Skip to main content
SpringerLink
Log in

Role of fructose concentration on cataractogenesis in senile diabetic and non-diabetic patients

  • Cataract
  • Published:
Graefe's Archive for Clinical and Experimental Ophthalmology Aims and scope Submit manuscript

Abstract

Background

Fructose intake has increased steadily during the past 2 decades. Fructose, like other reducing sugar, can react with proteins, which may account for aging and cataract formation. Fructose participates in glycation (fructation) and advanced glycation endproducts (AGE) formation some ten times faster than glucose. This study aims to determine the fructose concentration and correlate with antioxidant status in senile diabetic and non-diabetic cataract patients.

Methods

The study included 124 subjects. Of them, 31 were normal senile subjects, 33 were senile diabetic patients without cataract, 30 were senile diabetic patients with cataract, and 30 were senile non-diabetic patients with cataract. The patients were selected on clinical grounds from Eye Ward, Jinnah Postgraduate Medical Centre, Karachi, Pakistan.

Results

Serum fructose was significantly increased (P < 0.001) in senile diabetic patients with and without cataract and senile non-diabetic patients with cataract as compared with senile control subjects. Negative significant correlation was observed between serum fructose and serum total antioxidant status in diabetic and non-diabetic patients with cataract. Positive significant correlation was observed between serum fructose and s-AGEs in diabetic and non-diabetic patients with cataract. Serum total antioxidant status was found to be significantly decreased (P < 0.001) in senile diabetic patients with and without cataract and senile non-diabetic patients with cataract as compared with senile control subjects. Fasting blood glucose, HbA1C and serum fructosamine were significantly increased (P < 0.001) in senile diabetic patients with or without cataract as compared with senile non-diabetic patients with cataract and senile control subjects.

Conclusions

The results indicate that the increased fructose concentration which induces oxidative stress in diabetic and non-diabetic patients with cataract may be a predictor for cataractogenesis.

This is a preview of subscription content, log in via an institution to check access.

Access this article

Log in via an institution

Price excludes VAT (USA)
Tax calculation will be finalised during checkout.

Instant access to the full article PDF.

Institutional subscriptions

Fig. 1

Similar content being viewed by others

References

  1. Shera S (1998) Prevalence and prevention. Diabetes Dig 12:7–8

    Google Scholar 

  2. Kawasaki Y, Fujii J, Miyazawa N, Hoshi A, Okado A, Tano Y, Taniguchi N (1998) Specific detection of the early process of the glycation reaction by fructose and glucose in diabetic rat lens. FEBS Lett 441:116–120, doi:10.1016/S0014-5793(98)01529-4

    Article  PubMed  CAS  Google Scholar 

  3. Dills WL (1993) Protein fructosylation: fructose and the Maillard reaction. Am J Clin Nutr 58:779S–787S

    PubMed  CAS  Google Scholar 

  4. Suarez G, Maturana J, Oronsky AL, Raventos-Suarez C (1991) Fructose induces fluorescence generation of reductively methylated glycated bovine serum albumin: evidence of nonenzymatic glycosylation of Amadori adducts. Biochim Biophys Acta 1075:12–19

    PubMed  CAS  Google Scholar 

  5. Tagaki Y, Kashiwagi A, Tanaka Y, Asahina T, Kikkawa R, Shigeta Y (1995) Significance of fructose-induced protein oxidation and formation of advanced glycation endproduct. J Diabetes and its Complications 9:87–91

    Article  Google Scholar 

  6. Ding EL, Malik VS (2008) Convergence of obesity and high glycemic diet on compounding diabetes and cardiovascular risks in modernizing China: an emerging public health dilemma. Global Health 4:4–9, doi:10.1186/1744-8603-4-4

    Article  PubMed  Google Scholar 

  7. Levi B, Werman MJ (1998) Long term fructose consumption accelerates glycation and several age related variables in male rates. J Nutr 128:1442–1449

    PubMed  CAS  Google Scholar 

  8. Chung SS, Ho EC, Lam KS, Chung SK (2003) Contribution of polyol pathway to diabetes-induced oxidative stress. J Am Soc Nephrol 14:S233–S236, doi:10.1097/01.ASN.0000077408.15865.06

    Article  PubMed  CAS  Google Scholar 

  9. Lee AY, Chung SM (1999) Contributions of polyol pathway to oxidative stress in diabetic cataract. FASEB 13:23–30

    CAS  Google Scholar 

  10. Jedziniak JA, Chylack LT, Cheng HM, Gillis MK, Kalustian AA, Tung WH (1981) The sorbitol pathway in the human lens: aldose reductase and polyol dehydrogenase. Invest Ophthalmol Vis Sci 20:314–326

    PubMed  CAS  Google Scholar 

  11. Dawczynski J, Strobel J (2006) The aging lens—new concepts for lens aging. Ophthalmologe 103:759–764, doi:10.1007/s00347006-1410-z

    Article  PubMed  CAS  Google Scholar 

  12. Gabir MM, Roumain J, Hanson RL, Bennett PH, Dabelea D, Knowler WC, Imperatore G (2000) The 1997 American Diabetes Association and 1999 World Health Organization criteria for hyperglycemia in the diagnosis and prediction of diabetes. Diabetes Care 23:1108–1112, doi:10.2337/diacare.23.8.1108

    Article  PubMed  CAS  Google Scholar 

  13. Pogell BM (1954) The quantitative determination of fructose with skatole and hydrochloric acid. J Biol Chem 211:143–147

    PubMed  CAS  Google Scholar 

  14. Miller NJ, Rice-Evans C, Davies MJ, Gopinathan V, Milner A (1993) A novel method for measuring antioxidant capacity and its application for monitoring the antioxidant status in premature neonates. Clin Sci 84:407–412

    PubMed  CAS  Google Scholar 

  15. Ono Y, Aoki S, Ohnishi K, Yasuda T, Kawano K, Tsukada Y (1998) Increased serum levels of advanced glycation end-products and diabetic complications. Diabetes Res Clin Pract 41:131–137, doi:10.1016/S0168-8227(98)00074-6

    Article  PubMed  CAS  Google Scholar 

  16. Shah SP, Dineen B, Jadoon Z, Bourne R, Khan MA, Johnson GJ, De Stavola B, Gilbert C, Khan MD (2007) Lens opacities in adults in Pakistan: prevalence and risk factors. Ophthalmic Epidemiol 14:381–389, doi:10.1080/09286580701375179

    Article  PubMed  Google Scholar 

  17. Aronson D (2008) Hyperglycemia and the pathobiology of diabetic complications. Adv Cardiol 45:1–16, doi:10.1159/000115118

    Article  PubMed  CAS  Google Scholar 

  18. Park YK, Yetley EA (1993) Intakes and food sources of fructose in the United States. Am J Clin Nutr 58:737S–747S

    PubMed  CAS  Google Scholar 

  19. Miyazawa N, Kawasaki Y, Fujii J, Theingi M, Hamaoka R, Matsumoto A, Uozumi N, Teshima T, Taniguchi N (1998) Immunological detection of fructated proteins in vitro and in vivo. Biochem J 336:101–107

    PubMed  CAS  Google Scholar 

  20. Kawasaki T, Akanuma H, Yamanouchi T (2002) Increased fructose concentrations in blood and urine in patients with diabetes. Diabetes Care 25:353–357, doi:10.2337/diacare.25.2.353

    Article  PubMed  CAS  Google Scholar 

  21. Bell RC, Carlson JC, Storr KC, Herbert K, Sivak J (2000) High-fructose feeding of strptozotocin-diabetic rats is associated with increased cataract formation and increased oxidative stress in the kidney. Br J Nutr 84:575–582

    PubMed  CAS  Google Scholar 

  22. Franke S, Dawczynski J, Strobel J, Niwa T, Stahl P, Stein G (2003) Increased levels of advanced glycation end products in human cataractous lenses. J Cataract Refract Surg 29:998–1004, doi:10.1016/S0886-3350(02)01841-2

    Article  PubMed  Google Scholar 

  23. Johnson RJ, Segal MS, Sautin Y, Nakagawa T, Feig DI, Kang DH, Gersch MS, Benner S, Sánchez-Lozada LG (2007) Potential role of sugar (fructose) in the epidemic of hypertension, obesity and the metabolic syndrome, diabetes, kidney disease, and cardiovascular disease. Am J Clin Nutr 86:899–906

    PubMed  CAS  Google Scholar 

  24. Ahmed FN, Naqvi FN, Shafiq F (2006) Lipid peroxidation and serum antioxidant enzymes in patients with type 2 diabetes mellitus. Ann N Y Acad Sci 1084:481–489, doi:10.1196/annals.1372.022

    Article  PubMed  CAS  Google Scholar 

  25. Yamagishi S, Imaizumi T (2005) Diabetic vascular complications: pathophysiology, biochemical basis and potential therapeutic strategy. Curr Pharm Des 11:2279–2299, doi:10.2174/1381612054367300

    Article  PubMed  CAS  Google Scholar 

  26. Andriollo-Sanchez M, Hininger-Favier I, Meunier N, Venneria E, O’Connor JM, Maiani G, Coudray C, Roussel AM (2005) Age-related oxidative stress and antioxidant parameters in middle-aged and older European subjects. Eur J Clin Nutr 59:S58–S62, doi:10.1038/sj.ejcn.1602300

    Article  PubMed  CAS  Google Scholar 

  27. Hallfrisch J (1990) Metabolic effects of dietary fructose. FASEB J 4:2652–2660

    PubMed  CAS  Google Scholar 

  28. Rajasekar P, Palanisamy N, Anuradha CV (2007) Increase in nitric oxide and reductions in blood pressure, protein kinase C beta II and oxidative stress by L-carnitine: a study in the fructose-fed hypertensive rat. Clin Exp Hypertens 29:517–530, doi:10.1080/10641960701743998

    Article  PubMed  CAS  Google Scholar 

  29. Stanhope KL, Havel PJ (2008) Fructose consumption: potential mechanisms for its effects to increase visceral adiposity and induce dyslipidemia and insulin resistance. Curr Opin Lipidol 19:16–24

    Article  PubMed  CAS  Google Scholar 

  30. Basciano H, Federico L (2005) Adeli k. Fructose, insulin resistance, and metabolic dyslipidemia. Nutr Metab 2:5–11, doi:10.1186/1743-7075-2-5

    Article  CAS  Google Scholar 

  31. Sheikh MA, Robb DA (1995) Role of glucose and fructose in diabetic complications. Pak J Bioch Mol Biol 28:153–161

    Google Scholar 

  32. Abou-Seif MA, Youssef AA (2004) Evaluation of some biochemical changes in diabetic patients. Clin Chim Acta 346:161–170, doi:10.1016/j.cccn.2004.03.030

    Article  PubMed  CAS  Google Scholar 

Download references

Acknowledgement

This work was financially supported by a Pakistan science foundation grant. We are also grateful to Dr. Wasdev Harani, Head of Department, Eye Ward Jinnah Postgraduate Medical Centre, Karachi, Pakistan for providing human samples.

Author information

Authors and Affiliations

  1. Department of Biochemistry, Ziauddin University, 4/B Shahra-e-Ghalib, Clifton, Karachi, 75600, Pakistan

    Anjuman Gul & Syed Nazrul Hasnain

  2. H.E.J. Research Institute of Chemistry, University of Karachi, Karachi, 75270, Pakistan

    M. Ataur Rahman

Authors
  1. Anjuman Gul
    View author publications

    You can also search for this author in PubMed Google Scholar

  2. M. Ataur Rahman
    View author publications

    You can also search for this author in PubMed Google Scholar

  3. Syed Nazrul Hasnain
    View author publications

    You can also search for this author in PubMed Google Scholar

Corresponding author

Correspondence to Anjuman Gul.

Rights and permissions

Reprints and permissions

About this article

Cite this article

Gul, A., Rahman, M.A. & Hasnain, S.N. Role of fructose concentration on cataractogenesis in senile diabetic and non-diabetic patients. Graefes Arch Clin Exp Ophthalmol 247, 809–814 (2009). https://doi.org/10.1007/s00417-008-1027-9

Download citation

  • Received:

  • Revised:

  • Accepted:

  • Published:

  • Issue Date:

  • DOI: https://doi.org/10.1007/s00417-008-1027-9

Keywords

Search

Navigation