Menoufia Medical Journal

ORIGINAL ARTICLE
Year
: 2019  |  Volume : 32  |  Issue : 4  |  Page : 1338--1342

Visceral adiposity and insulin resistance in the prediction of gestational diabetes mellitus in early pregnancy: a prospective observational study


Osama A Elkelani1, Alaa E Elahalaby1, Ibrahim Saif Elnasr1, Abeer E Abo El-Fetouh2,  
1 Department of Obstetrics and Gynecology, Faculty of Medicine, Menoufia University, Shebin El-Kom, Menoufia, Egypt
2 Department of Obstetrics and Gynecology, Faculty of Medicine, Tanta University, Gharbia, Egypt

Correspondence Address:
Abeer E Abo El-Fetouh
Tanta, Gharbia
Egypt

Abstract

Objective The aim was to study the relationship between abdominal adiposity and insulin resistance in the prediction of gestational diabetes mellitus (GDM) in early pregnancy. Background There is a positive association between high prepregnancy BMI and risk of GDM. Patients and methods This prospective cohort study included 83 women at 11–14 weeks for abdominal adiposity measurement and at 16–22 weeks for oral glucose tolerance test measurement. The patients were divided into two groups: group 1included patients who did not develop GDM and group 2included patients who developed GDM. This study was conducted at the Obstetrics and Gynecology Department, Menoufia University Hospital between March 2015 and March 2017. Results There was a significant statistical difference between both groups as regards visceral adipose tissue (VAT) depth (P = 0.001) with a mean ± SD of VAT depth (5.85 ± 0.47) increase in group 2. There was a positive relationship between visceral adiposity and the homestatic model assessment of insulin resistance and a negative relationship between visceral adiposity and insulin sensitivity. The γ2 values examining the association between VAT depth and measured homestatic model assessment of insulin resistance or insulin sensitivity were higher than the γ2 examining the association between BMI and measured homestatic model assessment of insulin resistance or insulin sensitivity index. Conclusion Measurement of visceral adiposity during the 11–14 weeks' gestation by ultrasound might improve the performance of screening for GDM better than BMI.



How to cite this article:
Elkelani OA, Elahalaby AE, Elnasr IS, Abo El-Fetouh AE. Visceral adiposity and insulin resistance in the prediction of gestational diabetes mellitus in early pregnancy: a prospective observational study.Menoufia Med J 2019;32:1338-1342


How to cite this URL:
Elkelani OA, Elahalaby AE, Elnasr IS, Abo El-Fetouh AE. Visceral adiposity and insulin resistance in the prediction of gestational diabetes mellitus in early pregnancy: a prospective observational study. Menoufia Med J [serial online] 2019 [cited 2020 Apr 5 ];32:1338-1342
Available from: http://www.mmj.eg.net/text.asp?2019/32/4/1338/274235


Full Text



 Introduction



Gestational diabetes mellitus (GDM) affect 4–8% of pregnancies where maternal obesity and high prepregnancy BMI are considered major risk factors [1]. In the current practice, the 1-h glucose challenge test (GCT) is commonly used as a screening tool for GDM at 24–28 weeks' gestation, followed by a confirmatory 2-h oral glucose tolerance test (OGTT), or screening simply by a 2-h OGTT alone [2]. It is recommended to screen for GDM as early as possible in pregnancy because if we delay the screening to 24–28 weeks, it will make dietary and pharmacological therapy to be late which will affect the fetal growth or placental integrity [3]. General adiposity can be measured by prepregnancy BMI, and women with similar BMI values may have widely varying distributions of adipose tissue (AT) [4]. Excess visceral adipose tissue (VAT) is associated with dyslipidemia, insulin resistance, and high serum levels of free fatty acids [5]. Most obstetrical studies have used prepregnancy BMI to define the overweight and obese states [6]. Martin et al. [7] found that excess VAT depth in the first trimester of pregnancy is associated with hyperglycemia at 24–28 weeks' gestation. Insulin resistance assessment in the first trimester by using the homeostatic model assessment of insulin resistance (HOM-IR) or by insulin sensitivity index (ISI) appears to correlate well with the later development of GDM [8]. The aim of this study was to study the relationship between abdominal visceral adiposity and insulin resistance in the prediction of GDM in early pregnancy.

 Patients and Methods



This prospective cohort study was conducted at the Obstetrics and Gynecology Department, Menoufia University Hospital, on 83 pregnant women with viable singleton pregnancies for abdominal adiposity measurement at 11–14 weeks and then OGTT measurement at 16–22 weeks during the period between March 2015 and March 2017. The study protocol was reviewed and approved by the local ethics committee at our hospital. The study protocol was explained to the patients and informed written consent was taken from them after counseling and explanation of the benefits and unexpected risks of any procedure.

Women with pre-GDM, previous history of GDM, multiple pregnancies, and other medical disorders associated with pregnancy such as preeclampsia and antiphospholipid syndrome and patients under corticosteroid therapy were excluded. All patients were subjected to complete history taking, general examination, routine laboratory investigations, and ultrasound examination. The ultrasonographic examination was performed by experienced physicians to assess the subcutaneous adipose tissue (SAT) and VAT depth by using the machine IBE 2500D (MIS, Taiwan, China), China with curvilinear probe and 3.5–5.5 MHz frequency. Abdominal AT compartments were measured by ultrasound between 11 and 14 weeks' gestation [7]. SAT depth was distinguished and measured at the level of the linea alba and the umbilicus from the SAT layer to the outer border of the rectus abdominis muscle. In addition, VAT depth was distinguished and measured at the level of the linea alba from the inner border of the rectus abdominis muscle to the anterior wall of the abdominal aorta. Depth and zoom settings were standardized, such that the vertebral bodies were just visible and the aorta was at the bottom of the screen [7].

Then at 16–22 weeks gestation, the patients completed a 2 h 75 g OGTT and insulin resistance was estimated by homeostasis model assessment-insulin resistance (HOMA-IR) as well as by ISI. Each patient completed a 2 h, 75 g OGTT following an overnight fast. We measured the fasting, 1 h and 2 h serum glucose and serum insulin concentrations. The HOMA-IR and ISI at 0, 60, and 120 min were estimated. Glucose concentration was measured in mmol/l, so the data were converted to mg/dl to calculate the ISI. Insulin concentration was measured in pmol/l, so the data were converted to μU/ml to calculate the HOMA-IR [8]. The patients were then divided into two groups: group 1 included pregnant women who did not develop GDM and group 2 included pregnant women who developed GDM.

Statistical analysis

The collected data were tabulated and analyzed by SPSS V.20 (statistical package for the social sciences; SPSS Inc., Chicago, Illinois, USA). Quantitative data were expressed as mean and SD and analyzed by applying Student's t-test. Linear correlation coefficient (r) was used to test the relationship between SAT and VAT and ISI and HOMA-IR. P values less than 0.05 were used to determine the significance.

 Results



This study was conducted primarily on 110 pregnant women; five women were transferred to another hospital during the study and 22 women did not complete the OGTT. So, there were 83 pregnant women who completed the study with a mean age of 26.8 years. Thirty-three (40%) women were primigravida and 50 (60%) women were multigravida. Forty (48%) women had a previous cesarean section and 43 (52%) women had no previous CS. Twelve (14.5%) cases developed GDM and 71 (85.5%) cases did not develop GDM.

BMI was ranging from 20 to 30 in group 1 with mean ± SD of 23.32 ± 1.90, while it ranges from 24 to 43 in group 2 with mean ± SD of 33.92 ± 8.16 with a highly significant statistical difference (P = 0.001). There was a highly significant statistical difference between both groups as regards VAT, HOMA-IR, and ISI [Table 1]. In the current study, there was a positive relationship between visceral adiposity and HOMA-IR [Figure 1] and a negative relationship between visceral adiposity and insulin sensitivity [Figure 2]. In addition, there is no significant relationship between SAT and HOMA-IR and insulin sensitivity [Table 2].{Table 1}{Figure 1}{Figure 2}{Table 2}

The γ2 values which were used to examine the association between VAT depth and measured HOMA-IR or ISI were slightly higher than the γ2 which is used to examine the association between BMI and measured HOMA-IR or ISI [Table 3]. So, in this study, VAT explained the association between obesity and insulin resistance more efficiently than BMI.{Table 3}

 Discussion



Maternal obesity in pregnancy is a known risk factor for GDM, fetal macrosomia, and related adverse obstetrical outcomes. Obstetricians all over the world screen GDM routinely between 24 and 28 weeks of gestation as recommended in the guidelines. Recently, first-trimester assessment of insulin resistance by using HOMA-IR or ISI and VAT measurment appear to correlate well with the later development of GDM [9].

In our work, there was positive relationship between VAT and HOMA-IR with significant statistical difference. However, there is a negative relationship between VAT and ISI with significant statistical difference. Our result was in agreement with Gur et al. [10]. Their study was performed on 106 pregnant women between the ages of 18 and 40 years with singleton pregnancies from 4 to 14 weeks. They found that visceral fat thickness (VFT) in the early stage of gestation correlated with insulin resistance and hyperglycemia. Also, our result agreed with the results of Bartha et al. [11]. Their study performed on 30 pregnant women at 11–14 weeks of gestation. VFT and subcutaneous fat thickness (SFT) were measured by ultrasound. Fasting plasma glucose and insulin were measured. They found VFT that significantly correlated with insulinemia, glycemia, and insulin sensitivity. Insulin resistance was calculated by using the HOMA.

Martin et al. [7] performed a prospective cohort study on 62 pregnant women. Visceral fat was measured by ultrasonography at ±12 weeks' gestation. A 50-g GCT was performed at 24–28 weeks' gestation. They stated that VAT depth significantly correlated with a positive GCT in later pregnancy. In our results, we found that the VAT depth is significantly associated with positive OGTT in early pregnancy between 16 and 22 weeks. However, in Martin et al. [7] study, they found the same results in later pregnancy between 24 and 28 weeks [7].

Our result was not consistent with De Souza et al. [12]. They performed their study on 79 pregnant women. VAT depth was measured by ultrasonography at 11–14 weeks which ranged between 1.4 cm–9.1 cm with a mean of 3.9 ± 1.6 cm and then performed 75 g OGTT at 16–22 weeks to calculate HOMA-IR and ISI. They found that the VAT depth was not significantly correlated with HOMA-IR: each 1 cm increase in VAT depth was associated with an increase in HOMA-IR of 0.09. Each 1 cm increase in VAT depth was associated with a reduction in ISI of −0.09. In contrast to our study, Ross et al. [13] observed that VAT alone seemed to be an independent predictor of insulin resistance.

In our study, there was no significant relationship between SAT and ISI with no significant statistical difference. Also, there is no significant relationship between SAT and HOMA-IR without any significant statistical difference. Our result was in agreement with Bartha et al. [11]. In their study, they found that SFT is not significantly correlated with HOMA-IR. Also, our result was consistent with Martin et al. [7]. They found no significant association between SAT depth and HOMA-IR. In agreement with our work, Gur et al. [10] found that SFT was found to be similar in GDM and normal glucose metabolism. Forest et al. [14] determined that the SFT measurement was not effective in predicting DM, particularly in women. So, the effectiveness of the measurement is higher than those of waist/hip ratio and the WC. Contrary to our result, Ross et al. [13] found that subcutaneous AT of the abdomen was responsible for the association between abdominal obesity and insulin resistance. In this study, we found that the association between obesity and insulin resistance is better explained by VAT than BMI.

Our result was consistent with De Souza et al. [12]. They found that the γ2 value which was used to examine the association between VAT depth and the measured HOMA-IR (γ2 = 0.42) or ISI (γ2 = 0.36) is higher than the γ2 value which is used to examine the association between prepregnancy BMI and the measured HOMA-IR (γ2 = 0.40) or ISI (γ2 = 0.32). Bartha et al. [11] concluded that there was significant correlation between VFT and the metabolic risk factors than pregestational BMI and this was consistent with our result. Our result was in agreement withBrisson et al. [15]. They found that independent of BMI, visceral adiposity predicts insulin resistance and diabetes. So it was logic to use ultrasonography to measure visceral fat in relation to glucose intolerance in pregnancy. Our result was in agreement withGur et al. [10]. They studied that there were poor correlations between BMI and VFT, so VFT appeared to be a more sensitive predictor of GDM than BMI.

 Conclusion



From this study, we concluded that the measurement of VAT at 11–14 weeks' gestation by ultrasound might improve the performance of the screening for GDM and correlates well with metabolic risk factors better than BMI. Also, pregnant women with elevated visceral adiposity who are at high risk for GDM could benefit from either earlier screening or earlier dietary and lifestyle modifications. Women, who have been identified as having insulin resistance in early pregnancy, as indicated by increased VAT, may in the future be eligible for interventions in the first trimester of pregnancy aimed at lowering their risk of overt GDM and the perinatal complications associated with this diagnosis. However, this remains to be established in future large-scale prospective studies.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

References

1Morikawa M, Yamadia T, Sato S, Cho K, Minakami H. Prevalence of hyperglycemia during pregnancy according to maternal age and pre-pregnancy body mass index in Japan, 2001–2009. Int J Gynaecol Obstet 2012; 21:15–23.
2Retnakaran R, Qi Y, Sermer M, Connelly P, Hanley A, Zinman B. Glucose intolerance in pregnancy and future risk of pre-diabetes or diabetes. Diabetes Care 2008; 31:2026–2031.
3Canadian Diabetes Association Clinical Practice Guidelines Expert Committee. Canadian Diabetes Association 2013 clinical practice guidelines for the prevention and management of diabetes in Canada. Introduction. Can J Diabetes 2013; (Suppl 1):1–3.
4Chu S, Callaghan W, Kim S, Schmid C, Lau J, England L, et al. Maternal obesity and risk of gestational diabetes mellitus. Diabetes Care 2010; 30:2070–2076.
5Norman J, Reynolds R. The consequences of obesity and excess weight gain in pregnancy. Proc Nutr Soc 2011; 10:450–456.
6Romero-Corral A, Somers V, Sierra-Johnson J, Thomas R, Collazo-Clavell M, Korinek J, et al. Accuracy of body mass index in diagnosing obesity in the adult general population. Int J Obs (Lond) 2008; 32:959–966.
7Martin A, Berger H, Nisenbaum R, Lausman A, MacGarvie S, Crerar C, et al. Abdominal visceral adiposity in the first trimester predicts glucose intolerance in later pregnancy. Diabetes Care 2009; 32:1308–1310.
8Ozcimen E, Uckuyu A, Cifti F, Yanik F, Bakar C. Diagnosis of gestational diabetes mellitus by the use of the homeostasis model assessment insulin-resistance index in the first trimester. Gynecol Endocrinol 2008; 24:224–229.
9Koyanagi A, Zhang J, Dagvadorj A, Hirayama F, Shibuya K, Souza J, et al. Macrosomia in 23 developing countries: an analysis of a multicountry, facility-based, cross-sectional survey. Lancet 2013; 381:9865.
10Gur E, Ince O, Turan G, Karadeniz M, Tatar S, Celik E, et al. Ultrasonographic visceral fat thickness in the first trimester can predict metabolic syndrome and gestational diabetes mellitus. Endocrine 2014; 47:478–484.
11Bartha J, Marin-Segura P, Gonzalez-Gonzalez N, Wagner F, Aguilar-Diosdado M, Hervias-Vivancos B. Ultrasound evaluation of visceral fat and metabolic risk factors during early pregnancy. Obesity 2007; 15:2233–2239.
12De Souza L, Kogan E, Berger H, Alves J, Lebovic G, Retnakaran R, et al. Abdominal adiposity and insulin resistance in early pregnancy. J Obst Gynaecol Can 2014; 36:969–975.
13Ross R, Aru J, Freeman J, Hudson R, Janssen I. Abdominal adiposity and insulin resistance in obese men. Am J Physiol Endocrinol Metab 2002; 282:657–663.
14Forest J, Girouard J, Masse J, Moutquin JM, Kharfi A, Ness RB, et al. Early occurrence of metabolic syndrome after hypertension in pregnancy. Obstet Gynecol 2005; 105:1373–1380.
15Brisson D, Perron P, Guay S, Gaudet D, Bouchard L. The hypertriglyceridemicwaist phenotype and glucose intolerance in pregnancy. CMAJ 2010; 182:E722–E725.