Beta-Cell Function and Nutrient Intake

You Mi Lee

doi:10.4093/jkd.2016.17.3.190

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Lee: Beta-Cell Function and Nutrient Intake

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J Korean Diabetes 2016;17(3):190-195.

Published online: 10 January 2016

DOI: https://doi.org/10.4093/jkd.2016.17.3.190

Beta-Cell Function and Nutrient Intake

You Mi Lee

Department of Nutrition Consultation, Seoul National University Hospital Healthcare System Gangnam Center, Seoul, Korea

Corresponding author: You Mi Lee Department of Nutrition Consultation, Seoul National University Hospital Healthcare System Gangnam Center, 38∼40 F, 152 Teheran-ro, Gangnam-gu, Seoul 06236, Korea, E-mail: dldbal@snuh.org

Received 31 March 2016 Accepted 21 April 2016

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Pancreatic beta-cells have an important role in maintaining blood glucose homeostasis through insulin secretion. Therefore, decreased insulin secretion function induced by impaired beta-cell is one of the leading causes of diabetes mellitus. Accumulating data suggested that multiple factors such as age, body weight, smoking and alcohol intake may decrease beta-cell function. In addition, previous studies have reported that nutrient intake, such as carbohydrate, fat, vitamin and mineral intake, is associated with beta-cell function. The purpose of this study is to review the results regarding the association between nutrient intake and beta-cell function. We propose herein that nutrient intake helps prevent decreases in beta-cell function and preserves the optimal insulin secretion function.

Keywords: Insulin secretion function, Nutrient intake, Pancreatic beta-cells

References

1. Chiu KC, Lee NP, Cohan P, Chuang LM. Beta cell function declines with age in glucose tolerant Caucasians. Clin Endocrinol (Oxf). 2000; 53:569–75.

2. Ostgren CJ, Lindblad U, Ranstam J, Melander A, Råstam L. Skaraborg Hypertension and Diabetes Project. Associations between smoking and beta-cell function in a nonhypertensive and non-diabetic population. Skaraborg Hypertension and Diabetes Project. Diabet Med. 2000; 17:445–50.

3. Yamada Y, Noborisaka Y, Ishizaki M, Tsuritani I, Honda R, Yamada S. Alcohol consumption, homeostasis model assessment indices and blood pressure in middle-aged healthy men. J Hum Hypertens. 2004; 18:343–50.

4. Schuit FC, Huypens P, Heimberg H, Pipeleers DG. Glucose sensing in pancreatic beta-cells: a model for the study of other glucose-regulated cells in gut, pancreas, and hypothalamus. Diabetes. 2001; 50:1–11.

5. MacDonald PE, Joseph JW, Rorsman P. Glucose-sensing mechanisms in pancreatic beta-cells. Philos Trans R Soc Lond B Biol Sci. 2005; 360:2211–25.

6. Leahy JL. Natural history of beta-cell dysfunction in NIDDM. Diabetes Care. 1990; 13:992–1010.

7. Weyer C, Bogardus C, Mott DM, Pratley RE. The natural history of insulin secretory dysfunction and insulin resistance in the pathogenesis of type 2 diabetes mellitus. J Clin Invest. 1999; 104:787–94.

8. DeFronzo RA. Pathogenesis of type 2 diabetes mellitus. Med Clin North Am. 2004; 88:787–835.

9. Kim DJ, Lee MS, Kim KW, Lee MK. Insulin secretory dysfunction and insulin resistance in the pathogenesis of Korean type 2 diabetes mellitus. Metabolism. 2001; 50:590–3.

10. Yoon KH, Lee JH, Kim JW, Cho JH, Choi YH, Ko SH, Zimmet P, Son HY. Epidemic obesity and type 2 diabetes in Asia. Lancet. 2006; 368:1681–8.

11. Shin CS, Lee HK, Koh CS, Kim YI, Shin YS, Yoo KY, Paik HY, Park YS, Yang BG. Risk factors for the development of NIDDM in Younchon county, Korea. Diabetes Care. 1997; 20:1842–6.

12. Klöppel G, Löhr M, Habich K, Oberholzer M, Heitz PU. Islet pathology and the pathogenesis of type 1 and type 2 diabetes mellitus revisited. Surv Synth Pathol Res. 1985; 4:110–25.

13. Chang HH, Kim JW, Rhu MS, Park CY, Oh SJ, Woo JT, Kim SW, Kim YS, Choi YK. Homeostasis model assessment in Korean type 2 diabetes patients. J Korean Diabetes Assoc. 2002; 26:296–305.

14. Park SM, Choi MK, Ahn SH, Kim YH, Park CH, Choi SB. The effects of dietary caloric distribution on insulin secretion and insulin resistance in Sprague dawley rats. J Nutr Health. 2001; 34:485–92.

15. Garg MK, Dutta MK, Mahalle N. Study of beta-cell function (by HOMA model) in metabolic syndrome. Indian J Endocrinol Metab. 2011; 15:S44–S9.

16. Robertson RP, Harmon J, Tran PO, Poitout V. Beta-cell glucose toxicity, lipotoxicity, and chronic oxidative stress in type 2 diabetes. Diabetes. 2004; 53:S119–S24.

17. Won KC. Oxidative stress in pancreatic islet beta-cells exposed to high glucose concentration. Diabetes Metab J. 2004; 28:250–4.

18. Sartorelli DS, Franco LJ, Damião R, Gimeno S, Cardoso MA, Ferreira SR. Dietary glycemic load, glycemic index, and refined grains intake are associated with reduced beta-cell function in prediabetic Japanese migrants. Arq Bras Endocrinol Metabol. 2009; 53:429–34.

19. Lee YM, Chung HK, Kimm HJ, Jee SH. The relationship between β-cell function and nutrient intakes in korean adult-using 4th Korea National Health and Nutrition Examination Survey 2009-. Korean J Community Nutr. 2012; 17:243–57.

20. Korean Diabetes Association: Treatment guideline for diabetes. 5th ed.Seoul: Gold' Planning and Development;2015. p. 31–7.

21. Davis JN, Ventura EE, Weigensberg MJ, Ball GD, Cruz ML, Shaibi GQ, Goran MI. The relation of sugar intake to cell function in overweight Latino children. Am J Clin Nutr. 2005; 82:1004–10.

22. Ludwig DS. The glycemic index physiological mechanisms relating to obesity, diabetes, and cardiovascular disease. JAMA. 2002; 287:2414–23.

23. Wolever TM, Mehling C. Long-term effect of varying the source or amount of dietary carbohydrate on postprandial plasma glucose, insulin, triacylglycerol, and free fatty acid concentrations in subjects with impaired glucose tolerance. Am J Clin Nutr. 2003; 77:612–21.

24. López S, Bermúdez B, Pacheco YM, Villar J, Abia R, Muriana FJ. Distinctive postprandial modulation of beta cell function and insulin sensitivity by dietary fats: monounsaturated compared with saturated fatty acids. Am J Clin Nutr. 2008; 88:638–44.

25. Gower BA, Goree LL, Chandler-Laney PC, Ellis AC, Casazza K, Granger WM. A higher-carbohydrate, lower-fat diet reduces fasting glucose concentration and improves β-cell function in individuals with impaired fasting glucose. Metabolism. 2012; 61:358–65.

26. McGarry JD, Dobbins RL. Fatty acids, lipotoxicity and insulin secretion. Diabetologia. 1999; 42:128–38.

27. Chung HK, Cho Y, Shin MJ. Alcohol use behaviors, fat intake and the function of pancreatic β-cells in non-obese, healthy Korean males: findings from 2010 Korea National Health and Nutrition Examination Survey. Ann Nutr Metab. 2013; 62:129–36.

28. Weinberg JM. Lipotoxicity. Kidney Int. 2006; 70:1560–6.

29. Chung HK, Kang JH, Shin MJ. Assessment for nutrient intakes in Korean women according to obesity and metabolic syndrome. Korean J Community Nutr. 2010; 15:694–703.

30. Welters HJ, Tadayyon M, Scarpello JH, Smith SA, Morgan NG. Monounsaturated fatty acids protect against beta-cell apoptosis induced by saturated fatty acids, serum withdrawal or cytokine exposure. FEBS Lett. 2004; 560:103–8.

31. Bonnefont-Rousselot D. The role of antioxidant micronutrients in the prevention of diabetic complications. Treat Endocrinol. 2004; 3:41–52.

32. Frei B, Stocker R, Ames BN. Antioxidant defenses and lipid peroxidation in human blood plasma. Proc Natl Acad Sci USA. 1988; 85:9748–52.

33. Malone WF. Studies evaluating antioxidants and beta-carotene as chemopreventives. Am J Clin Nutr. 1991; 53:305S–13S.

34. Sardaş S, Yilmaz M, Oztok U, Cakir N, Karakaya AE. Assessment of DNA strand breakage by comet assay in diabetic patients and the role of antioxidant supplementation. Mutat Res. 2001; 490:123–9.

35. Opara EC. Oxidative stress, micronutrients, diabetes mellitus and its complications. J R Soc Promot Health. 2002; 122:28–34.

36. Moore WT, Bowser SM, Fausnacht DW, Staley LL, Suh KS, Liu D. Beta cell function and the nutritional state: dietary factors that influence insulin secretion. Curr Diab Rep. 2015; 15:76.

37. Cade C, Norman AW. Rapid normalization/stimulation by 1,25-dihydroxyvitamin D3 of insulin secretion and glucose tolerance in the vitamin D-deficient rat. Endocrinology. 1987; 120:1490–7.

38. Kadowaki S, Norman AW. Dietary vitamin D is essential for normal insulin secretion from the perfused rat pancreas. J Clin Invest. 1984; 73:759–66.

39. Huber AM, Gershoff SN. Effect of zinc deficiency in rats on insulin release from the pancreas. J Nutr. 1973; 103:1739–44.

40. Isaia G, Giorgino R, Adami S. High prevalence of hypovitaminosis D in female type 2 diabetic population. Diabetes Care. 2001; 24:1496.

41. Hagström E, Hellman P, Lundgren E, Lind L, Arnlöv J. Serum calcium is independently associated with insulin sensitivity measured with euglycaemic hyperinsulinaemic clamp in a community-based cohort. Diabetologia. 2007; 50:317–24.

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