Anthropometric Measurements and Analysis Results of Metabolic Parameters of Those with Impaired Fasting Glucose and Impaired Glucose Tolerance

Aim: Prediabetes is when the blood glucose level is between the normal value and the diabetes mellitus (DM) cut-off value. It is a metabolic disorder characterized by insulin resistance due to pancreatic β-cell dysfunction caused by primary or secondary causes. It is important due to the possibility of developing DM. Materials and Methods: We aimed to compare anthropometric and metabolic parameters in prediabetics and patients who applied to the internal medicine clinic of … University Health Education and Research Hospital between 01.06.2018-01.09.2018 included. Prediabetic individuals were divided into three as impaired fasting glucose, impaired glucose tolerance, and combined. Results: Of the 64 patients in our study, 35 were female, and 29 were male. While the age, body mass index (BMI), waist circumference, HBA1c, and homeostatic model assessment (HOMA)values did not differ significantly between the two genders, weight, height, hip circumference, waist/hip, and waist/height ratio showed significant difference (respectively p=0,040, p<0.001, p=0,040, p <0.001, p=0.003). When metabolic parameters were analyzed in prediabetic groups, HBA1c and HOMA-IR values showed statistically significant differences (p<0.001, p=0.004, respectively). While there was no difference in BMI and waist circumference from anthropometric parameters, hip circumference, waist/hip values, and Waist/Height ratio differed significantly between the genders (p=0.174, p=0.849, p=0.040, p<0.001, p=0.003 respectively). Conclusion: In comparing anthropometric parameters with metabolic parameters in prediabetics, it is recommended that the waist/height value shows a significant difference between the metabolic parameters and HBA1c, HOMA values in the clinical follow-up and treatment of these prediabetic agents.

Keywords:

Prediabetes Impaired fasting glucose, Impaired Glucose Tolerance, Anthropometric Measurement,

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1. American Diabetes Association. Diagnosis and classification of diabetes mellitus. Diabetes Care. 2013 Jan;36 Suppl 1:S67-74. https://doi.org/10.2337/dc13-S067
2. Polonsky KS, Given BD, Hirsch L, et al. Quantitative study of insulin secretion and clearance in normal and obese subjects. J Clin Invest. 1988; 81:435–41. https://doi.org/10.1172/JCI113338
3. Buysschaert M, Medina JL, Bergman M, et al. Prediabetes and associated disorders. Endocrine. 2015; 48:371–393. DOI 10.1007/s12020-014-0436-2
4. Lamparter J, Raum P, Pfeiffer N, et al. Prevalence and associations of diabetic retinopathy in a large cohort of prediabetic subjects: the Gutenberg Health Study. J Diabetes Complications. 2014; 28:482–487. https://doi.org/10.1016/j.jdiacomp.2014.02.008
5. The prevalence of retinopathy in impaired glucose tolerance and recent-onset diabetes in the Diabetes Prevention Program. Diabet Med. 2007; 24:137–144. https://doi.org/10.1111/j.1464-5491.2007.02043.x
6. Echouffo-Tcheugui JB, Narayan KM, Weisman D, et al. Association between prediabetes and risk of chronic kidney disease: a systematic review and meta-analysis. Diabet Med. 2016; 33:1615–1624. https://doi.org/10.1111/dme.13113
7. Nasr G, Sliem H. Silent myocardial ischemia in prediabetics in relation to insulin resistance. J Cardiovasc Dis Res. 2010 Jul;1 (3):116–21. https://doi.org/10.4103/0975-3583.70903
8. Taylor SE, Accili D, Imae Y. Insulin resistance or insulin deficiency. Which is the primary cause of NIDDM? Diabetes. 1994;43:735–740. https://doi.org/10.2337/diab.43.6.735
9. Belfiore F, Iannello S, Volpicelli G. Insulin sensitivity indices calculated from basal and OGTT-induced insulin, glucose, and FFA levels. Mol Genet Metab. 1998;63:134–41. https://doi.org/10.1006/mgme.1997.2658
10. Tabak AG, Jokela M, Akbaraly TN, et al. Trajectories of glycaemia, insulin sensitivity, and insulin secretion before diagnosis of type 2 diabetes: an analysis from the Whitehall II study. Lancet. 2009;373:2215–21. https://doi.org/10.1016/S0140-6736 (09)60619-X
11. Mason CC, Hanson RL, Knowler WC. Progression to type 2 diabetes characterized by moderate then rapid glucose increases. Diabetes. 2007; 56:2054–61. https://doi.org/10.2337/db07-0053
12. Weir GC, Bonner-Weir S. Five stages of evolving beta-cell dysfunction during progression to diabetes. Diabetes. 2004;53 (Suppl 3):S16–S21. https://doi.org/10.2337/diabetes.53.suppl_3.s16
13. Maestre GE. Reduction of cognitive decline in patients with or at high risk for diabetes. Curr Geriatr Rep. 2017; 6:188–195. https://doi.org/10.1007/s13670-017-0216-y
14. Ferrannini E, Nannipieri M, Williams K, et al. Mode of onset of type 2 diabetes from normal or impaired glucose tolerance. Diabetes. 2004; 53:160–5. https://doi.org/10.2337/diabetes.53.1.160
15. Gnatiuc, L., Alegre-Díaz, J., Wade, R., Ramirez-Reyes, R., Tapia-Conyer, R., Garcilazo-Ávila, A., Chiquete, E., Gonzáles-Carballo, C., Solano-Sanchez, M., Clarke, R., Collins, R., Herrington, W. G., Hill, M., Lewington, S., Peto, R., Emberson, J. R., & Kuri-Morales, P. (2019). General and Abdominal Adiposity and Mortality in Mexico City: A Prospective Study of 150000 Adults. Annals of internal medicine, 171 (6), 397–405. https://doi.org/10.7326/M18-3502
16. Abdul-Ghani MA, Tripathy D, DeFronzo RA (2006) Contributions of {beta}-cell dysfunction and insulin resistance to the pathogenesis of impaired glucose tolerance and impaired fasting glucose. Diabetes Care 29 (5):1130–1139. https://doi.org/10.2337/dc05-2179
17. Davies MJ, Raymond NT, Day JL, Hales C, Burden AC (2000) Impaired glucose tolerance and fasting hyperglycaemia have different characteristics. Diabet Med 17:433–440. https://doi.org/10.1046/j.1464-5491.2000.00246.x
18. Shimokata H, Tobin JD, Muller DC et al. Studies in body fat distribution: I. Effects of age, sex, and obesity. Journal of Gerontology, 1989, 44 (2):M66‐73. https://doi.org/10.1093/geronj/44.2.m66
19. Behboudi-Gandevani S, Ramezani Tehrani F, Cheraghi L, Azizl F Could "a body shape index"and"waist to height ratio"predict Insulin resistance and metabolic syndrome in polycystic ovary syndrome? Eur J Obstet Gynecol Reprod Biol. 2016; 205:110-4. https://doi.org/10.1016/j.ejogrb.2016.08.011
20. Meigs JB, Muller DC, Nathan DM, Blake DR, Andres R. The natural history of progression from normal glucose tolerace to type 2 diabetes in the Baltimore longitudinal study of aging. Diabetes 2003; 52 (6):1475–1484. https://doi.org/10.2337/diabetes.52.6.1475
21. Knowler WC, Barrett-Connor E, Fowler SE, et al. Reduction in the incidence of type 2 diabetes with lifestyle intervention or metformin. N Engl J Med. 2002;346 (6):393–403. https://doi.org/10.1056/NEJMoa012512
22. Hostalek U, Gwilt M, Hildemann S. Therapeutic use of metformin in prediabetes and diabetes prevention. Drugs. 2015;75 (10):1071–1094. https://doi.org/10.1007/s40265-015-0416-8
23. Armato JP, DeFronzo RA, Abdul-Ghani M, et al. Successful treatment of prediabetes in clinical practice using physiological assessment (STOP DIABETES). Lancet Diabetes Endo. 2018; 6 (10):781–789. https://doi.org/10.1016/S2213-8587 (18)30234-1
24. Rijkelijkhuizen J, Nijpels J, Heine R, Bouter L, Stehouwer C, Dekker J. High risk of cardiovascular mortality in individuals with impaired fasting glucose is explained by conversion to diabetes: the Hoorn study. Diabetes Care. 2007; 30 (2):332–336. https://doi.org/10.2337/dc06-1238
25. Papa G, Degano C, Iurato MP, Licciardello C, Maiorana R, Finocchiaro C. Macrovascular complication phenotypes in type 2 diabetic patients. Cardiovasc Diabetol. 2013; 12:20. https://doi.org/10.1186/1475-2840-12-20