跳到主要內容

臺灣博碩士論文加值系統

(18.97.14.83) 您好!臺灣時間:2025/01/25 16:25
字體大小: 字級放大   字級縮小   預設字形  
回查詢結果 :::

詳目顯示

: 
twitterline
研究生:顏琦恩
研究生(外文):Chi-En Yen
論文名稱:在標準抗糖尿病治療外,腎素-血管收縮素系統抑製劑可增進第二型糖尿病患者的血糖控制:一項前瞻性世代研究
論文名稱(外文):Renin–angiotensin system inhibitors in addition to standard glucose-lowering therapy enhance glycemic control in patients with type 2 diabetes mellitus: A prospective cohort study
指導教授:周明智周明智引用關係
指導教授(外文):Ming-Chin Chou
口試委員:顏旭亨林志立
口試日期:2023-06-29
學位類別:碩士
校院名稱:中山醫學大學
系所名稱:醫學研究所
學門:醫藥衛生學門
學類:醫學學類
論文種類:學術論文
論文出版年:2023
畢業學年度:111
語文別:中文
論文頁數:32
中文關鍵詞:第二型糖尿病腎素-血管收縮素系統葡萄糖代謝血壓管理
外文關鍵詞:Type 2 diabetes mellitusrenin-angiotensin systemglucose metabolismblood pressure management
DOI:10.6834/csmu202300159
相關次數:
  • 被引用被引用:0
  • 點閱點閱:64
  • 評分評分:
  • 下載下載:10
  • 收藏至我的研究室書目清單書目收藏:0
研究背景:第二型糖尿病 (T2DM) 是一種進展性的代謝疾病,其中有相當多的糖尿病患儘管服用降糖藥物仍無法維持血糖目標。腎素-血管收縮素系統(RAS)被認為與胰島素阻抗的發展有關,之前的研究也顯示腎素-血管收縮素系統(RAS)抑制可能會改善葡萄糖代謝。

研究目的:在標準降糖治療的基礎上添加腎素-血管收縮素系統(RAS)抑制劑可能改善第二型糖尿病 (T2DM) 病患者的血糖控制

研究方法:這項前瞻性世代研究調查了將腎素-血管收縮素系統(RAS)抑製劑Valsartan添加入標準降糖治療中對糖尿病患者血糖控制、血壓和血脂的影響。
收案標準是在研究收案時接受Metformin治療的第二型糖尿病(T2DM)成年人。對照組在無降壓藥物的情況下繼續接受Metformin治療,而實驗組在接受Metformin治療的基礎上額外服用80毫克的Valsartan。

研究結果:這項研究招募了203名患有第二型糖尿病(T2DM)的受試者,透過共同決策方式將他們分配到不同的治療組。在治療了24週後,接受額外Valsartan治療的受試者顯示出較低的平均糖化血色素(HbA1c)水平(6.22% vs 6.77%,P < 0.001),收縮壓(123 mm Hg vs 131 mm Hg,P < 0.001),舒張壓(73.6 mm Hg vs 77.4 mm Hg,P = 0.009),以及降低的低密度脂蛋白膽固醇水平(81 mg/dL vs 91.3 mg/dL,P = 0.0024),相較於接受Metformin單一療法的受試者。

研究限制:本研究為非隨機設計,可能會導致臨床結果的潛在偏差[13]。此外,觀察時間為24周可能不能代表長期結果,而且腎素-血管收縮素系統(RAS)抑制對血糖控制的有效性可能需要進一步研究,並具有更長的觀察時間。並且,飲食和生活習慣在血糖控制中起了重要的作用,所以兩組之間觀察到的血清糖化血色素(HbA1c)差異可能不僅僅是由於腎素-血管收縮素系統(RAS)抑制所引起的。

研究結論:第二型糖尿病患者合併有高血壓,使用Metformin 藥物治療無法達到適當的血糖控制,腎素-血管收縮素系統(RAS)抑制劑會是可行的選擇。


Background
Type 2 diabetes mellitus (T2DM) is a progressive metabolic disorder in which a considerable number of affected patients cannot maintain glycemic goals despite glucose-lowering medications. The renin-angiotensin system (RAS) has been implicated in the development of insulin resistance, and preceding studies suggest that RAS inhibition may improve glucose metabolism.

Objective
The investigators hypothesized that the addition of RAS inhibitors to standard glucose-lowering therapy may improve glycemic control in patients with T2DM.

Methods
This prospective study investigates the effect of adding the RAS inhibitor Valsartan to standard glucose-lowering therapy on glycemic control, blood pressure, and plasma lipid profile in diabetic patients. Inclusion criteria were adults with T2DM who were receiving metformin therapy at study enrolment. The control group continued metformin therapy without antihypertensive drug, whereas the experimental group received 80 milligrams of Valsartan in addition to metformin therapy.

Results
The study enrolled 203 participants with T2DM who were assigned to the treatment groups by shared decision making. After 24 weeks of therapy, participants receiving additional Valsartan demonstrated lower mean serum glycosylated hemoglobin A1c (HbA1c) (6.22% vs. 6.77%, P < 0.001), systolic blood pressure (123 mm Hg vs. 131 mm Hg, P < 0.001), diastolic blood pressure (73.6 mg Hg vs. 77.4 mm Hg, P = 0.009), and reduced low-density lipoprotein cholesterol levels (81 mg/dL vs. 91.3 mg/dL, P = 0.0024) compared to recipients of metformin monotherapy.

Limitations
The non-randomized design can lead to potential bias in the clinical findings[13]. Furthermore, the observation time of 24 weeks may not be representative of long-term outcomes, and the efficacy of RAS inhibition on glycemic control may require future studies with a longer observation time. Furthermore, dietary habits play an essential role in glycemic control, and the observed difference in serum HbA1c between treatment cohorts may not arise solely from RAS inhibition.

Conclusion
RAS inhibition may be a feasible option for diabetic patients with concomitant hypertension who are inadequately controlled with pharmacologic regimens involving metformin.
謝 誌 (致謝) --------------------------------------------------------------------- I
中文摘要-------------------------------------------------------------------------- II
英文摘要------------------------------------------------------------------------- IV
英文縮寫全名與中英文對照表---------------------------------------------- VI
表目錄---------------------------------------------------------------------------- IX
圖目錄----------------------------------------------------------------------------- X
第一章 緒論-----------------------------------------------------------------------1
第一節 研究背景與動機-------------------------------------------------- 3
第二節 研究目的----------------------------------------------------------- 5
第二章 文獻探討
第一節 糖尿病與併發症-------------------------------------------------- 6
第二節 糖尿病與腎素-血管收縮素系統(RAS)之間的關聯----- 7
第三節 腎素-血管收縮素系統(RAS)作用機轉--------------------- 8
第四節 腎素-血管收縮素系統(RAS)機轉與血糖的關聯性------ 10
第三章 研究設計
第一節 受試者選擇-------------------------------------------------------11
第二節 研究方案----------------------------------------------------------12
第三節 結果分析----------------------------------------------------------13
第四節 倫理聲明----------------------------------------------------------14
第五節 統計分析----------------------------------------------------------15
第四章 研究結果----------------------------------------------------------------16
第五章 討論--------------------------------------------------------------------- 18
第六章 研究限制--------------------------------------------------------------- 21
第七章 結論與建議------------------------------------------------------------ 22
參考文獻-------------------------------------------------------------------------- 23


表目錄

表格1 參加研究的參與者的基準特徵------------------------------------ 26
表格2 藥物治療24週後臨床參數的變化-------------------------------- 27
表格3 治療24週後達到血糖目標的勝算比----------------------------- 28


圖目錄

圖一 腎素-血管收縮素系統機轉------------------------------------------- 29
圖二 與腎素-血管收縮素系統相關有利於降血糖的機轉------------- 30
圖三 研究流程圖--------------------------------------------------------------- 31
圖四 腎素-血管收縮素系統抑制與血清糖化血紅蛋白水平相互作用的敏感性分析----------------------------------------------------------- 32
1. Khan MAB, Hashim MJ, King JK, Govender RD, Mustafa H, Al Kaabi J. Epidemiology of Type 2 Diabetes - Global Burden of Disease and Forecasted Trends. J Epidemiol Glob Health. 2020 Mar;10(1):107-111. doi: 10.2991/jegh.k.191028.001. PMID: 32175717; PMCID: PMC7310804
2. Cade WT. Diabetes-related microvascular and macrovascular diseases in the physical therapy setting. Phys Ther. 2008 Nov;88(11):1322-35. doi: 10.2522/ptj.20080008. Epub 2008 Sep 18. PMID: 18801863; PMCID: PMC2579903.
3. Davies MJ, D'Alessio DA, Fradkin J, Kernan WN, Mathieu C, Mingrone G, Rossing P, Tsapas A, Wexler DJ, Buse JB. Management of Hyperglycemia in Type 2 Diabetes, 2018. A Consensus Report by the American Diabetes Association (ADA) and the European Association for the Study of Diabetes (EASD). Diabetes Care. 2018 Dec;41(12):2669-2701. doi: 10.2337/dci18-0033. Epub 2018 Oct 4. PMID: 30291106; PMCID: PMC6245208.
4. Remedi MS, Emfinger C. Pancreatic β-cell identity in diabetes. Diabetes Obes Metab. 2016 Sep;18 Suppl 1(Suppl 1):110-6. doi: 10.1111/dom.12727. PMID: 27615139; PMCID: PMC5021188.
5. Nurun Nabi, A. H. M., & Ebihara, A. (2021). Diabetes and Renin-Angiotensin-Aldosterone System: Pathophysiology and Genetics. Renin-Angiotensin Aldosterone System. doi: 10.5772/intechopen.97518
6. Underwood PC, Adler GK. The renin angiotensin aldosterone system and insulin resistance in humans. Curr Hypertens Rep. 2013 Feb;15(1):59-70. doi: 10.1007/s11906-012-0323-2. PMID: 23242734; PMCID: PMC3551270.
7. Zorov DB, Juhaszova M, Sollott SJ. Mitochondrial reactive oxygen species (ROS) and ROS-induced ROS release. Physiol Rev. 2014 Jul;94(3):909-50. doi: 10.1152/physrev.00026.2013. PMID: 24987008; PMCID: PMC4101632.
8. Liemburg-Apers DC, Willems PH, Koopman WJ, Grefte S. Interactions between mitochondrial reactive oxygen species and cellular glucose metabolism. Arch Toxicol. 2015 Aug;89(8):1209-26. doi: 10.1007/s00204-015-1520-y. Epub 2015 Jun 6. PMID: 26047665; PMCID: PMC4508370.
9. Rattigan S, Clark MG, Barrett EJ. Acute vasoconstriction-induced insulin resistance in rat muscle in vivo. Diabetes. 1999 Mar;48(3):564-9. doi: 10.2337/diabetes.48.3.564. PMID: 10078557.
10. Ziyyat A, Ramdani N, Bouanani Nel H, Vanderpas J, Hassani B, Boutayeb A, Aziz M, Mekhfi H, Bnouham M, Legssyer A. Epidemiology of hypertension and its relationship with type 2 diabetes and obesity in eastern Morocco. Springerplus. 2014 Oct 30;3:644. doi: 10.1186/2193-1801-3-644. PMID: 25392811; PMCID: PMC4226801.
11. Jandeleit-Dahm KA, Tikellis C, Reid CM, Johnston CI, Cooper ME. Why blockade of the renin-angiotensin system reduces the incidence of new-onset diabetes. J Hypertens. 2005 Mar;23(3):463-73. doi: 10.1097/01.hjh.0000160198.05416.72. PMID: 15716683.
12. Ruilope LM, Solini A. RAS blockade for every diabetic patient: pro and con. Diabetes Care. 2011 May;34 Suppl 2(Suppl 2):S320-4. doi: 10.2337/dc11-s248. PMID: 21525476; PMCID: PMC3632200.
13. Phillips MR, Kaiser P, Thabane L, Bhandari M, Chaudhary V; Retina Evidence Trials InterNational Alliance (R.E.T.I.N.A.) Study Group. Risk of bias: why measure it, and how? Eye (Lond). 2022 Feb;36(2):346-348. doi: 10.1038/s41433-021-01759-9. Epub 2021 Sep 30. Erratum in: Eye (Lond). 2022 Jan 19;: PMID: 34594009; PMCID: PMC8807607.
14. Federation ID. IDF Diabetes Atlas, 10th edn. Brussels, Belgium; 2021
15. Nurun Nabi AHM and Ebihara A (2021) Diabetes and Renin-Angiotensin-Aldosterone System: Pathophysiology and Genetics. Renin-Angiotensin Aldosterone System. IntechOpen. DOI: 10.5772/intechopen.97518.
16. Perkins JM, Davis SN. The renin-angiotensin-aldosterone system: a pivotal role in insulin sensitivity and glycemic control. Curr Opin Endocrinol Diabetes Obes. 2008 Apr;15(2):147-52. doi: 10.1097/MED.0b013e3282f7026f. PMID: 18316950.
17. Jandeleit-Dahm KA, Tikellis C, Reid CM, Johnston CI, Cooper ME. Why blockade of the renin-angiotensin system reduces the incidence of new-onset diabetes. J Hypertens. 2005 Mar;23(3):463-73. doi: 10.1097/01.hjh.0000160198.05416.72. PMID: 15716683.
18. Gress TW, Nieto FJ, Shahar E, Wofford MR, Brancati FL. Hypertension and antihypertensive therapy as risk factors for type 2 diabetes mellitus. Atherosclerosis Risk in Communities Study. N Engl J Med 2000; 342:905–912.
19. Underwood PC, Adler GK. The renin angiotensin aldosterone system and insulin resistance in humans. Curr Hypertens Rep. 2013 Feb;15(1):59-70. doi: 10.1007/s11906-012-0323-2. PMID: 23242734; PMCID: PMC3551270.
20. Kahn SE, Hull RL, Utzschneider KM. Mechanisms linking obesity to insulin resistance and type 2
diabetes. Nature. 2006; 444:840–6. [PubMed: 17167471]
21. Skwiersky S, Iwuala S, Chillumuntala S, et al. (2021) Renin Angiotensin Aldosterone System, Glucose Homeostasis, and Prevention of Type 2 Diabetes: Mechanistic Insights and Evidence from Major Clinical Trials. Renin-Angiotensin Aldosterone System. IntechOpen. DOI: 10.5772/intechopen.97737.

連結至畢業學校之論文網頁點我開啟連結
註: 此連結為研究生畢業學校所提供,不一定有電子全文可供下載,若連結有誤,請點選上方之〝勘誤回報〞功能,我們會盡快修正,謝謝!
QRCODE
 
 
 
 
 
                                                                                                                                                                                                                                                                                                                                                                                                               
第一頁 上一頁 下一頁 最後一頁 top