VISCERAL ADIPOSITY INDEX: A SIMPLE TOOL FOR ASSESSING RISK OF TYPE 2 DIABETES MELLITUS
AbstractBackground: The prevalence of type 2 diabetes mellitus (T2DM) has increased recently in Pakistan. Visceral adiposity index (VAI) appears to be a better predictor for metabolic syndrome associated with insulin resistance. VAI has been shown to be linearly and positively associated with diabetes mellitus (DM) in many populations. It is, however, uncertain whether VAI could be associated with T2DM in the Pakistani adult population. Methods: This is a cross-sectional study of 300 outpatients with a newly diagnosed T2DM. Subjects were recruited from Lady Reading Hospital, Pakistan, during the period from April, 2020 to January, 2021. For all study subjects, anthropometric measurements were performed. Blood samples were collected for the assessment of high-density lipoproteins (HDL-C), triglycerides (TGs), glycated hemoglobin (HbA1c), and random blood glucose. Results: Participants with high VAI showed poor glycemic control. The number of patients with poor glycemic control increased across the VAI quartiles. VAI showed significant correlations with TGs (r=0.715, p=<0.001), total cholesterol (TC) (r=0.256, p=<0.001), low density lipoprotein (LDL-C) (r=0.154, p=0.007), uric acid (r=0.205, p=0.019), duration of diabetes (r=0.171, p=0.033), TSH (r=0.163, p=0.007), and random blood glucose (r=0.195, p=0.019). Conclusion: Our data suggest that VAI is significantly and positively correlated with the risk factors of DM such as random blood glucose, uric acid and TSH. The findings of the study do not imply a significant direct association between VAI and DM among the Pakistani adult population. Prospective-large scale studies can help inform an effectiveness of VAI for the prediction of the risk of T2DM among Pakistani population.
Stamler J, Vaccaro O, Neaton JD, Wentworth D. Diabetes, other risk factors, and 12-yr cardiovascular mortality for men screened in the Multiple Risk Factor Intervention Trial. Diabetes Care 1993;16(2):434–44.
Tancredi M, Rosengren A, Svensson AM, Kosiborod M, Pivodic A, Gudbjörnsdottir S, et al. Excess Mortality among Persons with Type 2 Diabetes. N Engl J Med 2015;373(18):1720–32.
Tobias DK, Pan A, Jackson CL, O'Reilly EJ, Ding EL, Willett WC, et al. Body-mass index and mortality among adults with incident type 2 diabetes. N Engl J Med 2014;370(3):233–44.
Nevill AM, Metsios GS. The need to redefine age- and gender-specific overweight and obese body mass index cutoff points. Nutr Diabetes 2015;5(11):e186.
Rothman KJ. BMI-related errors in the measurement of obesity. Int J Obes (Lond) 2008;32(Suppl 3):S56–9.
Bozorgmanesh M, Hadaegh F, Azizi F. Predictive performance of the visceral adiposity index for a visceral adiposity-related risk: type 2 diabetes. Lipids Health Dis 2011;10:88.
Cornier MA, Després JP, Davis N, Grossniklaus DA, Klein S, Lamarche B, et al. Assessing adiposity: a scientific statement from the American Heart Association. Circulation 2011;124(18):1996–2019.
Schulze MB, Thorand B, Fritsche A, Häring HU, Schick F, Zierer A, et al. Body adiposity index, body fat content and incidence of type 2 diabetes. Diabetologia 2012;55(6):1660–7.
Huang PL. A comprehensive definition for metabolic syndrome. Dis Model Mech 2009;2(5-6):231–7.
Amato MC, Giordano C. Visceral Adiposity Index: An Indicator of Adipose Tissue Dysfunction. Int J Endocrinol 2014;2014:730827.
Oh JY, Sung YA, Lee HJ. The visceral adiposity index as a predictor of insulin resistance in young women with polycystic ovary syndrome. Obesity (Silver Spring) 2013;21(8):1690–4.
Gârgavu SR, Clenciu D, Rosu MM, Tenea Cojan TS, Costache A, Vladu IM, et al. Visceral Adiposity Index (VAI) – a potential marker of cardiometabolic risk. Arch Balk Med Union 2018;53(2):246–51.
Goldani H, Adami FS, Antunes MT, Rosa LH, Fassina P, Quevedo Grave MT, et al. Applicatility of the visceral adiposity index (vai) in the prediction of the components of the metabolic syndrome in elderly. Nutr Hosp 2015;32(4):1609–15.
Randrianarisoa E, Lehn-Stefan A, Hieronimus A, Rietig R, Fritsche A, Machann J, et al. Visceral Adiposity Index as an Independent Marker of Subclinical Atherosclerosis in Individuals Prone to Diabetes Mellitus. J Atheroscler Thromb 2019;26(9):821–34.
Amato MC, Giordano C, Pitrone M, Galluzzo A. Cut-off points of the visceral adiposity index (VAI) identifying a visceral adipose dysfunction associated with cardiometabolic risk in a Caucasian Sicilian population. Lipids Health Dis 2011;10:183.
Saeedi P, Petersohn I, Salpea P, Malanda B, Karuranga S, Unwin N, et al. Global and regional diabetes prevalence estimates for 2019 and projections for 2030 and 2045: Results from the International Diabetes Federation Diabetes Atlas, 9(th) edition. Diabetes Res Clin Pract 2019;157:107843.
Basit A, Fawwad A, Qureshi H, Shera AS. Prevalence of diabetes, pre-diabetes and associated risk factors: second National Diabetes Survey of Pakistan (NDSP), 2016-2017. BMJ Open 2018;8(8):e020961.
Kahn SE, Hull RL, Utzschneider KM. Mechanisms linking obesity to insulin resistance and type 2 diabetes. Nature 2006;444(7121):840–6.
Frayn KN. Visceral fat and insulin resistance--causative or correlative? Br J Nutr 2000;83(Suppl 1):S71–7.
Cao YY, Tang X, Sun KX, Liu ZK, Xiang X, Juan J, et al. [Relationship between glycemic control and visceral adiposity index among the patients with type 2 diabetes mellitus]. Beijing Da Xue Xue Bao Yi Xue Ban 2017;49(3):446–50.
Alkhalaqi A, Al-Naimi F, Qassmi R, Shi Z, Ganji V, Salih R, et al. Visceral adiposity index is a better predictor of type 2 diabetes than body mass index in Qatari population. Medicine 2020;99(35):e21327.
Bowen ME, Xuan L, Lingvay I, Halm EA. Random blood glucose: a robust risk factor for type 2 diabetes. J Clin Endocrinol Metab 2015;100(4):1503–10.
Chaker L, Ligthart S, Korevaar TIM, Hofman A, Franco OH, Peeters RP, et al. Thyroid function and risk of type 2 diabetes: a population-based prospective cohort study. BMC Med 2016;14(1):150.
Canaris GJ, Manowitz NR, Mayor G, Ridgway EC. The Colorado thyroid disease prevalence study. Arch Intern Med 2000;160(4):526–34.
Bertrand C, Blanchet E, Pessemesse L, Annicotte JS, Feillet-Coudray C, Chabi B, et al. Mice lacking the p43 mitochondrial T3 receptor become glucose intolerant and insulin resistant during aging. PLoS One 2013;8(9):e75111.
Crunkhorn S, Patti ME. Links between thyroid hormone action, oxidative metabolism, and diabetes risk? Thyroid 2008;18(2):227–37.
Maratou E, Hadjidakis DJ, Kollias A, Tsegka K, Peppa M, Alevizaki M, et al. Studies of insulin resistance in patients with clinical and subclinical hypothyroidism. Eur J Endocrinol 2009;160(5):785–90.
Shah JH, Motto GS, Papagiannes E, Williams GA. Insulin metabolism in hypothyroidism. Diabetes 1975;24(10):922–5.
Stanická S, Vondra K, Pelikánová T, Vlcek P, Hill M, Zamrazil V. Insulin sensitivity and counter-regulatory hormones in hypothyroidism and during thyroid hormone replacement therapy. Clin Chem Lab Med 2005;43(7):715–20.
Chen RH, Chen HY, Man KM, Chen SJ, Chen W, Liu PL, et al. Thyroid diseases increased the risk of type 2 diabetes mellitus: A nation-wide cohort study. Medicine (Baltimore) 2019;98(20):e15631.
Dong H, Xu Y, Zhang X, Tian S. Visceral adiposity index is strongly associated with hyperuricemia independently of metabolic health and obesity phenotypes. Sci Rep 2017;7(1):8822.
Kim TH, Lee SS, Yoo JH, Kim SR, Yoo SJ, Song HC, et al. The relationship between the regional abdominal adipose tissue distribution and the serum uric acid levels in people with type 2 diabetes mellitus. Diabetol Metab Syndr 2012;4(1):3.
Xiong Q, Liu J, Xu Y. Effects of Uric Acid on Diabetes Mellitus and Its Chronic Complications. Int J Endocrinol 2019;2019:9691345.
Tassone EJ, Cimellaro A, Perticone M, Hribal ML, Sciacqua A, Andreozzi F, et al. Uric Acid Impairs Insulin Signaling by Promoting Enpp1 Binding to Insulin Receptor in Human Umbilical Vein Endothelial Cells. Front Endocrinol (Lausanne) 2018;9:98.
Katsiki N, Papanas N, Fonseca VA, Maltezos E, Mikhailidis DP. Uric acid and diabetes: Is there a link? Curr Pharm Des 2013;19(27):4930–7.
Journal of Ayub Medical College, Abbottabad is an OPEN ACCESS JOURNAL which means that all content is FREELY available without charge to all users whether registered with the journal or not. The work published by J Ayub Med Coll Abbottabad is licensed and distributed under the creative commons License CC BY ND Attribution-NoDerivs. Material printed in this journal is OPEN to access, and are FREE for use in academic and research work with proper citation. J Ayub Med Coll Abbottabad accepts only original material for publication with the understanding that except for abstracts, no part of the data has been published or will be submitted for publication elsewhere before appearing in J Ayub Med Coll Abbottabad. The Editorial Board of J Ayub Med Coll Abbottabad makes every effort to ensure the accuracy and authenticity of material printed in J Ayub Med Coll Abbottabad. However, conclusions and statements expressed are views of the authors and do not reflect the opinion/policy of J Ayub Med Coll Abbottabad or the Editorial Board.
USERS are allowed to read, download, copy, distribute, print, search, or link to the full texts of the articles, or use them for any other lawful purpose, without asking prior permission from the publisher or the author. This is in accordance with the BOAI definition of open access.
AUTHORS retain the rights of free downloading/unlimited e-print of full text and sharing/disseminating the article without any restriction, by any means including twitter, scholarly collaboration networks such as ResearchGate, Academia.eu, and social media sites such as Twitter, LinkedIn, Google Scholar and any other professional or academic networking site.