂，因为它们不仅提供 BHB 来提高酮水平，还提供在酮症期间可能耗尽的必需电解质。
例如，钠和镁对神经功能和肌肉收缩至关重要。然而，摄入大量 BHB 盐会导致这些矿物质摄入过量，这可能是监测矿物质摄入量的人所担心的问题。
BHB 盐以goBHB 的形式广泛存在，我们尤其喜欢钠和镁 BHB，只是注意在饮食中保持适当的钠钾比。
然而，随着饮料越来越受欢迎，一种新形式的 BHB 正在占领市场：
游离酸 BHB
游离酸 BHB也以goBHB的形式出售，它是纯 β-羟基丁酸，不含任何矿物质离子。液态时，它更容易被人体吸收，因为它在消化过程中不需要与盐化合物分离。这可以更快地提高血酮水平，提供快速的能量来源。
对于那些希望避免摄入过量 BHB 盐中存在的钠或钙等矿物质的人来说，游离酸 BHB 也是有利的。
酮酯（小心！）
酮酯是 β-羟基丁酸酯与酒精分子化学结合的化合物，通常以 1,3-丁二醇的形式出售。酮酯可以显著提高血液中的酮水平，但除了味道极差之外，还有一个大问题：摄入后，它们会在肝脏中代谢，释放出 BHB——连同酒精成分！
这引起了严重的安全问题，因为 1,3-丁二醇在体内的作用类似于酒精，可能会损害肝功能。今年早些时候，我们讨论了新的数据，表明1,3-丁二醇会降低肝脏 ATP 水平，而游离酸 D-BHB、游离酸 L-BHB 和 MCT会增加ATP。这类似于拆东墙补西墙，并不是一个好的长期解决方案。
上述文章详细介绍了这些酮酯的众多副作用，[58-62]具体如下：
体重减轻[58] 身体脱水[58] 生育能力下降[61] 胎儿骨骼生长延迟[61] 代谢性酸中毒[58] 生长迟缓[59] 肝毒性[59,60] 身体依赖性[62] 肝窦扩张[58]
毫不奇怪，1,3-丁二醇的代谢与乙醇类似。[63]
更糟糕的是酮酯 1,4-丁二醇，由于其毒性，它被列入司法部的监视名单[64]，因为已经发生过几起过量服用的情况——有时甚至是致命的。[65-67]
由于这些担忧，我们对酮酯非常警惕，更喜欢 BHB 盐或游离酸 BHB 作为更安全的替代品。
BHB 剂量
建议补充的 BHB 量取决于个人目标。虽然我们绝不会拒绝任何剂量的 BHB，但我们发现最佳体验确实始于5 克剂量水平。最方便的是使用粉末（作为 BHB 盐）和液体（作为 BHB 游离酸）。
然而，即使几克也能为许多人提供快速提升。Ketone Labs 允许将胶囊配制成每份 800 毫克，将软糖配制成每份400毫克。话虽如此，我们通常会尝试每天服用几份来增加这些剂量。
BHB不只是适合生酮饮食者
随着我们继续看到外源性 BHB 补充剂的复苏，很明显这些酮不再只是生酮饮食者的专利。虽然 goBHB 早期的营销专门针对生酮爱好者，但今天，我们认识到 BHB 对更广泛受众的潜在益处。无论您是寻求能量和耐力的高性能运动员，还是对增强大脑功能和代谢灵活性感兴趣的人，BHB 补充剂都具有广泛的优势。
BHB 复兴最令人兴奋的方面之一是它的多功能性。我们发现，游离酸 BHB 最适合用于能量饮料，可以快速、干净地补充能量，而 D-BHB 盐则适合用于粉状补充剂，尤其是当运动员需要更持久的能量时。这个行业已经发展，我们对如何最好地利用这些酮的理解也在不断发展。
越来越多的研究支持 BHB 的益处，从增强认知能力到提高运动表现，BHB 的前景一片光明。我们很高兴看到这些补充剂如何不断发展，为每个人提供更健康的生活方式。
Batch, Jennifer T et al. “Advantages and Disadvantages of the Ketogenic Diet: A Review Article.” Cureus vol. 12,8 e9639. 10 Aug. 2020, doi:10.7759/cureus.9639. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7480775/ Castellana, Marco, et al. “Efficacy and Safety of Very Low Calorie Ketogenic Diet (VLCKD) in Patients with Overweight and Obesity: A Systematic Review and Meta-Analysis.” Reviews in Endocrine and Metabolic Disorders, 9 Nov. 2019, 10.1007/s11154-019-09514-y; https://pubmed.ncbi.nlm.nih.gov/31705259/ Choi, Yeo Jin, et al. “Impact of a Ketogenic Diet on Metabolic Parameters in Patients with Obesity or Overweight and with or without Type 2 Diabetes: A Meta-Analysis of Randomized Controlled Trials.” Nutrients, vol. 12, no. 7, 6 July 2020, p. 2005, 10.3390/nu12072005; https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7400909/ Bueno, Nassib Bezerra, et al. “Very-Low-Carbohydrate Ketogenic Diet v. Low-Fat Diet for Long-Term Weight Loss: A Meta-Analysis of Randomised Controlled Trials.” British Journal of Nutrition, vol. 110, no. 07, 7 May 2013, pp. 1178–1187, 10.1017/s0007114513000548; https://pubmed.ncbi.nlm.nih.gov/23651522/ Yancy, W.S., Foy, M., Chalecki, A.M. et al. “A low-carbohydrate, ketogenic diet to treat type 2 diabetes”. Nutr Metab (Lond) 2, 34 (2005); https://nutritionandmetabolism.biomedcentral.com/articles/10.1186/1743-7075-2-34 Noakes M, Foster PR, Keogh JB, James AP, Mamo JC, Clifton PM. “Comparison of isocaloric very low carbohydrate/high saturated fat and high carbohydrate/low saturated fat diets on body composition and cardiovascular risk.” Nutr Metab (Lond). 2006 Jan 11;3:7. doi: 10.1186/1743-7075-3-7; https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1368980/ Wood, Richard J., et al. “Carbohydrate Restriction Alters Lipoprotein Metabolism by Modifying VLDL, LDL, and HDL Subfraction Distribution and Size in Overweight Men.” The Journal of Nutrition, vol. 136, no. 2, 1 Feb. 2006, pp. 384–389, doi:10.1093/jn/136.2.384. https://www.sciencedirect.com/science/article/pii/S0022316622080683 Foster, Gary D, et al. “A Randomized Trial of a Low-Carbohydrate Diet for Obesity.” The New England Journal of Medicine, vol. 348, no. 21, 22 May 2003, pp. 2082–90, doi:10.1056/NEJMoa022207. https://www.nejm.org/doi/10.1056/NEJMoa022207 Brinkworth, Grant D, et al. “Long-Term Effects of a Very-Low-Carbohydrate Weight Loss Diet Compared with an Isocaloric Low-Fat Diet after 12 Mo.” The American Journal of Clinical Nutrition, vol. 90, no. 1, 13 May 2009, pp. 23–32, doi:10.3945/ajcn.2008.27326 https://www.sciencedirect.com/science/article/pii/S0002916523232062 Li, Jian, et al. “Ketogenic Diet in Women with Polycystic Ovary Syndrome and Liver Dysfunction Who Are Obese: A Randomized, Open‐Label, Parallel‐Group, Controlled Pilot Trial.” Journal of Obstetrics and Gynaecology Research, vol. 47, no. 3, 18 Jan. 2021, pp. 1145–1152, doi:10.1111/jog.14650 https://pubmed.ncbi.nlm.nih.gov/33462940/ McKenzie, Amy L, et al. “A Novel Intervention Including Individualized Nutritional Recommendations Reduces Hemoglobin A1c Level, Medication Use, and Weight in Type 2 Diabetes.” JMIR Diabetes, vol. 2, no. 1, 7 Mar. 2017, p. e5, 10.2196/diabetes.6981; https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6238887/ Hallberg, Sarah J., et al. “Effectiveness and Safety of a Novel Care Model for the Management of Type 2 Diabetes at 1 Year: An Open-Label, Non-Randomized, Controlled Study.” Diabetes Therapy, vol. 9, no. 2, 7 Feb. 2018, pp. 583–612, 10.1007/s13300-018-0373-9; https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6104272/ Athinarayanan, Shaminie J., et al. “Long-Term Effects of a Novel Continuous Remote Care Intervention Including Nutritional Ketosis for the Management of Type 2 Diabetes: A 2-Year Non-Randomized Clinical Trial.” Frontiers in Endocrinology, vol. 10, 5 June 2019, 10.3389/fendo.2019.00348; https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6561315/ Firman, Chloe H et al. “Does a Ketogenic Diet Have a Place Within Diabetes Clinical Practice? Review of Current Evidence and Controversies.” Diabetes therapy : research, treatment and education of diabetes and related disorders vol. 15,1 (2024): 77-97. doi:10.1007/s13300-023-01492-4. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10786817/ Chinna-Meyyappan, Arun, et al. “Effects of the Ketogenic Diet on Cognition: A Systematic Review.” Nutritional Neuroscience, 10 Nov. 2022, pp. 1–21, doi:10.1080/1028415x.2022.2143609; https://pubmed.ncbi.nlm.nih.gov/36354157/ Altayyar, Mansour, et al. “The Implication of Physiological Ketosis on the Cognitive Brain: A Narrative Review.” Nutrients, vol. 14, no. 3, 25 Jan. 2022, p. 513, doi:10.3390/nu14030513; https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8840718/ Roekenes, Jessica, and Catia Martins. “Ketogenic diets and appetite regulation.” Current opinion in clinical nutrition and metabolic care vol. 24,4 (2021): 359-363. doi:10.1097/MCO.0000000000000760. https://journals.lww.com/co-clinicalnutrition/fulltext/2021/07000/ketogenic_diets_and_appetite_regulation.14.aspx Castaldo, Giuseppe, et al. “Effect of Very-Low-Calorie Ketogenic Diet on Psoriasis Patients: A Nuclear Magnetic Resonance-Based Metabolomic Study.” Journal of Proteome Research, vol. 20, no. 3, 9 Nov. 2020, pp. 1509–1521, 10.1021/acs.jproteome.0c00646; https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8016365/ Kashiwaya, Yoshihiro, et al. “A Ketone Ester Diet Exhibits Anxiolytic and Cognition-Sparing Properties, and Lessens Amyloid and Tau Pathologies in a Mouse Model of Alzheimer’s Disease.” Neurobiology of Aging, vol. 34, no. 6, June 2013, pp. 1530–1539, 10.1016/j.neurobiolaging.2012.11.023; https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3619192/ Ari, Csilla, et al. “Exogenous Ketone Supplements Reduce Anxiety-Related Behavior in Sprague-Dawley and Wistar Albino Glaxo/Rijswijk Rats.” Frontiers in Molecular Neuroscience, vol. 9, 6 Dec. 2016, 10.3389/fnmol.2016.00137; https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5138218/ Stubbs, Brianna J et al. “On the Metabolism of Exogenous Ketones in Humans.” Frontiers in physiology vol. 8 848. 30 Oct. 2017, doi:10.3389/fphys.2017.00848; https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5670148/ Soto‐Mota, Adrian, et al. “Exogenous D ‐β‐Hydroxybutyrate Lowers Blood Glucose in Part by Decreasing the Availability of L‐Alanine for Gluconeogenesis.” Endocrinology, Diabetes & Metabolism, vol. 5, no. 1, 16 Nov. 2021, doi:10.1002/edm2.300. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8754249/ Nakatani, T., et al. “Changes in Blood Glucose Levels in Relation to Blood Ketone Body Ratio Following Hypertonic Glucose Infusion in 70% Hepatectomized Rabbits.” European Surgical Research, vol. 16, no. 5, 1984, pp. 303–311, doi:10.1159/000128423. https://pubmed.ncbi.nlm.nih.gov/6468465/ Felts, P W, et al. “Effect of Infused Ketone Bodies on Glucose Utilization in the Dog*.” Journal of Clinical Investigation, vol. 43, no. 4, 1 Apr. 1964, pp. 638–646, doi:10.1172/jci104949. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC289541/ Müller, M J, et al. “Effect of Ketone Bodies on Glucose Production and Utilization in the Miniature Pig.” Journal of Clinical Investigation, vol. 74, no. 1, 1 July 1984, pp. 249–261, doi:10.1172/jci111408. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC425207/ Ari, et al. “Exogenous Ketones Lower Blood Glucose Level in Rested and Exercised Rodent Models.” Nutrients, vol. 11, no. 10, 1 Oct. 2019, p. 2330, doi:10.3390/nu11102330. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6835632/ Kovács, Zsolt, et al. “Beneficial Effects of Exogenous Ketogenic Supplements on Aging Processes and Age-Related Neurodegenerative Diseases.” Nutrients, vol. 13, no. 7, 26 June 2021, p. 2197, doi:10.3390/nu13072197. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8308443/ Kovács, Zsolt, et al. “Therapeutic Potential of Exogenous Ketone Supplement Induced Ketosis in the Treatment of Psychiatric Disorders: Review of Current Literature.” Frontiers in Psychiatry, vol. 10, 23 May 2019, doi:10.3389/fpsyt.2019.00363. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6543248/ Giza, Christopher C., and David A. Hovda. “The Neurometabolic Cascade of Concussion.” Journal of athletic training vol. 36,3 (2001): 228-235. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC155411/ Daines, Savannah Anne. “The Therapeutic Potential and Limitations of Ketones in Traumatic Brain Injury.” Frontiers in neurology vol. 12 723148. 22 Oct. 2021, doi:10.3389/fneur.2021.723148. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8579274/ McDougall, Alexandre et al. “The ketogenic diet as a treatment for traumatic brain injury: a scoping review.” Brain injury vol. 32,4 (2018): 416-422. doi:10.1080/02699052.2018.1429025; https://www.tandfonline.com/doi/abs/10.1080/02699052.2018.1429025 Davis, Laurie M et al. “Fasting is neuroprotective following traumatic brain injury.” Journal of neuroscience research vol. 86,8 (2008): 1812-22. doi:10.1002/jnr.21628. https://onlinelibrary.wiley.com/doi/10.1002/jnr.21628 Yamanashi, Takehiko, et al. “Beta-Hydroxybutyrate, an Endogenic NLRP3 Inflammasome Inhibitor, Attenuates Stress-Induced Behavioral and Inflammatory Responses.” Scientific Reports, vol. 7, no. 1, 9 Aug. 2017, doi:10.1038/s41598-017-08055-1. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5550422/ Naofumi Kajitani, et al. “Prefrontal Cortex Infusion of Beta‐Hydroxybutyrate, an Endogenous NLRP3 Inflammasome Inhibitor, Produces Antidepressant‐like Effects in a Rodent Model of Depression.” Neuropsychopharmacology Reports, vol. 40, no. 2, 3 Mar. 2020, pp. 157–165, doi:10.1002/npr2.12099. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7722664/ Stubbs, Brianna J., et al. “A Ketone Ester Drink Lowers Human Ghrelin and Appetite.” Obesity, vol. 26, no. 2, 6 Nov. 2017, pp. 269–273, 10.1002/oby.22051; https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5813183/ Wu, James T, and John G Kral. “Ghrelin: integrative neuroendocrine peptide in health and disease.” Annals of surgery vol. 239,4 (2004): 464-74. doi:10.1097/01.sla.0000118561.54919.61. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1356251/ Davis, Rachel A H et al. “Dietary R, S-1,3-butanediol diacetoacetate reduces body weight and adiposity in obese mice fed a high-fat diet.” FASEB journal : official publication of the Federation of American Societies for Experimental Biology vol. 33,2 (2019): 2409-2421. doi:10.1096/fj.201800821RR; https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6338649/ Holland, Angelia M., et al. “Blood and Cardiovascular Health Parameters after Supplementing with Ketone Salts for Six Weeks.” Journal of Insulin Resistance, vol. 4, no. 1, 24 Apr. 2019, 10.4102/jir.v4i1.47; https://insulinresistance.org/index.php/jir/article/view/47/172 Cuenoud, Bernard et al. “Metabolism of Exogenous D-Beta-Hydroxybutyrate, an Energy Substrate Avidly Consumed by the Heart and Kidney.” Frontiers in nutrition vol. 7 13. 19 Feb. 2020, doi:10.3389/fnut.2020.00013. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7042179/ Caminhotto, Rennan de Oliveira, et al. “Oral β-Hydroxybutyrate Increases Ketonemia, Decreases Visceral Adipocyte Volume and Improves Serum Lipid Profile in Wistar Rats.” Nutrition & Metabolism, vol. 14, no. 1, 24 Apr. 2017, 10.1186/s12986-017-0184-4; https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5404327/ Bertsch, Ruth Ann, and Maqdooda A Merchant. “Study of the Use of Lipid Panels as a Marker of Insulin Resistance to Determine Cardiovascular Risk.” The Permanente journal vol. 19,4 (2015): 4-10. doi:10.7812/TPP/14-237; https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4625988/ Bartlett, Jacquelaine, et al. “Is Isolated Low High-Density Lipoprotein Cholesterol a Cardiovascular Disease Risk Factor?” Circulation: Cardiovascular Quality and Outcomes, vol. 9, no. 3, May 2016, pp. 206–212, 10.1161/circoutcomes.115.002436; https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4871717/ Wang, T. D., et al. “Efficacy of Cholesterol Levels and Ratios in Predicting Future Coronary Heart Disease in a Chinese Population.” The American Journal of Cardiology, vol. 88, no. 7, 1 Oct. 2001, pp. 737–743, 10.1016/s0002-9149(01)01843-4; https://pubmed.ncbi.nlm.nih.gov/11589839 Jeppesen, Jørgen, et al. “Low Triglycerides–High High-Density Lipoprotein Cholesterol and Risk of Ischemic Heart Disease.” Archives of Internal Medicine, vol. 161, no. 3, 12 Feb. 2001, p. 361, 10.1001/archinte.161.3.361; https://jamanetwork.com/journals/jamainternalmedicine/fullarticle/647239 Castelli, William P. “Epidemiology of Triglycerides: A View from Framingham.” American Journal of Cardiology, vol. 70, no. 19, 14 Dec. 1992, pp. H3–H9, 10.1016/0002-9149(92)91083-G; https://www.ajconline.org/article/0002-9149(92)91083-G/abstract McLaughlin, Tracey, et al. “Use of Metabolic Markers to Identify Overweight Individuals Who Are Insulin Resistant.” Annals of Internal Medicine, vol. 139, no. 10, 18 Nov. 2003, p. 802, 10.7326/0003-4819-139-10-200311180-00007; https://pubmed.ncbi.nlm.nih.gov/14623617/ Harvey, Cliff J. d C., et al. “The Use of Nutritional Supplements to Induce Ketosis and Reduce Symptoms Associated with Keto-Induction: A Narrative Review.” PeerJ, vol. 6, 16 Mar. 2018, p. e4488, 10.7717/peerj.4488; https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5858534/ Okuda, Y., et al. “Ketone Body Utilization and Its Metabolic Effect in Resting Muscles of Normal and Streptozotocin-Diabetic Rats.” Endocrinologia Japonica, vol. 38, no. 3, 1 June 1991, pp. 245–251, 10.1507/endocrj1954.38.245; https://pubmed.ncbi.nlm.nih.gov/1838977/ Scott, Benjamin E., et al. “The Effect of 1,3-Butanediol and Carbohydrate Supplementation on Running Performance.” Journal of Science and Medicine in Sport, vol. 22, no. 6, 1 June 2019, pp. 702–706, 10.1016/j.jsams.2018.11.027; https://pubmed.ncbi.nlm.nih.gov/30553764/ Cox, Pete J., et al. “Nutritional Ketosis Alters Fuel Preference and Thereby Endurance Performance in Athletes.” Cell Metabolism, vol. 24, no. 2, Aug. 2016, pp. 256–268, 10.1016/j.cmet.2016.07.010; https://www.cell.com/cell-metabolism/fulltext/S1550-4131(16)30355-2 Dearlove, David J., et al. “Nutritional Ketoacidosis during Incremental Exercise in Healthy Athletes.” Frontiers in Physiology, vol. 10, 29 Mar. 2019, 10.3389/fphys.2019.00290; https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6450328/ Evans, Mark, and Brendan Egan. “Intermittent Running and Cognitive Performance after Ketone Ester Ingestion.” Medicine & Science in Sports & Exercise, vol. 50, no. 11, Nov. 2018, pp. 2330–2338, 10.1249/mss.0000000000001700; https://pubmed.ncbi.nlm.nih.gov/29944604/ d C. Harvey, Cliff J., et al. “The Effect of Medium Chain Triglycerides on Time to Nutritional Ketosis and Symptoms of Keto-Induction in Healthy Adults: A Randomised Controlled Clinical Trial.” Journal of Nutrition and Metabolism, vol. 2018, 22 May 2018, doi:10.1155/2018/2630565. https://www.hindawi.com/journals/jnme/2018/2630565/ Nair, K S et al. “Effect of beta-hydroxybutyrate on whole-body leucine kinetics and fractional mixed skeletal muscle protein synthesis in humans.” The Journal of clinical investigation vol. 82,1 (1988): 198-205. doi:10.1172/JCI113570 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC303494/ Thomsen, Henrik Holm et al. “Investigating effects of sodium beta-hydroxybutyrate on metabolism in placebo-controlled, bilaterally infused human leg with focus on skeletal muscle protein dynamics.” Physiological reports vol. 10,16 (2022): e15399. doi:10.14814/phy2.15399. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9391664/ Mose, M et al. “Anabolic effects of oral leucine-rich protein with and without β-hydroxybutyrate on muscle protein metabolism in a novel clinical model of systemic inflammation-a randomized crossover trial.” The American journal of clinical nutrition vol. 114,3 (2021): 1159-1172. doi:10.1093/ajcn/nqab148. https://www.sciencedirect.com/science/article/pii/S0002916522004397 Newman, John C., and Eric Verdin. “β-Hydroxybutyrate: A Signaling Metabolite.” Annual Review of Nutrition, vol. 37, no. 1, 21 Aug. 2017, pp. 51–76, doi:10.1146/annurev-nutr-071816-064916 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6640868/ McCarthy, Cameron G, et al. “Physiologic, Metabolic, and Toxicologic Profile of 1,3-Butanediol.” Journal of Pharmacology and Experimental Therapeutics, vol. 379, no. 3, 14 Sept. 2021, pp. 245–252, doi:10.1124/jpet.121.000796. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9164310/ McCarthy, Cameron G, et al. Ketone Body β-Hydroxybutyrate Is an Autophagy-Dependent Vasodilator. Vol. 6, no. 20, 22 Oct. 2021, doi:10.1172/jci.insight.149037. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8564907/ Pilon, Denis, et al. “1,3-Butanediol-Induced Increases in Ketone Bodies and Potentiation of CCl4 Hepatotoxicity.” Toxicology, vol. 40, no. 2, Aug. 1986, pp. 165–180, doi:10.1016/0300-483x(86)90076-4. https://pubmed.ncbi.nlm.nih.gov/3726892/ Hess, Frederick G., et al. “Reproduction and Teratology Study of 1,3-Butanediol in Rats.” Journal of Applied Toxicology, vol. 1, no. 4, Aug. 1981, pp. 202–209, doi:10.1002/jat.2550010404. https://pubmed.ncbi.nlm.nih.gov/7184938/ Frye, G. D., et al. “Effects of Acute and Chronic 1,3-Butanediol Treatment on Central Nervous System Function: A Comparison with Ethanol.” The Journal of Pharmacology and Experimental Therapeutics, vol. 216, no. 2, 1 Feb. 1981, pp. 306–314. https://pubmed.ncbi.nlm.nih.gov/7193248/ Mehlman, M A, et al. “Metabolic Fate of 1,3-Butanediol in the Rat: Liver Tissue Slices Metabolism.” The Journal of Nutrition, vol. 101, no. 12, 1 Dec. 1971, pp. 1711–1718, doi:10.1093/jn/101.12.1711. https://www.sciencedirect.com/science/article/abs/pii/S0022316623034144 United States Drug Enforcement Administration (DEA). “1,4-Butanediol”. February 2024. https://www.deadiversion.usdoj.gov/drug_chem_info/bdo.pdf Stefani, Maurizio, and Darren M. Roberts. “1,4-Butanediol Overdose Mimicking Toxic Alcohol Exposure.” Clinical Toxicology, 20 June 2019, pp. 1–4, doi:10.1080/15563650.2019.1617419. https://pubmed.ncbi.nlm.nih.gov/31218892/ Fischer, Victoria, et al. “Fatal Intoxication with 1,4‐Butanediol: Case Report and Comprehensive Review of the Literature.” Journal of Forensic Sciences, vol. 68, no. 4, 5 June 2023, pp. 1410–1418, doi:10.1111/1556-4029.15294. https://onlinelibrary.wiley.com/doi/10.1111/1556-4029.15294 Zvosec, Deborah L., et al. “Adverse Events, Including Death, Associated with the Use of 1,4-Butanediol.” New England Journal of Medicine, vol. 344, no. 2, 11 Jan. 2001, pp. 87–94, doi:10.1056/nejm200101113440202. https://www.nejm.org/doi/full/10.1056/NEJM200101113440202
转载须知
标注‘原创’仅代表原创编译，本平台不主张对原文的版权。本平台转载仅仅是出于学术交流和传播信息的需要，并不意味着代表本平台观点或证实其内容的真实性；转载文章版权归原作者所有，作者如果不希望被转载或有侵权行为，请联系本平台删除。
