FGF-21、CVAI在2型糖尿病肾病中的研究进展
Research Progress of FGF-21 and CVAI in Type 2 Diabetic Kidney Disease
DOI: 10.12677/ACM.2023.1371690, PDF,   
作者: 才巴央宗：青海大学研究生院，青海 西宁；张惠莉*：青海大学附属医院内分泌与代谢科，青海 西宁
关键词: FGF-21；CVAI；2型糖尿病；糖尿病肾病；胰岛素抵抗；FGF-21； CVAI； Type 2 Diabetes Mellitus； Diabetic Kidney Disease； Nephropathy Insulin Resistance
摘要: 2型糖尿病是一种异质病因的病理学，其特征是存在胰岛素抵抗、胰岛素分泌不足或两者兼而有之导致的高血糖，预计到2030年全球糖尿病患者人数约为4.39亿。糖尿病的延长与微血管有关，尤其是糖尿病肾病(DKD)。DKD是2型糖尿病最常见的并发症，是全球终末期肾病的主要原因。成纤维细胞生长因子21 (Fibroblast growth factor 21, FGF-21)是一种内分泌因子，参与机体物质代谢、维持脂肪和糖代谢的平衡。近年来研究发现FGF-21在糖尿病肾病(DKD)患者中呈异常高表达，且对DKD有较高的诊断价值。腹型肥胖被认为是心脏疾病、代谢疾病、糖尿病、和糖尿病并发症的重要危险因素之一。最近一项新的调查研究提示在中国成人糖尿病患者中，内脏脂肪指数(VAI)和中国人内脏脂肪指数(CVAI)与肾病的发生独立相关。本文对FGF-21、CVAI与糖尿病肾病相关性进行综述。
Abstract: Type 2 diabetes mellitus, a heteroetiological pathology characterized by hyperglycemia due to insu-lin resistance, inadequate insulin production, or both, is estimated to affect 439 million people worldwide by 2030. Prolongation of diabetes is associated with microvessels, especially diabetic kidney disease (DKD). DKD is the most common complication of type 2 diabetes and the leading cause of end-stage renal disease worldwide. Fibroblast growth factor 21 (Fibroblast growth factor 21, FGF-21) is a kind of endocrine factor, involved in the body’s metabolism, maintaining the bal-ance of metabolism of fat and sugar. Recent studies have found that FGF-21 is abnormally highly expressed in patients with diabetic kidney disease (DKD), and has high diagnostic value for DKD. Abdominal obesity is considered to be an important risk factor for heart disease, metabolic disease, diabetes, and diabetes complications. A new study suggests that visceral fat index (VAI) and Chinese visceral fat index (CVAI) are independently associated with the development of kidney disease in Chinese adults with diabetes. This paper reviews the correlation between FGF-21, CVAI and diabetic nephropathy.
文章引用：才巴央宗, 张惠莉. FGF-21、CVAI在2型糖尿病肾病中的研究进展[J]. 临床医学进展, 2023, 13(7): 12056-12061. https://doi.org/10.12677/ACM.2023.1371690

参考文献

[1] Alicic, R.Z., Rooney, M.T. and Tuttle, K.R. (2017) Diabetic Kidney Disease: Challenges, Progress, and Possibilities. Clinical Journal of the American Society of Nephrology, 12, 2032-2045. [Google Scholar] [CrossRef] 
[2] Gregg, E.W., Li, Y., Wang, J., Burrows, N.R., Ali, M.K., Rolka, D., et al. (2014) Changes in Diabetes-Related Complications in the United States, 1990-2010. The New England Journal of Medicine, 370, 1514-1523. [Google Scholar] [CrossRef] 
[3] Thomas, M.C., Brownlee, M., Susztak, K., Sharma, K., Jande-leitDahm, K.A., Zoungas, S., et al. (2015) Diabetic Kidney Disease. Nature Reviews Disease Primers, 1, Article No. 15018. [Google Scholar] [CrossRef] [PubMed]
[4] Anders, H.J., Huber, T.B., Isermann, B. and Schiffer, M. (2018) CKD in Diabetes: Diabetic Kidney Disease versus Nondiabetic Kidney Disease. Nature Reviews Nephrology, 14, 361-377. [Google Scholar] [CrossRef] [PubMed]
[5] Diabetes Control and Complications Trial Research Group, Nathan, D.M., Genuth, S., Lachin, J., Cleary, P., Crofford, O., et al. (1993) The Effect of Intensive Treatment of Diabetes on the Development and Progression of Long-Term Complications in Insulin-Dependent Diabetes Mellitus. The New England Journal of Medicine, 329, 977-986. [Google Scholar] [CrossRef] 
[6] American Diabetes Association (2018) 6. Glycemic Targets: Standards of Medical Care in Diabetes—2018. Diabetes Care, 41, S55-S64. [Google Scholar] [CrossRef] 
[7] ADV ANCE Collaborative Group, Patel, A., MacMahon, S., Chalmers, J., Neal, B., Billot, L., et al. (2008) Intensive Blood Glucose Control and Vascular Outcomes in Patients with Type 2 Dia-betes. The New England Journal of Medicine, 358, 2560-2572. [Google Scholar] [CrossRef] 
[8] Ismail-Beigi, F., Craven, T., Banerji, M.A., Basile, J., Calles, J., Cohen, R.M., et al. (2010) Effect of Intensive Treatment of Hyperglycaemia on Microvascular Outcomes in Type 2 Dia-betes: An Analysis of the ACCORD Randomised Trial. The Lancet, 376, 419-430. [Google Scholar] [CrossRef] 
[9] Tamborlane, W.V., Puklin, J.E., Bergman, M., Verdonk, C., Rudolf, M.C., Felig, P., et al. (1982) Long-Term Improvement of Metabolic Control with the Insulin Pump Does Not Reverse Diabetic Microangiopathy. Diabetes Care, 5, 58-64.
[10] Caramori, M.L., Fioretto, P. and Mauer, M. (2003) Low Glomerular Filtrationrate in Normoalbuminuric Type 1 Diabetic Patients: An Indicator of More Advanced Glomer-ular Lesions. Diabetes, 52, 1036-1040. [Google Scholar] [CrossRef] [PubMed]
[11] Lin, L., Tan, W., Pan, X., Tian, E., Wu, Z. and Yang, J. (2022) Metabolic Syndrome-Related Kidney Injury: A Review and Update. Frontiers in Endocrinology (Lausanne), 13, Article ID: 904001. [Google Scholar] [CrossRef] [PubMed]
[12] Lin, Y.C., Chang, Y.H., Yang, S.Y., Wu, K.D. and Chu, T.S. (2018) Update of Pathophysiology and Management of Diabetic Kidney Disease. Journal of the Formosan Medical As-sociation, 117, 662-675. [Google Scholar] [CrossRef] [PubMed]
[13] Sharma, D., Bhattacharya, P., Kalia, K. and Tiwari, V. (2017) Dia-betic Nephropathy: New Insights into Established Therapeutic Paradigms and Novel Molecular Targets. Diabetes Re-search and Clinical Practice, 128, 91-108. [Google Scholar] [CrossRef] [PubMed]
[14] Warren, A.M., Knudsen, S.T. and Cooper, M.E. (2019) Diabetic Nephropathy: An Insight into Molecular Mechanisms and Emerging Therapies. Expert Opinion on Therapeutic Targets, 23, 579-591. [Google Scholar] [CrossRef] [PubMed]
[15] Chow, F., Ozols, E., Nikolic-Paterson, D.J., Atkins, R.C. and Tesch, G.H. (2004) Macrophages in Mouse Type 2 Diabetic Nephropathy: Correlation with Diabetic State and Pro-gressive Renal Injury. Kidney International, 65, 116-128. [Google Scholar] [CrossRef] [PubMed]
[16] Shahzad, K., Bock, F., Dong, W., Wang, H., Kopf, S., Kohli, S., et al. (2015) Nlrp3-Inflammasome Activation in Non-Myeloid-Derived Cells Aggravates Diabetic Nephropa-thy. Kidney International, 87, 74-84. [Google Scholar] [CrossRef] [PubMed]
[17] Honda, T., Hirakawa, Y. and Nangaku, M. (2019) The Role of Oxidative Stress and Hypoxia in Renal Disease. Kidney Research and Clinical Practice, 38, 414-426. [Google Scholar] [CrossRef] [PubMed]
[18] Verma, S., Singh, P., Khurana, S., Ganguly, N.K., Kukreti, R., Saso, L., et al. (2021) Implications of Oxidative Stress in Chronic Kidney Disease: A Review on Current Concepts and Therapies. Kidney Research and Clinical Practice, 40, 183-193. [Google Scholar] [CrossRef] [PubMed]
[19] Sasaki, S. and Inoguchi, T. (2012) The Role of Oxidative Stress in the Pathogenesis of Diabetic Vascular Complications. Diabetes & Metabolism Journal, 36, 255-261. [Google Scholar] [CrossRef] [PubMed]
[20] Goligorsky, M.S., Chen, J. and Brodsky, S. (2001) Workshop: Endothelial Cell Dysfunction Leading to Diabetic Nephropathy: Focus on Nitric Oxide. Hypertension, 37, 744-748. [Google Scholar] [CrossRef] 
[21] 黄丽君, 占志平, 张琳静, 熊小琴, 童俊, 童惠. 血清FGF-21、FGF-23在糖尿病肾病中的表达及其临床意义[J]. 标记免疫分析与临床, 2020, 27(4): 598-602.
[22] Wu, Z., Yu, S., Kang, X., Liu, Y., Xu, Z., Li, Z., Wang, J., Miao, X., Liu, X., Li, X., Zhang, J., Wang, W., Tao, L. and Guo, X. (2022) Association of Visceral Adiposity Index with Incident Nephropathy and Retinopathy: A Cohort Study in the Diabetic Population. Cardiovascular Diabetology, 21, Article No. 32. [Google Scholar] [CrossRef] [PubMed]
[23] Potthoff, M.J., Inagaki, T., et al. (2009) FGF21 Induces PGC-1alpha and Regulates Carbohydrate and Fatty Acid Metabolism during the Adaptive Starvation Response. Pro-ceedings of the National Academy of Sciences of the United States of America, 106, 10853-10858. [Google Scholar] [CrossRef] [PubMed]
[24] 崔洪臣. 氧化应激与糖尿病肾病[J]. 临床内科杂志, 2015, 32(1): 65-66.
[25] Inoguchi, T., Li, P., Umeda, F., Yu, H.Y., Kakimoto, M., Imamura, M., Aoki, T., et al. (2000) High Glu-cose Level and Free Fatty Acid Stimulate Reactive Oxygen Species Production through Protein Kinase C-Dependent Ac-tivation of NAD(P)H Oxidase in Cultured Vascular Cells. Diabetes, 49, 1939-1945. [Google Scholar] [CrossRef] [PubMed]
[26] Bamba, R., Okamura, T., Hashimoto, Y., Hamaguchi, M., Obora, A., Kojima, T. and Fukui, M. (2020) The Visceral Adiposity Index Is a Predictor of Incident Chronic Kidney Disease: A Population-Based Longitudinal Study. Kidney and Blood Pressure Research, 45, 407-418. [Google Scholar] [CrossRef] [PubMed]

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