Serum Free Zinc as A Predictor for Excessive Function of Pancreatic Beta-Cells in Central-Obese Men

Miftakh Nur Rahman, Indriyanti Rafi Sukmawati, Irma Melyani Puspitasari, Miswar Fattah

Abstract


BACKGROUND: Central obesity is known as a risk factor for type 2 diabetes mellitus (T2DM). Its development is influenced by many factors such as a progressive failure of pancreatic beta cell function. The beta cells increase their function to secret insulin along T2DM development to compensate before it becomes exhausted. Zinc (Zn) plays a crucial role in beta cell function and insulin secretion. The majority of Zn in serum are bound to protein which is not readily available interact with cells. The free Zn in serum has been suggested as being more representative than total Zn in beta cell function. This research aimed to investigate the correlation between serum free Zn and homeostasis model assessment for beta cell function (HOMA-B) and to predict the pancreatic beta cell function in the development of T2DM.

METHODS: This study was designed as an observational with a cross-sectional approach. The subjects were centrally obese men aged 30-50 years and who had met the inclusion and exclusion criteria from the screening tests. Control subjects were lean men without T2DM. Serum free Zn and serum total Zn were measured by using inductively coupled plasma-mass spectrometry (ICP-MS).

RESULTS: There was positive correlation between serum free Zn and HOMA-B (R=0.361, p-value<0.001) but there was no correlation between serum total Zn and HOMA-B (R=-0.062, p-value=0.563). This study found that if the concentration of serum free Zn >1.7 ug/dL in central obese men was suggested as an excessive function of pancreatic beta cell and as an early warning before its exhausted.

CONCLUSION: This study suggested that serum free Zn had a correlation with beta cell function and had a predictive ability for beta cell excessive function before its exhausted.

KEYWORDS: Type 2 diabetes mellitus, HOMA-B, serum free zinc, central obesity

 


Full Text:

PDF

References


Castro AVB, Kolka CM, Kim SP, Bergman RN. Obesity, insulin resistance and comorbidities – Mechanisms of association. Arq Bras Endocrinol Metabol. 2014; 58: 600-9, CrossRef.

Ye J, McGuinness OP. Inflammation during obesity is not all bad: evidence from animal and human studies. Am J Physiol Endocrinol Metab. 2013; 304: E466-77, CrossRef.

Gerber PA, Rutter GA. The role of oxidative stress and hypoxia in pancreatic beta-cell dysfunction in diabetes mellitus. Antioxid Redox Signal. 2016; 26: 501-18, CrossRef.

Grarup N, Sandholt CH, Hansen T, Pedersen O. Genetic susceptibility to type 2 diabetes and obesity: from genome-wide association studies to rare variants and beyond. Diabetologia. 2014; 57: 1528-41, CrossRef.

Russo GT, Giorda CB, Cercone S, Nicolucci A, Cucinotta D, Group on behalf of BS. Factors associated with beta-cell dysfunction in type 2 diabetes: The BETADECLINE study. PLOS ONE. 2014; 9(10):e109702, CrossRef.

Weir GC, Bonner-Weir S. Five stages of evolving beta-cell dysfunction during progression to diabetes. Diabetes. 2004; 53 (Suppl. 3): S16-21, CrossRef.

Butler AE, Janson J, Bonner-Weir S, Ritzel R, Rizza RA, Butler PC. Beta-cell deficit and increased beta-cell apoptosis in humans with type 2 diabetes. Diabetes. 2003; 52: 102-10, CrossRef.

Butler AE, Dhawan S. β-cell identity in type 2 diabetes: lost or found? Diabetes. 2015; 64: 2698-700, CrossRef.

Maret W. Zinc in pancreatic islet biology, insulin sensitivity, and diabetes. Prev Nutr Food Sci. 2017; 22: 1–8, CrossRef.

Fukunaka A, Fujitani Y. Role of zinc homeostasis in the pathogenesis of diabetes and obesity. Int J Mol Sci. 2018; 19: 476, CrossRef.

Kaur K, Gupta R, Saraf SA, Saraf SK. Zinc: the metal of life. Compr Rev Food Sci Food Saf. 2014; 13: 358-76, CrossRef.

Hoeger J, Simon TP, Doemming S, Thiele C, Marx G, Schuerholz T, et al. Alterations in zinc binding capacity, free zinc levels and total serum zinc in a porcine model of sepsis. Biometals Int J Role Met Ions Biol Biochem Med. 2015; 28: 693-700, CrossRef.

International Obesity Task Force. The Asia Pacific Perspective: Redifining Obesity and Its Treatment. Geneva: WHO; 2000, article.

American Diabetes Association. Classification and diagnosis of diabetes. Diabetes Care. 2016; 39 (Suppl. 1): S13-22, CrossRef.

Charan J, Biswas T. How to calculate sample size for different study designs in medical research? Indian J Psychol Med. 2013; 35: 121-6, CrossRef.

Wallace TM, Levy JC, Matthews DR. Use and abuse of HOMA modeling. Diabetes Care. 2004; 27: 1487-95, CrossRef.

Tjokroprawiro A. Formula Klinik Praktis Bidang DiabetologiEndokrinologi-Metabolisme. 5th Edition. Surabaya: Pusat Diabetes dan Nutrisi Surabaya-FK Unair-RSUD Dr. Soetomo; 2017.

Foster M, Samman S. Zinc and regulation of inflammatory cytokines: implications for cardiometabolic disease. Nutrients. 2012; 4: 676- 94, CrossRef.

Rutter GA, Chabosseau P, Bellomo EA, Maret W, Mitchell RK, Hodson DJ, et al. Intracellular zinc in insulin secretion and action: a determinant of diabetes risk? Proc Nutr Soc. 2016; 75: 61-72, CrossRef.

Ashcroft FM, Rorsman P. Diabetes mellitus and the β cell: the last ten years. Cell. 2012; 148: 1160-71, CrossRef.




DOI: https://doi.org/10.18585/inabj.v11i3.618

Copyright (c) 2019 The Prodia Education and Research Institute

Creative Commons License
This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.

 

Indexed by:

                  

               

                   

 

 

The Prodia Education and Research Institute