脂肪細胞所分泌出具有活性的激素和因子統稱為脂肪細胞激素，與肥胖、糖尿病及其併發症有著緊密的關聯。Visfatin是個新鑑定出的脂肪細胞激素，具有類似胰島素的功能，可以刺激葡萄糖的代謝並降低血漿中葡萄糖的含量，還能夠促進脂肪細胞內脂質的合成與聚集。研究報告指出在病態型肥胖與第2型糖尿病患者的血漿visfatin濃度高於健康族群，這些發現似乎提供了visfatin可能在内臟型肥胖和代謝疾病中扮演著相關的危險性角色。而且visfatin基因上所產生的變異，也可能影響內臟和皮下的visfatin messenger RNA (mRNA)表現，及葡萄糖和胰島素的代謝。
本研究分析visfatin血漿濃度與基因多型性對於第2型糖尿病和糖尿病合併大血管併發症的影響。結果發現visfatin濃度愈高者其罹患大血管病變的相對危險性就愈增加。此外，visfatin濃度與腰臀圍比(WHR)也具正相關性 (p = 0.0196)。在基因多型性的研究結果發現visfatin -948變異型異合子G/T基因型，表現在第2型糖尿病合併大血管病變組中明顯高於第2型糖尿病對照組 (p = 0.0213)，且visfatin -948 G/T變異基因型也與高值的高密度脂蛋白膽固醇有關(p = 0.0484)。
在此研究中發現糖尿病合併大血管病變組血中visfatin濃度顯著高於糖尿病組，且visfatin濃度增加，糖尿病合併大血管病變的危險性就愈高。雖然visfatin在胰島素抗性和葡萄糖及脂質代謝上的生理機制仍不清楚，但是藉由觀察血漿visfatin濃度於第2型糖尿病對照組及合併大血管病變組中濃度的變化，可能對於visfatin的生理功能及其在慢性疾病影響的瞭解上是有所助益的，也可能有助於瞭解visfatin在大血管病變過程中所扮演的角色。

Adiposity has been shown to secrete bioactive cytokines and growth factor known as adipocytokines, they can contribute to obesity, diabetes and complications of diabetes. Visfatin is a novel adipocytokine, and it was shown to exert insulin-mimetic effects in stimulating glucose transport and induced triglyceride accumulation in preadipocytes and triglyceride synthesis from gluvose. Visfatin plasma levels are increased in morbid obesity and type 2 diabetes mellitus. These finding indicate that visfatin may play a role in the association between visceral obesity and increased metabolic risk, visfatin gene suggested that genetic variation in the visfatin gene may, indeed, have a minor effect on visceral and subcutaneous visfatin messenger RNA expression profiles and parameters of glucose and insulin metabolism.
In this study, we explored the relationships between the plasma level of visfatin and genetic single nucleotide polymorphisms (SNPs) of visfatin gene in type 2 diabetes mellitus (T2DM) with and without macrovascular disease. Plasma visfatin was found to be elevated significantly in T2DM with macrovascular disease patients. Moreover, waist to hip ratio was independently associated with plasma visfatin level. There were statistically significant differences in visfatin -948 G/T genetic variants distribution between T2DM with macrovascular disease and the T2DM control group. The visfatin -948 G/T heterozygotes showed higher mean high-density lipoprotein cholesterol than the carriers of the G allele.
The results of the current study indicated that plasma visfatin levels were associated with macrovascular complications in type 2 diabetes. However, the definite roles of visfatin in the pathogenesis of insulin resistance, glucose and lipid metabolism are unclear. The observation of changes in the plasma concentrations of visfatin seen in T2DM and T2DM with macrovascular diseases may exert beneficial effects in understanding roles of visfatin in physiologic activity and metabolic disorder. Further studies are needed to elucidate the mechanisms behind visfatin overexpression in humans.

中文摘要 1
英文摘要 3
第一章 緒論 5
第一節 國人第2型糖尿病疾病流行病學 6
第二節 第2型糖尿病之病因與危險因子 8
第三節 第2型糖尿病之大血管併發症 10
第四節糖尿病併發症之形成機轉 11
1.多元醇路徑 12
2.增加細胞內醣化終產物的形成 12
3.Protein kinase C路徑的活化 13
4.六醣胺路徑 14
第五節脂肪細胞與疾病之相關性 15
第六節visfatin作用及與疾病關係之文獻探討 17
第二章 研究目的與重要性 22
第三章 實驗材料及方法 23
第一節 研究族群及收集時間 23
第二節 臨床生理及生化檢查 25
第三節Visfatin酵素免疫分析 32
第四節Visfatin基因多型性的檢測 35
第五節 統計分析 39
第四章 研究結果 40
第五章 討論 44
第六章 結論與未來展望 50
參考文獻 52
表1、第2型糖尿病對照組與第2型糖尿病合併大血管病變疾病組臨床生理及生化資料之比較
表2、第2型糖尿病對照組、第2型糖尿病合併心血管疾病組與第2型糖尿病合併腦血管疾病組臨床生理及生化資料之比較
表3、邏輯式回歸分析血漿visfatin濃度於3個研究族群之間的相對危
險性
表4、線性回歸分析血漿visfatin與所有研究族群變異因子的相關性
表5、visfatin基因多型性於3個研究族群之間的分佈表現
表6、visfatin -948基因多型性於第2型糖尿病對照組與第2型糖尿病合併大血管病變組的分佈表現
表7、visfatin -948基因多型性與所有研究族群臨床生理及生化資料之比較
圖1、血漿visfatin濃度於3個族群中的濃度關係
附錄一、第2型糖尿病的主要危險因子
附錄二、血漿visfatin酵素結合免疫吸附法(ELISA)標準曲線
附錄三、Visfatin基因多型性引子序列
附錄四、Visfatin基因多型性分佈位置
附錄五、Visfatin -948基因多型性即時定量聚合酶連鎖反應(Real-time PCR)

1. King, H., Aubert, R. E., & Herman, W. H. (1998). Global burden of diabetes,
1995-2025: prevalence, numerical estimates, and projections. Diabetes Care, 21(9),
1414-1431.
2.行政院衛生署民國94 年衛生統計重要指標　
http://www.gov.tw/statistic/data 衛生統計重要指標/94/94.htm
3. Fukuhara, A., Matsuda, M., Nishizawa, M., Segawa, K., Tanaka, M., Kishimoto, K.,
et al. (2005). Visfatin: a protein secreted by visceral fat that mimics the effects of
insulin. Science, 307(5708), 426-430.
4. Zimmet, P., Alberti, K. G., & Shaw, J. (2001). Global and societal implications of the
diabetes epidemic. Nature, 414(6865), 782-787.
5.行政院衛生署國民健康局中老年保健-台灣糖尿病防治推動現況與展望
http://www.bhp.doh.gov.tw/BHP/index.jsp
6.白其卉、游山林、簡國龍、曾慶孝、蘇大成、黃麗卿、陳建仁. 台灣地區高血壓、
高血糖、高血脂之盛行率調查期末報告. p58-p83 行政院衛生署國民健康局
7. Castro, F. C., Delgado, E. F., Bezerra, R. M., & Lanna, D. P. (2004). Effects of
growth hormone on insulin signal transduction in rat adipose tissue maintained in
vitro. Endocr Res, 30(2), 225-238.
8. Prins, J. B. (2002). Adipose tissue as an endocrine organ. Best Pract Res Clin
Endocrinol Metab, 16(4), 639-651.
9. Jazet, I. M., Pijl, H., & Meinders, A. E. (2003). Adipose tissue as an endocrine
organ: impact on insulin resistance. Neth J Med, 61(6), 194-212.
10. Raben, N., Barbetti, F., Cama, A., Lesniak, M. A., Lillioja, S., Zimmet, P., et al.
(1991). Normal coding sequence of insulin gene in Pima Indians and Nauruans, two
groups with highest prevalence of type II diabetes. Diabetes, 40(1), 118-122.
11. Tai TY, Yang CL, Chang C J, et al. Epidemiology of diabetes mellitus among adults
in Taiwan, R.O.C. (1987). J Med Assoc, 70(supple 2): 42-48.
12. Chou P, Liao M J, Kuo HS, Hsiao K J, Tsai ST. A population survey on the
prevalence of diabetes in Kin-Hu, Kinmen. (1994) Diabetes Care ; 17: 1055-1058.
13. Prevention of diabetes mellitus. Report of a WHO Study Group. (1994). World
Health Organ Tech Rep Ser, 844, 1-100.
14. Semenkovich, C. F., & Heinecke, J. W. (1997). The mystery of diabetes and
atherosclerosis: time for a new plot. Diabetes, 46(3), 327-334.
15. Meigs, J. B., Singer, D. E., Sullivan, L. M., Dukes, K. A., D'Agostino, R. B.,
Nathan, D. M., et al. (1997). Metabolic control and prevalent cardiovascular
disease in non-insulin-dependent diabetes mellitus (NIDDM): The NIDDM
Patient Outcome Research Team. Am J Med, 102(1), 38-47.
16.行政院衛生署民國95 年衛生統計重要指標　
http://www.gov.tw/statistic/data衛生統計重要指標/95/95.htm
17. Beckman, J. A., Creager, M. A., & Libby, P. (2002). Diabetes and atherosclerosis:
epidemiology, pathophysiology, and management. Jama, 287(19), 2570-2581.
18. Steiner, G. (2000). Lipid intervention trials in diabetes. Diabetes Care, 23 Suppl 2,
B49-53.
19. Haffner, S. M., Lehto, S., Ronnemaa, T., Pyorala, K., & Laakso, M. (1998).
Mortality from coronary heart disease in subjects with type 2 diabetes and in
nondiabetic subjects with and without prior myocardial infarction. N Engl J Med,
339(4), 229-234.
20. Bonora, E., Formentini, G., Calcaterra, F., Lombardi, S., Marini, F., Zenari, L., et
al. (2002). HOMA-estimated insulin resistance is an independent predictor of
cardiovascular disease in type 2 diabetic subjects: prospective data from the
Verona Diabetes Complications Study. Diabetes Care, 25(7), 1135-1141.
21. Du, X. L., Edelstein, D., Rossetti, L., Fantus, I. G., Goldberg, H., Ziyadeh, F., et al.
(2000). Hyperglycemia-induced mitochondrial superoxide overproduction activates
the hexosamine pathway and induces plasminogen activator inhibitor-1 expression
by increasing Sp1 glycosylation. Proc Natl Acad Sci U S A, 97(22), 12222-12226.
22. Garcia Soriano, F., Virag, L., Jagtap, P., Szabo, E., Mabley, J. G., Liaudet, L., et
al. (2001). Diabetic endothelial dysfunction: the role of poly(ADP-ribose)
polymerase activation. Nat Med, 7(1), 108-113.
23. Brownlee, M., Cerami, A., & Vlassara, H. (1988). Advanced glycosylation end
products in tissue and the biochemical basis of diabetic complications. N Engl J
Med, 318(20), 1315-1321.
24. Gonzalez, R. G., Barnett, P., Aguayo, J., Cheng, H. M., & Chylack, L. T., Jr.
(1984). Direct measurement of polyol pathway activity in the ocular lens.
Diabetes, 33(2), 196-199.
25. Yamagishi, H., Yoshiyama, M., Shirai, N., Akioka, K., Takeuchi, K., &
Yoshikawa, J. (2005). Protective effect of high diastolic blood pressure during
exercise against exercise-induced myocardial ischemia. Am Heart J, 150(4),
790-795.
26. MacGregor, L. C., & Matschinsky, F. M. (1986). Altered retinal metabolism in
diabetes. II. Measurement of sodium-potassium ATPase and total sodium and
potassium in individual retinal layers. J Biol Chem, 261(9), 4052-4058.
27. Makita, Z., Yanagisawa, K., Kuwajima, S., Yoshioka, N., Atsumi, T., Hasunuma,
Y., et al. (1995). Advanced glycation endproducts and diabetic nephropathy. J
Diabetes Complications, 9(4), 265-268.
28. Raj, D. S., Choudhury, D., Welbourne, T. C., & Levi, M. (2000). Advanced
glycation end products: a Nephrologist's perspective. Am J Kidney Dis, 35(3),
365-380.
29. Sheetz, M. J., & King, G. L. (2002). Molecular understanding of hyperglycemia'sadverse
effects for diabetic complications. JAMA, 288(20), 2579-2588.
30. Tanaka, S., Avigad, G., Brodsky, B., & Eikenberry, E. F. (1988). Glycation
induces expansion of the molecular packing of collagen. J Mol Biol, 203(2),
495-505.
31. Haitoglou, C. S., Tsilibary, E. C., Brownlee, M., & Charonis, A. S. (1992).
Altered cellular interactions between endothelial cells and nonenzymatically
glucosylated laminin/type IV collagen. J Biol Chem, 267(18), 12404-12407.
32. Okamoto, T., Yamagishi, S., Inagaki, Y., Amano, S., Takeuchi, M., Kikuchi, S., et
al. (2002). Incadronate disodium inhibits advanced glycation end
products-induced angiogenesis in vitro. Biochem Biophys Res Commun, 297(2),
419-424.
33. Yamagishi, S., Fujimori, H., Yonekura, H., Yamamoto, Y., & Yamamoto, H.
(1998). Advanced glycation endproducts inhibit prostacyclin production and
induce plasminogen activator inhibitor-1 in human microvascular endothelial
cells. Diabetologia, 41(12), 1435-1441.
34. Yamagishi, S., Yamamoto, Y., Harada, S., Hsu, C. C., & Yamamoto, H. (1996).
Advanced glycosylation end products stimulate the growth but inhibit the
prostacyclin-producing ability of endothelial cells through interactions with their
receptors. FEBS Lett, 384(1), 103-106.
35. Moore, T. C., Moore, J. E., Kaji, Y., Frizzell, N., Usui, T., Poulaki, V., et al.
(2003). The role of advanced glycation end products in retinal microvascular
leukostasis. Invest Ophthalmol Vis Sci, 44(10), 4457-4464.
36. Koya, D., & King, G. L. (1998). Protein kinase C activation and the development
of diabetic complications. Diabetes, 47(6), 859-866.
37. Brownlee, M. (2000). Negative consequences of glycation. Metabolism, 49(2
Suppl 1), 9-13.
38. Inoguchi, T., Li, P., Umeda, F., Yu, H. Y., Kakimoto, M., Imamura, M., et al.
(2000). High glucose level and free fatty acid stimulate reactive oxygen species
production through protein kinase C--dependent activation of NAD(P)H oxidase
in cultured vascular cells. Diabetes, 49(11), 1939-1945.
39. Hink, U., Li, H., Mollnau, H., Oelze, M., Matheis, E., Hartmann, M., et al. (2001).
Mechanisms underlying endothelial dysfunction in diabetes mellitus. Circ Res,
88(2), E14-22.
40. Dashwood, M. R., & Tsui, J. C. (2002). Endothelin-1 and atherosclerosis:
potential complications associated with endothelin-receptor blockade.
Atherosclerosis, 160(2), 297-304.
41. Cosentino, F., Eto, M., De Paolis, P., van der Loo, B., Bachschmid, M., Ullrich,
V., et al. (2003). High glucose causes upregulation of cyclooxygenase-2 and alters
prostanoid profile in human endothelial cells: role of protein kinase C and reactive
oxygen species. Circulation, 107(7), 1017-1023.
42. Omi, H., Okayama, N., Shimizu, M., Okouchi, M., Ito, S., Fukutomi, T., et al.
(2002). Participation of high glucose concentrations in neutrophil adhesion and
surface expression of adhesion molecules on cultured human endothelial cells:
effect of antidiabetic medicines. J Diabetes Complications, 16(3), 201-208.
43. Kouroedov, A., Eto, M., Joch, H., Volpe, M., Luscher, T. F., & Cosentino, F.
(2004). Selective inhibition of protein kinase Cbeta2 prevents acute effects of high
glucose on vascular cell adhesion molecule-1 expression in human endothelial
cells. Circulation, 110(1), 91-96.
44. Feng, J., Han, J., Pearce, S. F., Silverstein, R. L., Gotto, A. M., Jr., Hajjar, D. P.,
et al. (2000). Induction of CD36 expression by oxidized LDL and IL-4 by a
common signaling pathway dependent on protein kinase C and PPAR-gamma. J
Lipid Res, 41(5), 688-696.
45. Li, L., Sawamura, T., & Renier, G. (2004). Glucose enhances human macrophage
LOX-1 expression: role for LOX-1 in glucose-induced macrophage foam cellformation. Circ Res, 94(7), 892-901.
46. Marshall, S., Bacote, V., & Traxinger, R. R. (1991). Discovery of a metabolic
pathway mediating glucose-induced desensitization of the glucose transport
system. Role of hexosamine biosynthesis in the induction of insulin resistance. J
Biol Chem, 266(8), 4706-4712.
47. Hanover, J. A., Lai, Z., Lee, G., Lubas, W. A., & Sato, S. M. (1999). Elevated
O-linked N-acetylglucosamine metabolism in pancreatic beta-cells. Arch Biochem
Biophys, 362(1), 38-45.
48. Kolm-Litty, V., Sauer, U., Nerlich, A., Lehmann, R., & Schleicher, E. D. (1998).
High glucose-induced transforming growth factor beta1 production is mediated by
the hexosamine pathway in porcine glomerular mesangial cells. J Clin Invest
, 101(1), 160-169.
49. James, L. R., Fantus, I. G., Goldberg, H., Ly, H., & Scholey, J. W. (2000).
Overexpression of GFAT activates PAI-1 promoter in mesangial cells. Am J
Physiol Renal Physiol, 279(4), F718-727.
50. Goldberg, H. J., Scholey, J., & Fantus, I. G. (2000). Glucosamine activates the
plasminogen activator inhibitor 1 gene promoter through Sp1 DNA binding sites
in glomerular mesangial cells. Diabetes, 49(5), 863-871.
51. Fogo, A. B. (2000). The role of angiotensin II and plasminogen activator
inhibitor-1 in progressive glomerulosclerosis. Am J Kidney Dis, 35(2), 179-188.
52. Kougias, P., Chai, H., Lin, P. H., Yao, Q., Lumsden, A. B., & Chen, C. (2005).
Effects of adipocyte-derived cytokines on endothelial functions: implication of
vascular disease. J Surg Res, 126(1), 121-129.
53. Fantuzzi, G. (2005). Adipose tissue, adipokines, and inflammation. J Allergy Clin
Immunol, 115(5), 911-919; quiz 920.
54. Arner, P. (2005). Insulin resistance in type 2 diabetes -- role of the adipokines.
Curr Mol Med, 5(3), 333-339.
55. Lau, D. C., Dhillon, B., Yan, H., Szmitko, P. E., & Verma, S. (2005). Adipokines:
molecular links between obesity and atheroslcerosis. Am J Physiol Heart Circ
Physiol, 288(5), H2031-2041.
56. Bloomgarden, Z. T. (2002). Adiposity and diabetes. Diabetes Care, 25(12),
2342-2349.
57. Steppan, C. M., Bailey, S. T., Bhat, S., Brown, E. J., Banerjee, R. R., Wright, C.
M., et al. (2001). The hormone resistin links obesity to diabetes. Nature,409 (6818),
307-312.
58. Nystrom, T., Nygren, A., & Sjoholm, A. (2006). Increased levels of tumour
necrosis factor-alpha (TNF-alpha) in patients with Type II diabetes mellitus after
myocardial infarction are related to endothelial dysfunction. Clin Sci (Lond),
110(6), 673-681.
59. Tsiavou, A., Hatziagelaki, E., Chaidaroglou, A., Manginas, A., Koniavitou, K.,
Degiannis, D., et al. (2004). TNF-alpha, TGF-beta1, IL-10, IL-6, gene
polymorphisms in latent autoimmune diabetes of adults (LADA) and type 2
diabetes mellitus. J Clin Immunol, 24(6), 591-599.
60. Danielsson, P., Truedsson, L., Eriksson, K. F., & Norgren, L. (2005).
Inflammatory markers and IL-6 polymorphism in peripheral arterial disease with
and without diabetes mellitus. Vasc Med, 10(3), 191-198.
61. Yanagawa, T., Taniguchi, A., Fukushima, M., Nakai, Y., Nagasaka, S., Ohgushi,
M., et al. (2007). Leptin, triglycerides, and interleukin 6 are independently
associated with C-reactive protein in Japanese type 2 diabetic patients. Diabetes
Res Clin Pract, 75(1), 2-6.
62. Kim, C., Park, J., Park, J., Kang, E., Ahn, C., Cha, B., et al. (2006). Comparison
of body fat composition and serum adiponectin levels in diabetic obesity and
non-diabetic obesity. Obesity (Silver Spring), 14(7), 1164-1171.
63. Thamer, C., Haap, M., Heller, E., Joel, L., Braun, S., Tschritter, O., et al. (2006).
Beta cell function, insulin resistance and plasma adiponectin concentrations are
predictors for the change of postprandial glucose in non-diabetic subjects at risk
for type 2 diabetes. Horm Metab Res, 38(3), 178-182.
64. Kralisch, S., Klein, J., Lossner, U., Bluher, M., Paschke, R., Stumvoll, M., et al.
(2005). Hormonal regulation of the novel adipocytokine visfatin in 3T3-L1
adipocytes. J Endocrinol, 185(3), R1-8.
65. Hammarstedt, A., Pihlajamaki, J., Rotter Sopasakis, V., Gogg, S., Jansson, P. A.,
Laakso, M., et al. (2006). Visfatin is an adipokine, but it is not regulated by
thiazolidinediones. J Clin Endocrinol Metab, 91(3), 1181-1184.
66. Sandeep, S., Velmurugan, K., Deepa, R., & Mohan, V. (2007). Serum visfatin in
relation to visceral fat, obesity, and type 2 diabetes mellitus in Asian Indians.
Metabolism, 56(4), 565-570.
67. Dahl, T. B., Yndestad, A., Skjelland, M., Oie, E., Dahl, A., Michelsen, A., et al.
(2007). Increased expression of visfatin in macrophages of human unstable carotid
and coronary atherosclerosis: possible role in inflammation and plaque
destabilization. Circulation, 115(8), 972-980.
68. Korner, A., Bottcher, Y., Enigk, B., Kiess, W., Stumvoll, M., & Kovacs, P. (2007).
Effects of genetic variation in the visfatin gene (PBEF1) on obesity, glucose
metabolism, and blood pressure in children. Metabolism, 56(6), 772-777.
69. Bottcher, Y., Teupser, D., Enigk, B., Berndt, J., Kloting, N., Schon, M. R., et al.
(2006). Genetic variation in the visfatin gene (PBEF1) and its relation to glucose
metabolism and fat-depot-specific messenger ribonucleic acid expression in
humans. J Clin Endocrinol Metab, 91(7), 2725-2731.
70. Alberti, K. G., & Zimmet, P. Z. (1998). Definition, diagnosis and classification of
diabetes mellitus and its complications. Part 1: diagnosis and classification of
diabetes mellitus provisional report of a WHO consultation. Diabet Med, 15(7),
539-553.
71. Berndt, J., Kloting, N., Kralisch, S., Kovacs, P., Fasshauer, M., Schon, M. R., et al.
(2005). Plasma visfatin concentrations and fat depot-specific mRNA expression in
humans. Diabetes, 54(10), 2911-2916.
72. Bray, G. A., Lovejoy, J. C., Smith, S. R., DeLany, J. P., Lefevre, M., Hwang, D.,
et al. (2002). The influence of different fats and fatty acids on obesity, insulin
resistance and inflammation. J Nutr, 132(9), 2488-2491.
73. Ognjanovic, S., Bao, S., Yamamoto, S. Y., Garibay-Tupas, J., Samal, B., &
Bryant-Greenwood, G. D. (2001). Genomic organization of the gene coding for
human pre-B-cell colony enhancing factor and expression in human fetal
membranes. J Mol Endocrinol, 26(2), 107-117.
74. Chen, M. P., Chung, F. M., Chang, D. M., Tsai, J. C., Huang, H. F., Shin, S. J., et
al. (2006). Elevated plasma level of visfatin/pre-B cell colony-enhancing factor in
patients with type 2 diabetes mellitus. J Clin Endocrinol Metab, 91(1), 295-299.
75. Cinti, S., Mitchell, G., Barbatelli, G., Murano, I., Ceresi, E., Faloia, E., et al.
(2005). Adipocyte death defines macrophage localization and function in adipose
tissue of obese mice and humans. J Lipid Res, 46(11), 2347-2355.
76. Lumeng, C. N., Bodzin, J. L., & Saltiel, A. R. (2007). Obesity induces a
phenotypic switch in adipose tissue macrophage polarization. J Clin Invest, 117(1),
175-184.
77. Curat, C. A., Wegner, V., Sengenes, C., Miranville, A., Tonus, C., Busse, R., et al.
(2006). Macrophages in human visceral adipose tissue: increased accumulation in
obesity and a source of resistin and visfatin. Diabetologia, 49(4), 744-747.
78. Haider, D. G., Handisurya, A., Storka, A., Vojtassakova, E., Luger, A., Pacini, G.,
et al. (2007). Visfatin response to glucose is reduced in women with gestational
diabetes mellitus. Diabetes Care, 30(7), 1889-1891.
79. Choi, K. C., Ryu, O. H., Lee, K. W., Kim, H. Y., Seo, J. A., Kim, S. G., et al.
(2005). Effect of PPAR-alpha and -gamma agonist on the expression of visfatin,adiponectin,
and TNF-alpha in visceral fat of OLETF rats. Biochem Biophys Res
Commun, 336(3), 747-753.
80. Bailey, S. D., Loredo-Osti, J. C., Lepage, P., Faith, J., Fontaine, J., Desbiens, K. M.,
et al. (2006). Common polymorphisms in the promoter of the visfatin gene (PBEF1)
influence plasma insulin levels in a French-Canadian population. Diabetes, 55(10),
2896-2902.
81. Jian, W. X., Luo, T. H., Gu, Y. Y., Zhang, H. L., Zheng, S., Dai, M., et al. (2006).
The visfatin gene is associated with glucose and lipid metabolism in a Chinese
population. Diabet Med, 23(9), 967-973.