碳水阻断剂(白芸豆提取物)真实有效吗?

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Keto Cheat减脂胶囊完好评测

Keto Cheat 是 Sheer Strength公司的一种新型天然减脂助剂。Sheer Strength 造造了许多健美补剂,他们是一个受欢送的品牌,他们似乎正在相当不变的增长。

那么那个产物有什么感化吗?

Keto Cheat 显然是 Sheer Strength 的 KETO SERIES 的一部门。它不像我们在那个网站上评论的大大都产物,因为它似乎更像是一种饮食辅助而不是健美补剂。

在盒子上,Keto Cheat 被描述为“生酮一号,碳水化合物阻断剂”。

按照瓶子的说法,那种弥补剂供给了以下次要益处:

削减碳水化合物的吸收减轻做弊餐损害撑持减肥

任何提到“碳水化合物阻塞”对我们来说都是一个次要的危险信号。

若是您是一名正在为大型角逐训练的运发动,那么您需要切当地晓得您每天的食物摄入量是几。

碳水化合物是饮食的重要构成部门。没有碳水化合物,您将无法成立任何新的肌肉量量,而且您将无法获得完成熬炼所需的能量。

是的,节食包罗削减热量摄入。

但那其实不意味着你需要脱节碳水化合物;那意味着你需要摄入更少的卡路里。

那当然其实不意味着您能够完全不晓得您每天现实吸收了几碳水化合物。

我们也对整个“生酮圈”的时髦深感不满。

稍后将详细介绍所有那些。

如今,我们需要起头更详细地研究地道的力量酮做弊。

它能否做到了它在瓶身上所说的一切?

你实的想要“碳水化合物阻滞剂”吗?

如许的工作现实上可能吗?

生酮做弊平安吗?可能的安康风险是什么?

Keto Cheat减脂胶囊营养成分表

我们看到那份营养成分表时,第一印象觉得很欠好。

我们很遗憾地说那是一个十分可悲的营养成分表。

就减肥补剂而言,那长短常蹩脚的配方架构设想。

在利用此成分时,很少有人可能会看到实正的成果,也就是毫无感化。

我们当然不认为它合适庄重的拳击手、健美运发动等。

我们以至认为那关于那些只想在炎天减脂的人来说不是一个好的选择。

我们有关于 Keto Cheat 的三个次要问题,我们如今将不按特定挨次逐个讨论。

Keto Cheat减脂胶囊的错误宣传

要晓得,没有一小我能实正从碳水化合物阻断剂中受益。

许多人错误地认为碳水化合物会让你发胖,任何想要变瘦的人都需要完全戒掉那一类食物。

那是错的!!!

碳水化合物是安康人类饮食的需要构成部门。

碳水化合物不会让你发胖。

过多的卡路里才会让你发胖!

清洁的白米饭和清洁的全麦面包,你会选哪个?伶俐人两者城市选。只要愚蠢的韭菜才会选择全麦面包,因为在韭菜心中,全麦面包要比白米饭热量更低。那是多么好笑啊!

良多人发现他们在削减碳水化合物后体重减轻了,但那只是因为他们凡是是人生中第一次控造饮食。

他们发现本身不克不及那么容易在外面吃饭,所以他们被迫愈加自律。

摄入的食物体积变小,热量摄入量也下降。

碳水化合物不是那个过程的重要部门;饮食控造是关键。

因而,即便 Keto Cheat 阻遏了你摄入的每一种碳水化合物,你仍然会越来越胖,除非你摄入的卡路里少于消耗的卡路里。

我们都需要碳水化合物

若是您希望既瘦又强健,那么您就不想从饮食中削减碳水化合物。

健美运发动的肌肉看起来如斯厚实和圆润的原因是因为肌肉里充满了糖原。

若是你耗尽了你的糖原储蓄,你的肌肉会看起来很瘪。

碳水化合物使你的肌肉看起来又大又厚。

你还需要碳水化合物来帮忙你增肌。

是的,卵白量很重要,但训练肌肉所需的卵白量量十分少。

但是除非你摄入大量碳水化合物,不然你会发现很难成立任何新的肌肉量量。

若是你是一个健美运发动,完全不吃碳水化合物是个坏主意(除非你打针类固醇,那在心理上是实正的底层逻辑变化行为)。

更重要的是,若是您是一名运发动,试图在重要角逐(无论是肉搏、举重角逐仍是健美演出)中竭尽全力,那么您需要在前几周的训练中连结 100% 的表示.

削减碳水化合物的摄入会危及那一切,包罗影响你的表示、你的训练强度和你的恢复。

碳水化合物阻滞剂毁坏饮食方案

想象一下,若是以上所有内容都不是实的。

想象一下,要蹲下 700 磅或看起来像杰·卡特勒,你所要做的就是吃牛排和芦笋。

那么你仍然需要可以准确地方案你的饮食。

碳水化合物阻滞剂说它们会削减碳水化合物的“摄取”,但我们不晓得削减了几。

我们不晓得它们有多有效,它们能持续多久,或者它们能否会阻遏吸收所有形式的碳水化合物。

它们可能会阻遏可乐中的糖分被吸收,但它们可能不会阻遏您在服用 Keto Cheat减脂胶囊3 小时后吃的所有燕麦片。

所以你不克不及准确地方案你的饮食。

你无法准确地权衡你的碳水化合物摄入量。

向我们展现一个认实的运发动,他能够在重要角逐之前用他们的食物摄入量停止赌博,我们将向您展现一个必定要失败的人。

Keto Cheat减脂胶囊所谓的生酮快速通道

虽然我们认为 Keto Cheat 的既定目的完全被误导,但那并非故事的结局。

若是它确实以其他体例帮忙削减脂肪,我们仍然能够拥有优良的弥补剂。

不幸的是,事实并不是如斯。

次要成分是白芸豆提取物。

据我们所知,没有任何证据表白那种工具能够加强脂肪削减的效果。

以至没有关于白芸豆,撑持藤黄果之类的传说风闻证据。

Keto Cheat减脂胶囊还含有肉桂成分肉桂是一种廉价、普遍利用的香料,对减脂没有任何感化。

那对你在健身房的表示没有帮忙。

它不会阻遏碳水化合物的吸收。

它只会让您的卡布奇诺味道更好。

绿茶提取物是一种很好的天然脂肪燃烧器,但那款产物中含有的 250 毫克是微不敷道的份量。

更好的燃脂补剂含有两倍的量,若是不是更多的话。

因为其他两种成分是如斯无用,我们不克不及对绿茶提取物太兴奋。

即便份量更大,当今市场上大大都更好的脂肪燃烧器都利用绿茶和 5-8 种其他有效的脂肪削减促进剂。

250mg 的绿茶提取物无法挽救那种虚弱、无效的配方。

Keto Cheat减脂胶囊的副感化

关于地道的生酮做弊,你可能会说的独一益处是副感化似乎十分不成能。

成分都十分暖和。

绿茶有一些严峻的脂肪燃烧潜力,但 250 毫克底子不会做太多。

白芸豆与肉桂对减脂毫无感化

与往常一样,仅仅因为成分对我们来说看起来平安其实不意味着它对每小我都是平安的。

在利用 Keto Cheat 等补剂之前,您需要领会本身的不耐受性、敏感性和过敏性。

我们不是医生,如今告诉您购置 Keto Cheat 的人并没有将您的更大利益放在心上。

在利用 Keto Cheat 减脂胶囊之前,您必需先征询医生。在继续之前,请从您本身的医生那里获得合格的医疗定见。若是您在利用那种产物时碰到任何副感化,请停行利用并就医。

若是您严峻瘦削,那么一切减脂补剂都不合适你!

那些减脂补剂产物专为安康、运动的人而设想,他们需要帮忙在减脂阶段获得更大帮忙,或者在健美角逐中处于更佳形态。

要记住!减脂补剂不克不及治愈瘦削症。为此,您需要优良的饮食、歇息和体育计划。

Keto Cheat减脂胶囊评测总结

总而言之,很难找到关于 Keto Cheat 减脂胶囊的任何益处。

若是您完好阅读了上面的Keto Cheat减脂胶囊评测,您就会晓得我们不喜好那个产物。

起首,我们认为碳水化合物阻滞剂对任何人来说都不是一个好选择。

碳水化合物不会让你发胖。过多的卡路里才会让你发胖。

另一方面,缺乏碳水化合物会让你变得平展,你的肌肉萎缩,你在地板上的情感以及你在健身房的表示会敏捷恶化。

若是你是一名为角逐而减脂的运发动,碳水化合物阻滞剂是你最不需要的工具。

它们还意味着您无法准确方案您的饮食,因为您不晓得有几碳水化合物被阻遏。

最最关键的就是那款产物的配方只是两种完全虚假的、完全无害的成分和一小份绿茶。

若是你想要实正的成果和任何物有所值的外表,看看此外产物吧!

最初,再反复一遍!

若是您严峻瘦削,那么一切减脂补剂都不合适你!

那些减脂补剂产物专为安康、运动的人而设想,他们需要帮忙在减脂阶段获得更大帮忙,或者在健美角逐中处于更佳形态。

要记住!市道上所有减脂补剂都不克不及治愈瘦削症。为此,您需要优良的饮食、歇息和体育计划。

我们的评测尺度是什么?

我们将阐发产物的配方、成分、剂量以及消费者对那款产物的评价,然后我们会停止成分风险评估与副感化评估,最初得出一个合理的综合评分。

优良的燃脂补剂应兼具特征和特征。要实正做到有效,它必需是:

1.完全天然,也没有尝试室造造的兴奋剂成分2.不含任何违禁物量(任何药检制止的的成分)3.仅由最有效的成分以及高剂量有效成分构成,没有混合隐藏成分4.价格实惠,具备性价比,物超所值留意!

如今市道上有太多的补剂含有“填充剂”成分。那些凡是是廉价的物量,除了帮忙填补剂量不敷的配方外,没有其他益处,好比在卵白粉傍边填充麦芽糊精、食用胶、抗结块剂等。

最重要的是,应将那些有效剂量设定在更大有效的剂量且副感化最小的剂量,就咖啡因而言,摄入太多纷歧定老是更好。

参考文献:

1. Oda M, Satta Y, Takenaka O, Takahata N. Loss of urate oxidase activity in hominoids and its evolutionary implications. Mol Biol Evol. 2002;19(5):640–653.

2. Masako Oda, Yoko Satta, Osamu Takenaka, Naoyuki Takahata.Loss of urate oxidase activity in hominoids and its evolutionary implications.Mol Biol Evol. 2002 May;19(5):640-53.

3. Ackerman Z., Oron-Herman M., Grozovski M., Rosenthal T., Pappo O., Link G., and Sela B. A. (2005) Fructose-induced fatty liver disease: hepatic effects of blood pressure and plasma triglyceride reduction. Hypertension 45, 1012–1018.

4. Ishimoto T., Lanaspa M. A., Le M. T., Garcia G. E., Diggle C. P., Maclean P. S., Jackman M. R., Asipu A., Roncal-Jimenez C. A., Kosugi T., Rivard C. J., Maruyama S., Rodriguez-Iturbe B., Sánchez-Lozada L. G., Bonthron D. T., et al. (2012) Opposing effects of fructokinase C and A isoforms on fructose-induced metabolic syndrome in mice. Proc. Natl. Acad. Sci. U.S.A. 109, 4320–4325

5. Lanaspa M. A., Sanchez-Lozada L. G., Choi Y. J., Cicerchi C., Kanbay M., Roncal-Jimenez C. A., Ishimoto T., Li N., Marek G., Duranay M., Schreiner G., Rodriguez-Iturbe B., Nakagawa T., Kang D. H., Sautin Y. Y., et al. (2012) Uric acid induces hepatic steatosis by generation of mitochondrial oxidative stress: potential role in fructose-dependent and -independent fatty liver. J. Biol. Chem. 287, 40732–40744

6. Lanaspa M. A., Cicerchi C., Garcia G., Li N., Roncal-Jimenez C. A., Rivard C. J., Hunter B., Andrés-Hernando A., Ishimoto T., Sánchez-Lozada L. G., Thomas J., Hodges R. S., Mant C. T., and Johnson R. J. (2012) Counteracting roles of AMP deaminase and AMP kinase in the development of fatty liver. PLoS One 7.

7. Tana C., Ticinesi A., Prati B., Nouvenne A., Meschi T. (2018). Uric Acid and Cognitive Function in Older Individuals. Nutrients 10, 97

8. Kimura T., Takahashi M., Yan K., Sakurai H. (2014). Expression of SLC2A9 Isoforms in the Kidney and Their Localization in Polarized Epithelial Cells. PLoS One 9, e84996.

9. Laura G. Sanchez-Lozada1 , Ana Andres-Hernando2 , Fernando E. Garcia-Arroyo1 , Christina Cicerchi2 , Nanxing Li2 , Masanari Kuwabara2 , Carlos A. Roncal-Jimenez2 , Richard J. Johnson2 and Miguel A. Lanaspa 2* . Uric acid

activates aldose reductase and the polyol pathway for endogenous fructose and fat production causing development of fatty liver in rats.JBC Papers in Press. Published on January 16, 2019 as Manuscript RA118.006158.

10. Johnson RJ, Kang DH, Feig D, Kivlighn S, Kanellis J, Watanabe S, et al. Is there a pathogenetic role for uric acid in hypertension and cardiovascular and renal disease? Hypertension. 2003;41(6):1183–1190.

11. Mene P, Punzo G. Uric acid: bystander or culprit in hypertension and progressive renal disease? Journal of Hypertension. 2008;26(11):2085–2092.

12. Khosla UM, Zharikov S, Finch JL, Nakagawa T, Roncal C, Mu W, et al. Hyperuricemia induces endothelial dysfunction. Kidney International. 2005;67(5):1739–1742.

13. Farquharson CA, Butler R, Hill A, Belch JJ, Struthers AD. Allopurinol improves endothelial dysfunction in chronic heart failure. Circulation. 2002;106(2):221–226.

14. Doehner W, Schoene N, Rauchhaus M, Leyva-Leon F, Pavitt DV, Reaveley DA, et al. Effects of xanthine oxidase inhibition with allopurinol on endothelial function and peripheral blood flow in hyperuricemic patients with chronic heart failure: results from 2 placebo-controlled studies. Circulation. 2002;105(22):2619–2624.

15. Toma I, Kan J, Meer E, Pet-Peterdi J. Uric acid triggers renin release via a macula densa-dependent pathway. Presented at: American Society of Nephrology Annual Meeting; San Francisco, CA. 2007. F-P0240.

16. Perlstein TS, Gumieniak O, Hopkins PN, Murphey LJ, Brown NJ, Williams GH, et al. Uric acid and the state of the intrarenal renin-angiotensin system in humans. Kidney International. 2004;66(4):1465–1470.

17. S. E. Kocyigit, P. Soysal, E. Ates Bulut & A. T. Isik.Malnutrition and Malnutrition Risk Can Be Associated with Systolic Orthostatic Hypotension in Older Adults.The journal of nutrition, health & aging volume 22, pages 928–933 (2018).

18. Joel B Gunter.Fasting, halothane, and hypotension.Anesth Analg. 2003 May;96(5):1537-8; author reply 1538.

19. T D Williams 1 , J B Chambers, R P Henderson, M E Rashotte, J M Overton.Cardiovascular responses to caloric restriction and thermoneutrality in C57BL/6J http://mice.Am J Physiol Regul Integr Comp Physiol. 2002 May;282(5):R1459-67.

20. B N Ames, R Cathcart, E Schwiers, and P Hochstein.Uric acid provides an antioxidant defense in humans against oxidant- and radical-caused aging and cancer: a hypothesis.Proc Natl Acad Sci U S A. 1981 Nov; 78(11): 6858–6862.

21. Masako Oda, Yoko Satta, Osamu Takenaka, Naoyuki Takahata.Loss of urate oxidase activity in hominoids and its evolutionary implications.Mol Biol Evol. 2002 May;19(5):640-53.

22. Fatemeh Dabbagh, Mohammad B Ghoshoon, Shiva Hemmati, Mozhdeh Zamani, Milad Mohkam, Younes Ghasemi.Engineering Human Urate Oxidase: Towards Reactivating It as an Important Therapeutic Enzyme.Curr Pharm Biotechnol.2015;17(2):141-6.

23. Jessica Maiuolo, Francesca Oppedisano, Santo Gratteri, Carolina Muscoli, Vincenzo Mollace.Regulation of uric acid metabolism and http://excretion.Int J Cardiol. 2016 Jun 15;213:8-14.

24. Jessica Maiuolo, Gratteri S, Muscoli C, Mollace V.(2016). Regulation of Uric Acid Metabolism and Excretion. Int.J.Cardiol.15,8–14.

25. Nieto C. I. F. J., Gross M. D., Comstock G. W., Cutler R. G. (2000). Uric Acid and Serum Antioxidant Capacity: a Reaction to Atherosclerosis? Atherosclerosis 148, 131–139.

26. Wang Q., Wen X., Kong J. (2020). Recent Progress on Uric Acid Detection: A Review. Crit. Rev. Anal Chem. 50, 359–375.

27. Bassanese G., Wlodkowski T., Servais A., Heidet L., Roccatello D., Emma F., et al. (2021). The European Rare Kidney Disease Registry (ERKReg): Objectives, Design and Initial Results. Orphanet J. Rare Dis. 16, 251.

28. So A., Thorens B. (2010). Uric Acid Transport and Disease. J. Clin. Invest 120, 1791–1799.

29. Bardin T., Richette P. (2014). Definition of Hyperuricemia and Gouty Conditions. Curr. Opin. Rheumatol. 26, 186–191.

30. Latourte, Augustina,b; Bardin, Thomasa,b; Richette, Pascala,b.Uric acid and cognitive decline: a double-edge sword?.Current Opinion in Rheumatology: March 2018 - Volume 30 - Issue 2 - p 183-187.

31. Ebert K., Ludwig M., Geillinger K. E., Schoberth G. C., Essenwanger J., Stolz J., et al. (2017). Reassessment of GLUT7 and GLUT9 as Putative Fructose and Glucose Transporters. J. Membr. Biol. 250, 171–182.

32. Akaoka I, Nishizawa T, Yano E, Takeuchi A, Nishida Y. Familial hypouricaemia due to renal tubular defect of urate transport. Ann Clin Res. 1975;7(5):318–324.

33. Wakasugi M, Kazama JJ, Narita I, Konta T, Fujimoto S, Iseki K, et al. Association between hypouricemia and reduced kidney function: a cross-sectional population-based study in Japan. Am J Nephrol. 2015;41(2):138–146.

34. Suzuki T, Kidoguchi K, Hayashi A. Genetic heterogeneity of familial hypouricemia due to isolated renal tubular defect. Jinrui Idengaku Zasshi. 1981;26(3):243–248.

35. Kikuchi Y., Koga H., Yasutomo Y., Kawabata Y., Shimizu E., Naruse M., Kiyama S., Nonoguchi H., Tomita K., Sasatomi Y. Patients with renal hypouricemia with exercise-induced acute renal failure and chronic renal dysfunction. Clin. Nephrol. 2000;53:467–472.

36. Diamond H.S., Paolino J.S. Evidence for a postsecretory reabsorptive site for uric acid in man. J. Clin. Invest. 1973;52:1491–1499.

37. Hosoyamada M., Ichida K., Enomoto A., Hosoya T., Endou H. (2004). Function and Localization of Urate Transporter 1 in Mouse Kidney. J. Am. Soc. Nephrol. 15, 261–268.

38. Enomoto A., Kimura H., Chairoungdua A., Shigeta Y., Jutabha P., Cha S. H., et al. (2002). Molecular Identification of a Renal Urate Anion Exchanger that Regulates Blood Urate Levels. Nature 417, 447–452.

39. Zhou F., Zhu L., Cui P. H., Church W. B., Murray M. (2010). Functional Characterization of Nonsynonymous Single Nucleotide Polymorphisms in the Human Organic Anion Transporter 4 (hOAT4). Br. J Pharmacol 159, 419–427.

40. Skwara P., Sch?mig E., Gründemann D. (2017). A Novel Mode of Operation of SLC22A11: Membrane Insertion of Estrone Sulfate versus Translocation of Uric Acid and Glutamate. Biochem. Pharmacol. 15, 74–82.

41. Zhu C., Sun Bao., Zhang B., Zhou Z. (2021). An Update of Genetics, Co-morbidities and Management of Hyperuricemia. Clin. Exp. Pharmacol. Physiol.

42. Pasquale Strazzullo, Juan Garcia Puig.Uric acid and oxidative stress: relative impact on cardiovascular risk?.Nutr Metab Cardiovasc Dis. 2007 Jul;17(6):409-14.

43. Mandal A. K., Mount D. B. (2019). Interaction between ITM2B and GLUT9 Links Urate Transport to Neurodegenerative Disorders.

44. Ascherio A., LeWitt P. A., Xu K., Eberly S., Watts A., Matson W. R., et al. (2009). Urate as a Predictor of the Rate of Clinical Decline in Parkinson Disease. Randomized Controlled Trial 66, 1460–1468.

45. Du N., Xu D., Hou X., Song X., Liu C., Chen Y., et al. (2016). Inverse Association between Serum Uric Acid Levels and Alzheimers Disease Risk. Mol. Neurobiol. 53, 2594–2599.

46. Ye B. S., Lee W. W., Ham J. H., Lee J. J., Lee P. H., Sohn Y. H. (2016). Does Serum Uric Acid Act as a Modulator of Cerebrospinal Fluid Alzheimers Disease Biomarker Related Cognitive Decline? Eur. J. Neurol. 23, 948–957.

47. Cunningham R., Brazie M., Kanumuru S., Xiaofei E., Biswas R., Wang F., et al. (2007). Sodium-hydrogen Exchanger Regulatory Factor-1 Interacts with Mouse Urate Transporter 1 to Regulate Renal Proximal Tubule Uric Acid Transport. J. Am. Soc. Nephrol. 18, 1419–1425.

48. Shenolikar S., Voltz J. W., Minkoff C. M., Wade J. B., Weinman E. J. (2002). Targeted Disruption of the Mouse NHERF-1 Gene Promotes Internalization of Proximal Tubule Sodium-Phosphate Cotransporter Type IIa and Renal Phosphate Wasting. Proc. Natl. Acad. Sci. U S A. 99, 11470–11475.

49. Houlihan L. M., Wyatt N. D., Harris S. E., Hayward C., Gow A. J., Marioni R. E., et al. (2010). Variation in the Uric Acid Transporter Gene (SLC2A9) and Memory Performance. Hum. Mol. Genet. 19, 2321–2330.

50. Maliepaard M., Scheffer G. L., Faneyte I. F., van Gastelen M. A., Pijnenborg A. C., Schinkel A. H., et al. (2001). Subcellular Localization and Distribution of the Breast Cancer Resistance Protein Transporter in Normal Human Tissues. Cancer Res. 61, 3458–3464.

51. Yun-Hong Lu Y.-P. C., Li T., Han F., Li C-J., Li X-Y., Xue M., et al. (2020). Empagliflozin Attenuates Hyperuricemia by Upregulation of ABCG2 via AMPK/AKT/CREB Signaling Pathway in Type 2 Diabetic Mice. Int. J. Biol. Sci. 16, 529–542.

52. Matsuo H., Takada T., Ichida K., Nakamura T., Nakayama A., Ikebuchi Y., et al. (2009). Common Defects of ABCG2, a High-Capacity Urate Exporter, Cause Gout: A Function-Based Genetic Analysis in a Japanese Population. Sci. Transl Med. 1, 5ra11.

53. Ichida K., Matsuo H., Takada T., Nakayama A., Murakami K., Shimizu T., et al. (2012). Decreased Extra-renal Urate Excretion Is a Common Cause of Hyperuricemia. Nat. Commun. 3, 764.

54. Yano H., Tamura Y., Kobayashi K., Tanemoto M., Uchida S. (2014). Uric Acid Transporter ABCG2 Is Increased in the Intestine of the 5/6 Nephrectomy Rat Model of Chronic Kidney Disease. Clin. Exp. Nephrol. 18, 50–55.

55. Nigam S. K. (2015). What Do Drug Transporters Really Do? Nat. Rev. Drug Discov. 14, 29–44.

56. Bhatnagar V., Richard E. L., Wu W., Nievergelt C. M., Lipkowitz M. S., Jeff J., et al. (2016). Analysis of ABCG2 and Other Urate Transporters in Uric Acid Homeostasis in Chronic Kidney Disease: Potential Role of Remote Sensing and Signaling. Clin. Kideny J. 9, 444–453.

57. Cleophas M. C., Joosten L. A., Stamp L. K., Dalbeth N., Woodward O. M., Merriman T. R. (2017). ABCG2 Polymorphisms in Gout: Insights into Disease Susceptibility and Treatment Approaches. Pharmgenomics Pers Med. 10, 129–142.

58. Nigam S. K., Bhatnagar V. (2018). The Systems Biology of Uric Acid Transporters: the Role of Remote Sensing and Signaling. Curr. Opin. Nephrol. Hypertens. 27, 305–313.

59. Sorensen L. B. Role of the intestinal tract in the elimination of uric acid. Arthritis Rheum. 8, 694–706 (1965).

60. Sica D. A. & Schoolwerth A. in Brenner and Rectors The Kidney (ed. B.M. Brenner) 645–649 (Saunders, 2004).

61. Enomoto A. et al.. Molecular identification of a renal urate anion exchanger that regulates blood urate levels. Nature 417, 447–452 (2002).

62. Li S. et al.. The GLUT9 gene is associated with serum uric acid levels in Sardinia and Chianti cohorts. PLoS Genet. 3, e194 (2007).

63. D?ring A. et al.. SLC2A9 influences uric acid concentrations with pronounced sex-specific effects. Nat. Genet. 40, 430–436 (2008).

64. Vitart V. et al.. SLC2A9 is a newly identified urate transporter influencing serum urate concentration, urate excretion and gout. Nat. Genet. 40, 437–442 (2008).

65. Anzai N. et al.. Plasma urate level is directly regulated by a voltage-driven urate efflux transporter URATv1 (SLC2A9) in humans. J. Biol. Chem. 283, 26834–26838 (2008).

66. Dehghan A. et al.. Association of three genetic loci with uric acid concentration and risk of gout: a genome-wide association study. Lancet 372, 1953–1961 (2008).

67. Kolz M. et al.. Meta-analysis of 28,141 individuals identifies common variants within five new loci that influence uric acid concentrations. PLoS Genet. 5, e1000504 (2009).

68. Kamatani Y. et al.. Genome-wide association study of hematological and biochemical traits in a Japanese population. Nat. Genet. 42, 210–215 (2010).

69. X. W. Wu, C. C. Lee, D. M. Muzny, C. T. Caskey, Urate oxidase: Primary structure and evolutionary implications. Proc. Natl. Acad. Sci. U.S.A. 86, 9412–9416 (1989).

70. C. C. Lee, X. W. Wu, R. A. Gibbs, R. G. Cook, D. M. Muzny, C. T. Caskey, Generation of cDNA probes directed by amino acid sequence: Cloning of urate oxidase. Science 239, 1288–1291 (1988).

71. R. G. Cutler, Urate and ascorbate: Their possible roles as antioxidants in determining longevity of mammalian species. Arch. Gerontol. Geriatr. 3, 321–348 (1984).

72. Robinson PC. Gout-an update of aetiology, genetics, co-morbidities and management. Maturitas. 2018;118:67–73.

73. Wang H, Zhang H, Sun L, Guo W. Roles of hyperuricemia in metabolic syndrome and cardiac-kidney-vascular system diseases. Am J Transl Res. 2018;10:2749–2763.

74. Roddy E, Choi HK. Epidemiology of gout. Rheum Dis Clin North Am. 2014;40:155–175.

75. Ni Q, Lu X, Chen C, Du H, Zhang R. Risk factors for the development of hyperuricemia: a STROBE-compliant cross-sectional and longitudinal study. Medicine (Baltimore) 2019;98:e17597.

76. Chaudhary NS, Bridges SL Jr, Saag KG, Rahn EJ, Curtis JR, Gaffo A, Limdi NA, Levitan EB, Singh JA, Colantonio LD, Howard G, Cushman M, Flaherty ML, Judd S, Irvin MR, Reynolds RJ. Severity of hypertension mediates the association of hyperuricemia with stroke in the REGARDS case cohort study. Hypertension. 2020;75:246–256.

77. Steiger S, Ma Q, Anders HJ. The case for evidence-based medicine for the association between hyperuricaemia and CKD. Nat Rev Nephrol. 2020;16:422.

78. Sato Y, Feig DI, Stack AG, Kang DH, Lanaspa MA, Ejaz AA, Sanchez-Lozada LG, Kuwabara M, Borghi C, Johnson RJ. The case for uric acid-lowering treatment in patients with hyperuricaemia and CKD. Nat Rev Nephrol. 2019;15:767–775.

79. Terkeltaub RA. Clinical practice. Gout. N Engl J Med. 2003;349:1647–1655.

80. Becker MA, Jolly M. In: Arthritis and Allied Conditions. 15. Koopman WJ, Moreland LW, editor. Philadelphia: Lippincott, Williams & Wilkins; 2005. Clinical gout and the pathogenesis of hyperuricemia; pp. 2303–2339.

81. Wyngaarden JB, Kelley WN. Gout and Hyperuricemia. New York: Grune & Stratton; 1976. pp. 1–512.

82. Li T, Walsh JR, Ghishan FK, Bai L. Molecular cloning and characterization of a human urate transporter (hURAT1) gene promoter. Biochim Biophys Acta 2004; 1681:53–58.

83. Fellstrom B., Danielson B.G., Karlstrom B., Lithell H., Ljunghall S., Vessby B. The influence of a high dietary intake of purine-rich animal protein on urinary urate excretion and supersaturation in renal stone disease. Clin. Sci. 1983;64:399–405.

84. Dalbeth N., Merriman T.R., Stamp L.K. Gout. Lancet. 2016;388:2039–2052.

85. Perez-Ruiz F., Calabozo M., Erauskin G.G., Ruibal A., Herrero-Beites A.M. Renal underexcretion of uric acid is present in patients with apparent high urinary uric acid output. Arthritis Rheum. 2002;47:610–613.

86. Qiong Yang, Chao-Yu Guo, L Adrienne Cupples, Daniel Levy, Peter W F Wilson, Caroline S Fox.Genome-wide search for genes affecting serum uric acid levels: the Framingham Heart Study.Metabolism. 2005 Nov;54(11):1435-41.

87. Juan García Puig 1 , María Angeles Martínez.Hyperuricemia, gout and the metabolic syndrome.Curr Opin Rheumatol. 2008 Mar;20(2):187-91.

88. Veronique Vitart et al.SLC2A9 is a newly identified urate transporter influencing serum urate concentration, urate excretion and gout.Nat Genet. 2008 Apr;40(4):437-42.

89. Adrienne Tin.et al.Target genes, variants, tissues and transcriptional pathways influencing human serum urate levels.Nat Genet. 2019 Oct; 51(10): 1459–1474.

90. US Department of Health and Human Services. Physical Activity and Health: A Report of the Surgeon General. DIANE Publishing; 1996.

91. Katzmarzyk P, Janssen I, Ardern C. Physical inactivity, excess adiposity and premature mortality. Obesity Rev. 2003;4(4):257–290.

92. Chau JY, Grunseit AC, Chey T, et al. Daily sitting time and all-cause mortality: a meta-analysis. PLoS One. 2013;8(11):e80000.

93. Thyfault JP, Du M, Kraus WE, et al. Physiology of sedentary behavior and its relationship to health outcomes. Med Sci Sports Exerc. 2015;47(6):1301.

94. Yuan H, Yu C, Li X, et al. Serum uric acid levels and risk of metabolic syndrome: a dose-response meta-analysis of prospective studies. J Clin Endocrinol Metab. 2015;100(11):4198–4207.

95. Facchini F, Chen Y-DI, Hollenbeck CB, Reaven GM. Relationship between resistance to insulin-mediated glucose uptake, urinary uric acid clearance, and plasma uric acid concentration. Jama. 1991;266(21):3008–3011.

96. Katzmarzyk P, Janssen I, Ardern C. Physical inactivity, excess adiposity and premature mortality. Obesity Rev. 2003;4(4):257–290.

97. Chau JY, Grunseit AC, Chey T, et al. Daily sitting time and all-cause mortality: a meta-analysis. PLoS One. 2013;8(11):e80000.

98. Bouchard C, Blair SN, Katzmarzyk PT, et al. Less sitting, more physical activity, or higher fitness? Mayo Clinic Proc. 2015. Elsevier. doi:10.1016/j.mayocp. 2015;90(11):1533–1540

99. Wannamethee SG, Shaper AG, Alberti KGM. Physical activity, metabolic factors, and the incidence of coronary heart disease and type 2 diabetes. Arch Intern Med. 2000;160(14):2108–2116.

100. Bey L, Hamilton MT. Suppression of skeletal muscle lipoprotein lipase activity during physical inactivity: a molecular reason to maintain daily low‐intensity activity. J Physiol. 2003;551(2):673–682.

101. Hamilton TM, Hamilton GD, Zderic WT. Exercise physiology versus inactivity physiology: an essential concept for understanding lipoprotein lipase regulation. Exerc Sport Sci Rev. 2004;32(4):161–166.

102. Hu FB, Leitzmann MF, Stampfer MJ, et al. Physical activity and television watching in relation to risk for type 2 diabetes mellitus in men. (Original Investigation). Arch Internal Med. 2001;161(12):1542.

103. Hu F, Li T, Colditz G, Willett W, Manson JE. Television watching and other sedentary behaviors in relation to risk of obesity and type 2 diabetes mellitus in women. JAMA. 2003;289(14):1785–1791.

104. Lee I.R., Yang L., Sebetso G., Allen R., Doan T.H., Blundell R., Lui E.Y., Morrow C.A., Fraser J.A. Characterization of the complete uric acid degradation pathway in the fungal pathogen Cryptococcus neoformans. PLoS ONE. 2013;8:e64292.

105. Shulten P, Thomas J, Miller M, Smith M, Ahern M. The role of diet in the management of gout: a comparison of knowledge and attitudes to current evidence. J Hum Nutr Diet. 2009;22:3–11.

106. Winnard D, Wright C, Taylor WJ, Jackson G, Te Karu L, Arroll B, et al. National prevalence of gout derived from administrative health data in Aotearoa New Zealand. Rheumatology (Oxford) 2012;51:901–909.

107. Lee C-YJ, Isaac HB, Huang SH, Long LH, Wang H, Gruber J, et al. Limited antioxidant effect after consumption of a single dose of tomato sauce by young males, despite a rise in plasma lycopene. Free Radic Res. 2009;43:622–628.

108. Johnson RJ, Nakagawa T, Sanchez-Lozada LG, Lanaspa MA, Tamura Y, Tanabe K, et al. Umami: the taste that drives purine intake. J Rheumatol. 2013;40:1794–1796.

109. Raivio KO, Seegmiller JE. Role of glutamine in purine synthesis and in guanine nucleotide formation in normal fibroblasts and in fibroblasts deficient in hypoxanthine phosphoribosyltransferase activity. Biochim Biophysic Acta. 1973;299:283–292.

110. Tanya J Flynn, Murray Cadzow, Nicola Dalbeth, Peter B Jones, Lisa K Stamp, Jennie Harré Hindmarsh, Alwyn S Todd, Robert J Walker, Ruth Topless, and Tony R Merrimancorresponding author.Positive association of tomato consumption with serum urate: support for tomato consumption as an anecdotal trigger of gout flares.BMC Musculoskelet Disord. 2015; 16: 196.

111. Maersk M., Belza A., Stødkilde-Jorgensen H., Ringgaard S., Chabanova E., Thomsen H., Pedersen S. B., Astrup A., and Richelsen B. (2012) Sucrose-sweetened beverages increase fat storage in the liver, muscle, and visceral fat depot: a 6-mo randomized intervention study. Am. J. Clin. Nutr. 95, 283–289

112. Ackerman Z., Oron-Herman M., Grozovski M., Rosenthal T., Pappo O., Link G., and Sela B. A. (2005) Fructose-induced fatty liver disease: hepatic effects of blood pressure and plasma triglyceride reduction. Hypertension 45, 1012–1018 10.1161/01.HYP.

113. Ishimoto T., Lanaspa M. A., Le M. T., Garcia G. E., Diggle C. P., Maclean P. S., Jackman M. R., Asipu A., Roncal-Jimenez C. A., Kosugi T., Rivard C. J., Maruyama S., Rodriguez-Iturbe B., Sánchez-Lozada L. G., Bonthron D. T., et al. (2012) Opposing effects of fructokinase C and A isoforms on fructose-induced metabolic syndrome in mice. Proc. Natl. Acad. Sci. U.S.A. 109, 4320–4325.

114. Lanaspa M. A., Ishimoto T., Li N., Cicerchi C., Orlicky D. J., Ruzycki P., Rivard C., Inaba S., Roncal-Jimenez C. A., Bales E. S., Diggle C. P., Asipu A., Petrash J. M., Kosugi T., Maruyama S., et al. (2013) Endogenous fructose production and metabolism in the liver contributes to the development of metabolic syndrome. Nat. Commun. 4, 2434

115. Lanaspa M. A., Kuwabara M., Andres-Hernando A., Li N., Cicerchi C., Jensen T., Orlicky D. J., Roncal-Jimenez C. A., Ishimoto T., Nakagawa T., Rodriguez-Iturbe B., MacLean P. S., and Johnson R. J. (2018) High salt intake causes leptin resistance and obesity in mice by stimulating endogenous fructose production and metabolism. Proc. Natl. Acad. Sci. U.S.A. 115, 3138–3143

116. Na K. Y., Woo S. K., Lee S. D., and Kwon H. M. (2003) Silencing of TonEBP/NFAT5 transcriptional activator by RNA interference. J. Am. Soc. Nephrol. 14, 283–288.

117. Woo S. K., Lee S. D., and Kwon H. M. (2002) TonEBP transcriptional activator in the cellular response to increased osmolality. Pflugers Arch. 444, 579–585

118. Lanaspa M. A., Sanchez-Lozada L. G., Cicerchi C., Li N., Roncal-Jimenez C. A., Ishimoto T., Le M., Garcia G. E., Thomas J. B., Rivard C. J., Andres-Hernando A., Hunter B., Schreiner G., Rodriguez-Iturbe B., Sautin Y. Y. et al. (2012) Uric acid stimulates fructokinase and accelerates fructose metabolism in the development of fatty liver. PLoS One 7, e47948

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