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The Change of Tissue Lipid Levels and Fatty Acid Compositions by Alloxan-induced Diabetes in Rats

Alloxan 유도 당뇨성 흰쥐에서 조직 중 지질 수준 및 지방산 조성 변화에 관한 연구

  • Lee, Joon-Ho (Dept. of Consumers' Life Information, Chungnam National University) ;
  • Jun, In-Nyo (Dept. of Consumers' Life Information, Chungnam National University)
  • 이준호 (충남대학교 소비자생활정보학과) ;
  • 전인녀 (충남대학교 소비자생활정보학과)
  • Published : 2004.10.01

Abstract

The change of tissue lipid levels and fatty acid compositions in alloxan-induced diabetes was studied in rats (SD, male) in order to examine the pathway of diabetic complications. Rats were injected with alloxan 20 mg/kg BW or 40 mg/kg BW to induce diabetes. In rats injected with alloxan (40 mg/kg BW), the body weight was significantly decreased, food intake and liver weight per 100 g (BW) were significantly increased, compared with other groups. The blood glucose levels were apparently elevated as about 2 times in rats injected with alloxan (40 mg/kg BW) than the other groups. The concentrations of serum total cholesterol, triglyceride and HDL-cholesterol were not significantly different among the groups. However, the levels of serum triglyceride tended to increase according to amount of alloxan injected. Liver cholesterol levels were significantly decreased in rats injected with alloxan (40 mg/kg BW) compared with other groups, but triglyceride levels of those were not significantly different among groups. Concerning the fatty acid compositions of serum, liver, kidney, spleen phosphatidylcholine, the percentage of linoleic acid in rats injected with alloxan (40 mg/kg BW) was significantly increased, while that of arachidonic acid was significantly decreased compared with the other groups. Therefore, the ratios of arachidonic/linoleic acid in tissue phosphatidylcholine tended to be low in rats injected with alloxan (40 mg/kg BW) and especially significant low levels were found in serum and spleen. Thus, it was suggested that insulin deficiency can affect on fatty acid biosynthesis and induce diabetic complications.

당뇨병의 합병증 중 지질대사성 질환으로 유도되는 대사경로를 규명하고자 6주령의 흰쥐(Sprague-Dawley) 24마리를 3군으로 나누어 4주간 chemical pure diet로 사육하였다. 당뇨병을 유발하고자 alloxan을 20 mg/kg BW 또는 40 mg BW를 매주 1회 투여하였다. 혈당치를 측정하여 당뇨증상을 확인하였으며 혈청 및 간의 지질수준과 각 조직의 지방산 조성을 측정하여 당뇨병에 의한 지질대사의 변화를 비교 검토하였다. Alloxan 40 mg 투여군에서 심한 당뇨병 유발로 체중감소가 크게 나타났으며, 식이섭취량과 간중량/100 g BW도 다른 군에 비하여 유의적으로 높았다. 혈당의 변화는 alloxan 40 mg/kg BW 투여한 군이 다른 군에 비해 약 2배정도로 높게 나타나 당뇨병이 유발되었음을 확실하게 알 수 있었다. 혈청지질에서 cholesterol 함량은 alloxan 40 mg/kg BW 투여한 군에서 다른 군보다 다소 증가된 경향을 보였다. Triglyceride도 역시 alloxan 투여군에서 높은 경향으로 나타났다. 혈청 HDL-cholesterol은 군간의 유의적인 차이가 없었으며 HDL-/total cholesterol 비율도 군간에 유의적인 차이는 없었으나, 다른 군보다 alloxan 40 mg/kg BW을 투여한 군이 다소 높은 경향이었다. 간 지질에서 cholesterol 함량은 alloxan 40 mg/kg BW 투여군이 다른 군에 비해 유의적으로 낮았다. Triglyceride 함량은 군간에 유의적인 차이가 없었다. 각 조직의 인지질 지방산 조성을 보면 alloxan 40 mg/kg BW 투여군에서 lionleic acid는 증가하고 반면 arachidonic acid는 감소되어 그 결과 arachidonic/linoleic acid의 비율이 낮은 경향을 보였으며 특히 혈청과 비장에서는 그 경향이 뚜렷하여 유의적인 차이를 나타냈다. 이상의 결과를 종합하면, 당뇨병이 유도된 흰쥐에서 간의 중량 및 혈청의 지질이 증가되었고, 조직의 인지질에서 desaturation이 억제되었으므로 그로 인하여 지질대사에 관련된 합병증이 유도되는 것으로 판단되었다.

Keywords

References

  1. Yoon JY, Lee JH, Lee YC, Lee HC, Huh KB. 1997. Visceral fat accumulation and the fatty acid composition of serum phospholipids in middle-aged woman with different degrees of glucose tolerance. J Korean Diabetes Assoc 21: 444-456
  2. Pelikanova T, Kohout M, Valek J, Base J, Kazdova L. 1989. Insulin secretion and insulin action related to the serum phospholipid fatty acid pattern in healthy men. Metabolism 38: 188-192 https://doi.org/10.1016/0026-0495(89)90261-8
  3. Poisson JP. 1985. Comparative in vivo and in vitro study of the influence of experimental diabetes in rat liver linileic acid $\Delta$6- and $\Delta$5-desaturation. Enzyme 34: 1-14 https://doi.org/10.1159/000469353
  4. Padly FB, Podmore J. 1985. The role of fats in human nutrition. Academic Press, London. p 23-34
  5. Clark DL, Hamel FG, Queener SF. 1983. Changes in renal phospholipid fatty acids in diabetes mellitus: Correlation with changes in adenylate cyclase activity. Lipids 18: 696- 705 https://doi.org/10.1007/BF02534536
  6. 최영길, 이태희, 신순현, 김영설. 1998. 당뇨병성 혈관합병증 진단과 치료. 도서출판 한의학, 서울. p 69-86
  7. Stevens MJ, Feldman EL, Greene DA. 1995. The etiology of diabetic neuropathy: The combined roles of metabolic and vascular defects. Diabetic Med 12: 1566-1579
  8. Kim DM. 1998. Diabetic angiopathy and vascular adhesion molecule. J Korean Diabetes Assoc 22: 19-22
  9. American Diabetes Association. 1989. Role of cardiovascular risk factors in prevention and treatment of macrovascular disease. Diabetes Care 12: 573-579 https://doi.org/10.2337/diacare.12.8.573
  10. Roh MR. 1986. Studies on the serum lipoprotein in diabetes. MS Thesis. Ewha Woman Univ. p 19-22
  11. Kramer-Guth T. 1997. Structural and compositional modifications of diabetic low-density lipoproteins influence their receptor-mediated up-take by hepatocytes. Eur J Clin Invest 27: 460-468 https://doi.org/10.1046/j.1365-2362.1997.1460695.x
  12. Georgopoulos A, Phair RD. 1991. Abnormal clearance of postprandial Sf 100-400 plasma lipoproteins in insulin- dependent diabetes mellitus. J Lipid Res 32: 1133-1141
  13. Tomkin GH, Owens D. 1991. Abnormalities of cholesterol metabolism in diabetes. Proc Nutr Soc 50: 583-589 https://doi.org/10.1079/PNS19910072
  14. Kim JY, Kim MS, Kim JM, Park JH, Lee JH, Yang SW, Chung DJ, Chung MY, Lee TH. 1998. Lipoprotein(a) level and vascular complications in NIDDM. J Korean Diabetes Assoc 22: 65-73
  15. American Institute of Nutrition. 1977. Report of AIN ad hoc Committee on Standard for Nutrition Studies. J Nutr 107: 1340 https://doi.org/10.1093/jn/107.7.1340
  16. Folch J, Lees M, Sloane-Stanley GH. 1957. A simple method for the isolation and purification of total lipids from animal tissues. J Biol Chem 226: 497-509
  17. Sperry WM, Webb M. 1950. A revision of the Schoenheimer-Sperry method for cholesterol determination. J Biol Chem 187: 97-106
  18. Fletcher MJ. 1968. A colorimetric method for estimating serum triglycerides. Clin Chim Acta 22: 393-397 https://doi.org/10.1016/0009-8981(68)90041-7
  19. Wada M, Sugano M. 1972. The practical methods for utilization of thin layer chromatography to the analysis of glycerolipids from animal tissues. Sci Bull Fac Agric Kyushu Univ 26: 505-516
  20. Morrison WR, Smith LM. 1964. Preparation of fatty acid methylesters and dimethylacetyls from lipids with Boron Flouride-methanol. J Lipid Res 5: 600
  21. Chung YH. 1991. Delta 6 desaturase activity and fatty acid composition in experimental diabetic rats. PhD Dissertation. Seoul Nat'l Univ. p 25-66
  22. Hwang HS. 1985. Effect of $Ca^2^+$-antagonists on alloxan- induced diabetes. Master theses of Chonbug Nat'l Univ. p 4-6
  23. Okubo M. 1996. Hypertriglyceridemia and low HDL cholesterol in Japanese patients with NIDDM. Diabetes 45 (Suppl 3): 123-125 https://doi.org/10.2337/diab.45.3.S123
  24. Taskinen MR. 1992. Quantitative and qualitative lipoprotein abnormalities in diabetes mellitus. Diabetes 41 (Suppl 2): 12-17 https://doi.org/10.2337/diabetes.41.1.12
  25. Yoon JY, Song YD, Lee JH, Park EJ, Kim SM, Lim HS, Lee HC, Huh KB. 1995. Effect of different levels of carbohydrate and fat intake on glucose and lipid metabolism in patients with NIDDM. J Korean Diabetes Assoc 19: 208-218
  26. Min YK. 1985. HDL subfractions in diabetes. Master theses of Seoul Nat'l Univ. p 6-8
  27. Reilly FD. 1985. Innervation and Vascular pharmocodynamic of the mammallian spleen. Experientia 41: 187-192 https://doi.org/10.1007/BF02002612
  28. Zuniga ME, Lokesh BR, Kinsella JE. 1987. Dietary n-3 polyunsaturated fatty acid alter lipid composition and decrease prostaglandin synthesis in rat spleen. Nutr Res 7: 299-306 https://doi.org/10.1016/S0271-5317(87)80019-2

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