Int J Diabetes Dev Ctries (October–December 2015) 35(4):439–447

DOI 10.1007/s13410-015-0302-7

ORIGINAL ARTICLE

Association of abdominal obesity, hypertriglyceridemia,

and hypertriglyceridemic waist phenotype with hypertension
and type 2 diabetes mellitus
Surapon Tangvarasittichai & Chintana Seangsuk &
Chaiwat Chaisomboon & Suwadee Meemark &
Orathai Tangvarasittichai

Received: 12 June 2013 / Accepted: 14 January 2015 / Published online: 17 March 2015
# Research Society for Study of Diabetes in India 2015

Abstract The present study tested the hypothesis that simple Abbreviations
variables, such as waist circumference, hypertriglyceridemia AO Abdominal obesity
(eTG), and hypertriglyceridemic waist (eTGWC) phenotype eTG Hypertriglyceridemia
could be used as screening tools for the identification of those eTGWC Hypertriglyceridemic waist phenotype
at high risk in hypertension (HT) and type 2 diabetes mellitus T2DM Type 2 diabetes mellitus
(T2DM). Based on data from our health survey, check of 4206 HT Hypertension
participants (997 men and 3209 women) were 420 (42.1 %) CVD Cardiovascular disease
and 2394 (74.6 %) AO men and women, 370 (37.1 %) and WC Waist circumference
1340 (41.8 %) eTG men and women, and 236 (23.7 %) and SBP Systolic blood pressure
1131 (35.2 %) eTGWC men and women. We demonstrated DBP Diastolic blood pressure
that AO, eTG, and eTGWC phenotype associated with in- Glu Fasting blood glucose
creased risk of HT and T2DM. In men, the largest area under TC Total cholesterol
curve (AUC) of the receiver operating characteristic (ROC) TG Triglyceride
curves demonstrated that AO was the best marker for HT and HDL-C High-density lipoprotein-cholesterol
eTG was the best marker for T2DM in men, while eTGWC LDL-C Low-density lipoprotein-cholesterol
was the best marker for both HT and T2DM in women. In OR Odds ratio
conclusion, it is suggested AO may serve as the early 95 % CI 95 % confident interval
phenotype-associated sequel to eTG reach to eTGWC. Waist
circumference measurements and fasting triglycerides can
serve as inexpensive screening tools for HT and T2DM to
Introduction
identify those at high risk of HT and T2DM.
Hypertension (HT) and diabetes mellitus (T2DM) are public
Keywords Abdominal obesity . Waist circumference . health concern in both developed and developing countries.
Hypertriglyceremia . Hypertriglyceridemic waist . Obesity is considered to be the link between insulin resistance
Hypertension . Type 2 diabetes mellitus and metabolic abnormalities inclusive of diabetes, hyperten-
sion, and dyslipidemia, all of which are risk factors for coro-
S. Tangvarasittichai (*) : C. Seangsuk : C. Chaisomboon : nary artery disease (CAD). Obesity has now become an im-
O. Tangvarasittichai
portant health problem in developing countries particularly in
Chronic Disease Research Unit, Department of Medical Technology,
Faculty of Allied Health Sciences, Naresuan University, Thailand, which is currently experiencing a rapid epidemio-
Phitsanulok 65000, Thailand logical transition. Clinical evidence proved that abdominal
e-mail: surapon14t@yahoo.com obesity (AO) is a strong predictor of adverse cardiovascular
disease (CVD) outcomes and risk of T2DM [1, 2]. The devel-
S. Meemark
Health Promotion Center, Faculty of Allied Health Sciences, opment of AO promotes insulin resistance and risk factors for
Naresuan University, Phitsanulok 65000, Thailand CVD, inflammation, and/or altered hemostasis [3]. However,
440
increased risk for CVD associated with insulin resistance (IR)
states begins long before patients could be clinically diag-
nosed of T2DM [4]. AO and hypertriglyceridemia (eTG) are
the major components of metabolic syndrome (MetS) [5]
whose joint role is demonstrated in CVD. Both AO and MetS
are pathophysiologically linked to IR [6]. Many studies have
shown a positive association of eTG with CVD risk factors
[7]. Both AO and eTG are independent risk factors for CVD
and have potential role in identifying subjects at risk for car-
diovascular events [8, 9]. Excess intra-abdominal adiposity
increases overall cardiometabolic risk through the alterations
in the secretion of adipokines. These include increased secre-
tion of free fatty acids (which can induce IR in muscle and β-
cell toxicity in the pancreas), inflammatory mediators
(TNF-α, IL-6, resistin, and plasminogen activator inhibitor)
and decreased secretion of adiponectin (cardioprotective
adipokine) [10, 11].
AO and eTG are interrelated metabolic disorders [12]. TG
is a surrogate marker for atherogenic disturbances in lipopro-
tein moieties that are found to be associated with increased
abdominal fat and IR [13]. Understanding the role of the joint
occurrence of eTG and AO may provide useful HT and T2DM
prevention approaches. Okosun and Boltri [14] demonstrated
that the comorbid condition of eTG and large AO was shown
as hypertriglyceridemic waist (eTGWC) phenotype and the
association of joint occurrence of AO (waist circumference
(WC) of ≥90 cm in men, and ≥80 cm in women [15]), eTG
(≥1.69 mmol/l or 150 mg/dl), and eTGWC with T2DM was
used as markers. TG is a major lipid in chylomicrons and
very-low-density lipoprotein particles. A TG level of less than
1.69 mmol/l (150 mg/dl) is considered normal [12]. eTGWC
phenotype is a marker of the atherogenic metabolic triad that
includes hyperinsulinemia, hyperapolipoprotenemia, and
small density low-density lipoprotein cholesterol [13, 16].
Our present study tested the hypothesis that simple variables,
such as WC, eTG, and eTGWC phenotypes, could be used as
screening tools for the identification of those at high risk of
HT and T2DM.
Material and methods
Subjects
A total of 4206 participants were included in this study. Sam-
pling criteria was person aged ≥40 years from seven provinces
of the Lower Northern Region of Thailand (Phitsanulok,
Phichit, Kampaengpetch, Uttraradit, Nakhornsawan,
Uthaithani, and Phechabun Provinces), by using survey data
from a project of the Mobile Unit for Health and Occupation
Development of Naresuan University (Fig. 1). All participants
had the medical examination in the morning. Detailed infor-
mation including smoking, alcohol drinking, and medical
Int J Diabetes Dev Ctries (October–December 2015) 35(4):439–447
history was collected in the questionnaire. Data were collected
as a cross-sectional health survey during 2008–2011. All par-
ticipants provided written informed consent, and the Ethics
committees of the Naresuan University approved the study
protocol. Four hundred and sixty-three participants had
known end-stage renal failure, cancer, infection, and any
life-threatening diseases that were excluded from the study.
Anthropometric measurement
The participants’ WC was measured at their midsection be-
tween the rib cage and the top of the lateral border of the iliac
crest during relaxed respiration. The blood pressure was taken
after the participants were seated and rested for 5 min. Blood
pressure was measured twice at 5-min intervals with a digital
blood pressure monitor (ES-P 110, Terumo cooperation, Ja-
pan). The average of the two measurements was used for data
analysis.
Biochemical measurements
Blood samples were collected from participants in the morn-
ing after an overnight fasting. The fasting time was verified
before the blood specimen was taken. Biochemical examina-
tions included fasting glucose (Glu; GOD-PAP method), total
cholesterol (TC; CHOD-PAP method), and triglyceride (TG;
GPO-PAP method), as well as high-density lipoprotein cho-
lesterol (HDL-C) which were performed by using a homoge-
neous enzymatic methods on the Photometer Humanlyzer
2000 (Human, Wiesbaden, Germany). We calculated the
low-density lipoprotein cholesterol (LDL-C) with
Friedewald’s formula in specimens with TG levels less than
4.52 mmol/l (<400 mg/dl). All determinations were performed
at the site in each survey. The control material was Humatrol
(Human, Wiesbaden, Germany). The intra- and inter-assay
coefficients of variation (CV) of glucose, total cholesterol,
triglyceride, and HDL-C levels were 2.43, 3.86, 3.48, 3.21,
and 4.74, and 4.43, 5.38, and 4.12 %, respectively.
Definition of terms
Abdominal obesity was defined as waist circumference values
of ≥90 and ≥80 cm in men and women, respectively [5].
Hypertriglyceridemia was defined as TG levels of
1.69 mmol/l (150 mg/dl) or greater [12, 16].
Hypertriglyceridemic waist phenotype was defined as co-
occurrence of eTG and AO [12, 14]. T2DM was defined as
diagnosed diabetes on insulin or other hypoglycemic agents or
fasting blood glucose value ≥6.93 mmol/l (126 mg/dl) or an
oral glucose tolerance test ≥11.0 mmol/l (200 mg/dl) [17].
Hypertension was defined as an average blood pressure (BP)
≥1 40/9 0 mmHg or i f t he participant was taking
Int J Diabetes Dev Ctries (October–December 2015) 35(4):439–447
Fig 1 Demographic map of the
seven provinces (star mark) of
Lower Northern Thailand in the
present study
antihypertensive medications or had been diagnosed with hy-
pertension [18].
Statistical analysis
Categorical data are presented as percentages, and continuous
data are presented as median and interquartile range for these
non-normally distributed data and were tested by using
Shapiro-Wilk test. Comparisons between groups were per-
formed using the Mann-Whitney U test. Odds ratios (OR)
from logistic regression analyses were used to estimate the
risk of HT and T2DM; those were associated with AO, eTG,
and eTGWC. We also used the receiver operating
441
characteristic (ROC) curve for comparison of AO, eTG, and
eTGWC phenotypes (markers). An ROC curve is a plot be-
tween sensitivity (Y-axis) versus false positive (X-axis). Areas
under the curve (AUC) of the ROC curves and their 95 %
confidence intervals (CI) were evaluated as a measure of di-
agnostic accuracy. The discrimination analysis was performed
to identify AO, eTG, and eTGWC phenotypes (markers) that
provided the best identification of HT and T2DM. Greater
AUC of ROC curve indicated better markers of the study. In
general, an AUC of a ROC of 0.5 suggests no discrimination,
whereas a maximal AUC of a ROC of 1 suggests outstanding
discrimination [19]. The results of all analyses were evaluated
for statistical significance using p value <0.05. All analysis
442 Int J Diabetes Dev Ctries (October–December 2015) 35(4):439–447

Table 1 Comparison of general characteristics of abdominal obesity with non-abdominal obese participants

Variables All man participants All woman participants

AO (n=420) Non-AO (n=577) p value AO (n=2394) Non-AO (n=815) p value

Age (year) 55.0 (46.0–62.0) 55.0 (46.5–63.0) 0.669 51.0 (43.0–59.0) 48.0 (41.0–58.0) <0.001
WC (cm) 95.0 (91.6–99.0) 83.0 (78.0–87.0) <0.001 89.0 (84.0–95.0) 77.0 (74.0–78.0) <0.001
SBP (mmHg) 135.0 (126.3–142.0) 127.0 (118.0–135.0) <0.001 127.0 (114.0–137.0) 121.0 (110.0–128.0) <0.001
DBP (mmHg) 84.0 (76.0–88.0) 77.0 (69.0–82.0) <0.001 80.0 (73.0–87.0) 75.0 (68.0–80.0) <0.001
Glu (mmol/l) 5.39 (4.84–5.89) 5.28 (4.73–5.67) 0.007 5.23 (4.79–5.72) 5.06 (4.68–5.50) <0.001
TC (mmol/l) 5.42 (4.80–6.30) 4.85 (4.39–5.52) <0.001 5.30 (4.64–6.09) 4.90 (4.44–5.50) <0.001
TG (mmol/l) 2.14 (1.58–2.81) 1.47 (1.17–1.91) <0.001 1.65 (1.23–2.19) 1.34 (1.07–1.71) <0.001
HDL-C (mmol/l) 1.37 (1.11–1.61) 1.52 (1.28–1.77) <0.001 1.53 (1.30–1.79) 1.67 (1.43–1.92) <0.001
LDL-C (mmol/l) 2.98 (2.35–3.72) 2.62 (2.16–3.22) <0.001 2.95 (2.31–3.67) 2.60 (2.14–3.19) <0.001
Drinking (%) 68.1 10.9 <0.001 17.3 6.3 <0.001
Smoking (%) 68.8 34.3 <0.001 28.3 11.0 <0.001
Diabetes (%) 20.2 7.8 <0.001 23.6 14.9 <0.001
Hypertension (%) 40.7 15.42 <0.001 24.4 16.3 <0.001

WC waist circumference, SBP systolic blood pressure, DBP diastolic blood pressure, Glu fasting blood glucose, TC total cholesterol, TG triglyceride,
HDL-C high density lipoprotein-cholesterol; LDL-C, low density lipoprotein-cholesterol

was performed using the SPSS computer program version
13.0 (SPSS, Chicago, IL).
Results
The characteristics of the total 4206 eligible participants
consisted of 997 (23.7 %) men and 3209 (76.3 %) women.
The prevalence of AO phenotype was 420 (42.1 %) in men
and 2394 (74.6 %) in women, eTG phenotype was 370
(37.1 %) in men and 1340 (41.8 %) in women, and eTGWC
phenotype was 236 (23.7 %) in men and 1131 (35.2 %) in
women. Participants with AO phenotype demonstrated that
WC, systolic BP (SBP), diastolic BP (DBP), Glu, TC, TG,
LDL-C, number of alcohol drinking, smoking, HT, and
T2DM were significantly higher and lower in HDL-C
(p<0.05). Women AO phenotype was significantly older
and also higher in the same variables in men than non-AO

Table 2 Comparison of general characteristics of hypertriglyceridemia with non-hypertriglyceridemia participants

Variables All man participants All woman participants

eTG (n=370) Non-eTG (n=627) p value eTG (n=1340) Non-eTG (n=1869) p value

Age (year) 54.0 (45.0–61.0) 56.0 (47.0–63.0) 0.051 54.0 (46.0–63.0) 48.0 (41.0–56.0) <0.001
WC (cm) 91.0 (87.0–96.0) 86.0 (79.0–91.0) <0.001 88.0 (82.0–94.0) 84.0 (78.0–92.0) <0.001
SBP (mmHg) 135.0 (124.0–142.0) 127.0 (119.0–136.0) <0.001 130.0 (119.0–140.0) 121.0 (110.0–129.0) <0.001
DBP (mmHg) 85.0 (76.0–88.0) 78.0 (69.0–82.0) <0.001 82.0 (74.0–88.0) 77.0 (70.0–82.0) <0.001
Glu (mmol/l) 5.39 (4.90–5.90) 5.28 (4.73–5.72) 0.007 5.28 (4.84–5.83) 5.12 (4.68–5.56) <0.001
TC ( mmol/l) 5.55 (4.88–6.51) 4.82 (4.36–5.52) <0.001 5.55 (4.83–6.35) 4.98 (4.46–5.62) <0.001
TG ( mmol/l) 2.59 (2.27–3.23) 1.37 (1.15–1.65) <0.001 2.19 (1.91–2.74) 1.23 (1.03–1.44) <0.001
HDL-C (mmol/l) 1.23 (1.00–1.53) 1.55 (1.35–1.78) <0.001 1.38 (1.23–1.62) 1.68 (1.45–1.92) <0.001
LDL-C (mmol/l) 2.96 (2.24–3.71) 2.65 (2.2–3.28) <0.001 2.97 (2.35–3.78) 2.76 (2.22–3.42) <0.001
Drinking (%) 68.7 15.2 <0.001 24.2 21.8 0.118
Smoking (%) 96.5 20.8 <0.001 22.8 20.4 0.103
Diabetes (%) 22.4 7.5 <0.001 21.5 9.5 <0.001
Hypertension (%) 41.9 16.8 <0.001 33.0 17.4 <0.001

WC waist circumference, SBP systolic blood pressure, DBP diastolic blood pressure, Glu fasting blood glucose, TC total cholesterol, TG triglyceride,
HDL-C high density lipoprotein-cholesterol, LDL-C low density lipoprotein-cholesterol, eTG hypertriglyceridemia
Int J Diabetes Dev Ctries (October–December 2015) 35(4):439–447 443

Table 3 Comparison of general characteristics of hypertriglyceridemic waist with non-hypertriglyceridemic waist participants

Variables All man participants All woman participants

eTGWC (n=236) Non-eTGWC (n=761) p value eTGWC (n=1131) Non-eTGWC (n=2078) p value

Age (year) 54.0 (45.0–60.0) 55.0 (47.0–63.0) 0.023 54.0 (46.0–63.0) 48.0 (41.0–57.0) <0.001
WC (cm) 95.0 (92.0–98.0) 86.0 (79.0–89.3) <0.001 89.0 (85.0–96.0) 82.0 (78.0–91.0) <0.001
SBP (mmHg) 137.0 (130.0–142.0) 128.0 (120.0–137.0) <0.001 131.0 (120.0–140.0) 121.0 (110.0–130.0) <0.001
DBP (mmHg) 85.0 (79.0–89.0) 78.0 (70.0–83.5) <0.001 84.0 (76.0–88.0) 77.0 (70.0–82.0) <0.001
Glu (mmol/l) 5.45 (4.95–6.04) 5.28 (4.73–5.72) <0.001 5.28 (4.84–5.83) 5.12 (4.68–5.56) <0.001
TC (mmol/l) 5.62 (5.01–6.66) 4.90 (4.41–5.62) <0.001 5.62 (4.88–6.40) 5.01 (4.49–5.65) <0.001
TG (mmol/l) 2.70 (2.33–3.28) 1.48 (1.19–1.84) <0.001 2.24 (1.94–2.79) 1.28 (1.06–1.51) <0.001
HDL-C (mmol/l) 1.20 (0.99–1.54) 1.50 (1.30–1.74) <0.001 1.37 (1.23–1.61) 1.67 (1.45–1.92) <0.001
LDL-C (mmol/l) 2.98 (2.29–3.86) 2.67 (2.20–3.34) <0.001 3.04 (2.38–3.80) 2.76 (2.22–3.43) <0.001
Drinking (%) 94.9 16.4 <0.001 23.6 22.4 0.428
Smoking (%) 97.5 33.8 <0.001 22.1 21.1 0.498
Diabetes (%) 26.3 8.9 <0.001 23.5 9.6 <0.001
Hypertension (%) 46.7 19.8 <0.001 35.2 17.8 <0.001

WC waist circumference, SBP systolic blood pressure, DBP diastolic blood pressure, Glu fasting blood glucose, TC total cholesterol, TG triglyceride,
HDL-C high density lipoprotein-cholesterol, LDL-C low density lipoprotein-cholesterol, eTGWC hypertriglyceridemic waist

phenotype as shown in Table 1 (p<0.05). Participants with (p<0.05). Women with eTG phenotype were significantly
eTG phenotype demonstrated that WC, SBP, DBP, Glu, TC, older than non-eTG phenotype as shown in Table 2
TG, LDL-C, number of alcohol drinking, smoking, HT, and (p<0.05). The number of alcohol drinking and smoking was
T2DM were also significantly higher and lower in HDL-C not significantly different in women with eTG (p<0.05).

Table 4 Bivariate correlation of variables among abdominal obesity participants

Correlation between Correlation coefficient Correlation between Correlation coefficient

parameters (men) parameters (women)
r p value r p value

WC Diast BP 0.124 0.011 WC Diast BP 0.169 <0.001

HDL-C −0.106 0.030 Glu Glu 0.185 <0.001
Glu TG 0.167 0.001 Syst BP 0.163 <0.001
HDL-C −0.112 0.022 TC 0.111 <0.001
TG Syst BP 0.149 0.002 TG 0.108 0.001
Diast BP 0.287 <0.001 TG Age 0.257 <0.001
TC 0.293 <0.001 Syst BP 0.280 <0.001
HDL-C −0.407 <0.001 Diast BP 0.242 <0.001
HDL-C Syst BP −0.107 0.028 TC 0.286 <0.001
Diast BP −0.191 <0.001 HDL-C −0.465 <0.001
TC Syst BP 0.178 <0.001 HDL-C Age −0.138 <0.001
Diast BP 0.212 <0.001 Syst BP −0.194 <0.001
LDL-C 0.860 <0.001 Diast BP −0.186 <0.001
LDL-C Syst BP 0.155 0.001 LDL-C −0.121 <0.001
Diast BP 0.158 0.001 TC Age 0.250 <0.001
Syst BP 0.187 <0.001
Diast BP 0.164 <0.001
LDL-C 0.903 <0.001
LDL-C Age 0.198 <0.001
Syst BP 0.147 0.001
Diast BP 0.134 0.001
444 Int J Diabetes Dev Ctries (October–December 2015) 35(4):439–447

Table 5 Impact of the association of abdominal obesity, hypertriglyceridemia, and hypertriglyceridemic waist phenotype with hypertension and type 2
diabetes mellitus

Abdominal obesity OR (men) 95 % confidence p value OR (women) 95 % confidence p value

interval (CI) interval (CI)

Model 1
Hypertension 3.14 2.14–4.59 <0.001 2.59 2.02–3.31 <0.001
Diabetes 1.86 1.13–3.06 0.015 2.39 1.75–3.29 <0.001
Hypertriglyceridemia 1.27 0.75–2.17 0.377 1.91 1.57–2.32 <0.001
Decreased HDL-C 1.02 0.62–1.67 0.943 1.34 1.06–1.70 0.016
Hypercholesterolemia 1.58 0.99–2.52 0.053 1.61 1.35–1.92 <0.001
Drinking 24.96 15.32–40.66 <0.001 0.41 0.24–0.69 0.001
Smoking 0.41 0.23–0.72 0.002 4.32 2.49–7.51 <0.001
Age 1.00 0.99–1.02 0.669 0.99 0.99–1.01 0.182
Model 2
Hypertension 1.77 1.09–2.86 0.020 1.54 1.28–1.85 <0.001
Diabetes 2.94 1.51–5.73 0.002 1.47 1.17–1.84 0.001
Abdominal obesity 1.31 0.72–2.38 0.372 1.87 1.54–2.28 <0.001
Decreased HDL-C 14.59 6.74–31.58 <0.001 5.11 4.19–6.22 <0.001
Hypercholesterolemia 2.99 1.65–5.41 <0.001 2.22 1.88–2.61 <0.001
Drinking 1.43 0.76–2.68 0.263 1.14 0.66–1.98 0.633
Smoking 88.58 42.38–185.16 <0.001 1.01 0.58–1.77 0.967
Age 0.99 0.97–1.01 0.458 1.02 1.02–1.04 <0.001
Model 3
Hypertension 1.74 11.07–2.84 0.025 1.84 1.54–2.21 <0.001
Diabetes 2.07 1.13–3.79 0.018 1.87 1.49–2.33 <0.001
Decreased HDL-C 5.24 2.80–9.81 <0.001 4.67 3.86–5.64 <0.001
Hypercholesterolemia 2.13 1.19–3.79 0.010 2.41 2.03–2.85 <0.001
Drinking 44.14 21.79–89.39 <0.001 1.16 0.67–1.99 0.594
Smoking 7.94 3.18–19.79 <0.001 0.97 0.56–1.68 0.906
Age 0.99 0.97–1.01 0.276 0.99 1.01–1.02 <0.001

Model 1: after adjusted with hypertriglyceridemia, reduced HDL, hypercholesterolemia, drinking, smoking, and age. Model 2: after adjusted with
reduced HDL, hypercholesterolemia, drinking, smoking, and age. Model 3: after adjusted with reduced HDL, hypercholesterolemia, drinking, smoking,
and age

Participants with eTGWC phenotype also demonstrated that
WC, SBP, DBP, Glu, TC, TG, LDL-C, number of alcohol
drinking, smoking, HT, and T2DM were also significantly
higher and lower in HDL-C in eTGWC phenotype
(p<0.05). Men with eTGWC phenotype were younger, but
women with eTGWC phenotype were significantly older as
shown in Table 3 (p<0.05). The number of alcohol drinking
and smoking was not significantly different in women with
eTGWC phenotype (p<0.05). Bivariate correlation of all AO
men and women are shown in Table 4.
Association of AO, eTG, and eTGWC phenotype with HT and
T2DM In multiple logistic regression analysis, models
showed the association of AO, eTG, and eTGWC phenotype
with increased risk of HT and T2DM after adjusting with the
other variables in each gender. In men, model 1 AO associated
with increased risk for HT (OR=3.14, 95 % CI 2.14–4.59)
and T2DM (OR=1.86, 95 % CI 1.13–3.06), model 2 eTG
associated with increased risk for HT (OR=1.77, 95 % CI
1.09–2.86) and T2DM (OR=2.94, 95 % CI 1.51–5.73), and
model 3 eTGWC associated with increased risk for HT (OR=
1.74, 95 % CI 1.07–2.84) and T2DM (OR=2.07, 95 % CI
1.13–3.79). In women, model 1 AO associated with increased
risk for HT (OR=2.59, 95 % CI 2.02–3.31) and T2DM (OR=
2.39, 95 % CI 1.75–3.29), model 2 eTG associated with in-
creased risk for HT (OR=1.54, 95 % CI 1.09–2.86) and
T2DM (OR=1.47, 95 % CI 1.17–1.84), and model 3 eTGWC
associated with increased risk for HT (OR=1.84, 95 % CI
1.54–2.21) and T2DM (OR=1.87, 95 % CI 1.49–2.33). The
prevalence of HT and T2DM was also greater in subjects with
eTG and eTGWC phenotype in both genders (Table 5).
ROC curves analysis We plotted the ROC curves for AO,
eTG, and eTGWC. The results of AO, eTG, and eTGWC
Int J Diabetes Dev Ctries (October–December 2015) 35(4):439–447 445

ROC curve analysis showed that each phenotype (marker) is a
significant discriminator for HT and T2DM. The AUC of the
ROC curves were used for prediction of better phenotype
(marker) for HT and T2DM. In men, the largest AUC was
obtained with the AO and eTG, indicating that the model with
this phenotype (marker) was superior for estimating the HT
and T2DM, respectively, in the present study. In women, the
largest AUC was obtained with the eTGWC, indicating that
the model with this phenotype (marker) was superior for esti-
mation both HT and T2DM in the present study as shown in
Table 6 and Fig 2.
Discussion
Obesity is considered to be the link between insulin resistance
and metabolic abnormalities inclusive of diabetes, hyperten-
sion, and dyslipidemia, all of which are risk factors for CAD
[1, 2, 8, 9]. Measures commonly used for assessing obesity are
BMI and WC. BMI is not considered to be a good estimate of
obesity in Asian population, as they have a characteristic obe-
sity phenotype, with relatively lower BMI but with central
obesity. Hence, abdominal adiposity assessed using WC is
considered to be more appropriate to predict metabolic disor-
ders than generalized adiposity assessed by BMI. It has been
suggested that fat distributed in the abdominal region, partic-
ularly visceral fat, is more metabolically important than other
fat depots. Our study aimed to find a simple approach to iden-
tify individuals apparently healthy, who were high risk in HT
and T2DM and at increased risk of CVD and other clinical
syndromes related to defect in metabolism. In the present
study, both men and women that had AO, eTG, and eTGWC
demonstrated higher SBP, DBP, Glu, TC, TG, LDL-C, num-
ber of alcohol drinking, smoking, HT, and T2DM and lower
HDL-C levels. The eTGWC phenotype occurred in younger
men but older in women especially in postmenopausal.
Because of its simple determinations, the AO, eTG, and
eTGWC are easily available to the clinician with lipid profile
ordered, thus eliminating any additional costs. In our present
study, in men, the AO and eTG phenotypes (markers) depicted
the stronger risk of HT and T2DM, respectively, both in mul-
tiple logistic regression and ROC analysis. In women, the AO
phenotype (marker) had the highest OR risk association for
HT and T2DM. In ROC analysis, the largest AUC was
eTGWC, indicating that the model with this phenotype
(marker) was superior for estimating both HT and T2DM.
Our findings in women were the same as the study of Okosun
and Boltri [14] which showed that the risk of HT and T2DM
was stronger for eTGWC phenotype when compared to AO or
eTG phenotypes. The sequence of the prevalence phenotype
of the present population was AO, eTG, and eTGWC in both
genders. Then, AO may be taken as a risk factor and an indi-
cator for early prediction of HT and T2DM.
The development of obesity, especially AO, is also fre-
quently associated with vascular diseases and dyslipidemia.
The major features are initially recognized eTG, decreased
HDL-C levels, and normal or borderline-elevated levels of
LDL-C with an altered composition. These appear to be prob-
lems of VLDL and HDL concentrations, but not LDL concen-
trations, and increase in circulating insulin levels [14, 16], as
risk factor for CVD, and T2DM [1, 8, 14, 16]. AO is now
recognized by the third report of the National Cholesterol
Education Program Adult Treatment Panel (NCEP ATP III)
and the World Health Organization as a component of the
metabolic syndrome [20, 21], which is also considered a risk
factor for type 2 diabetes mellitus. Small, dense LDL particles
are highly prevalent in abdominally obese and insulin-
resistant patients, and both increase coronary heart disease risk
[16, 20]. Pouliot et al. [21] documented that waist circumfer-
ence was best correlated with the amount of visceral adipose
tissue. AO is a surrogate marker for visceral adiposity. In-
creased secretion of interleukin-6 and tumor necrosis

Table 6 Area under the receiver-operating characteristic curves of abdominal obesity, hypertriglyceridemia, and hypertriglyceridemic waist for
hypertension (A) and type 2 diabetes (B)

Phenotype Area under the ROC 95 % confidence p value Phenotype Area under the ROC 95 % confidence p value
curve±SE (men) interval curve±SE (women) interval

(A)
AO 0.616±0.020 0.579–0.655 <0.001 eTGWC 0.609±0.012 0.586–0.632 <0.001
eTG 0.590±0.020 0.551–0.630 <0.001 eTG 0.604±0.012 0.581–0.627 <0.001
eTGWC 0.574±0.021 0.534–0.615 <0.001 AO 0.590±0.011 0.568–0.612 <0.001
(B)
eTG 0.654±0.026 0.603–0.705 <0.001 eTGWC 0.628±0.014 0.600–0.656 <0.001
eTGWC 0.638±0.028 0.583–0.693 <0.001 eTG 0.617±0.014 0.590–0.645 <0.001
AO 0.634±0.026 0.583–0.685 <0.001 AO 0.584±0.013 0.559–0.610 <0.001

Null hypothesis: true area=0.5

eTGWC hypertriglyceridemic waist, eTG hypertriglyceridemia, AO abdominal obesity
446
Fig 2 ROC curves for abdominal obesity, hypertriglyceridemia, and hypertriglyceridemic waist for the hypertension (a) and type 2 diabetes prediction
(b) in a1 and b1 in men and a2 and b2 in women
factor-α from intra-abdominal adipocytes has been shown to
stimulate hepatic secretion of C-reactive protein, a marker of
low-grade systemic inflammation. These factors are signifi-
cantly associated with the development of arterial stiffness,
an early sign of atherosclerosis [22]. Case control studies
[23] have clearly indicated that visceral fat is associated with
diabetes.
Lemieux et al. [16] first suggested that the simulta-
neous interpretation of waist circumference and fasting
TG concentration may be a comprehensive and cost-
effective screening method for the identification of pa-
tients characterized by a cluster of atherogenic risk factors
and also indicates that hyperglycemia by itself is not pre-
dictive of CVD risk in the absence of hypertriglyc-
eridemia and abdominal adiposity comorbidity. Studies
have shown that the cardiovascular disease risk attribut-
able to glycemia may be caused by the co-occurrence of
abdominal adiposity and eTG [6]. Determination of WC
Int J Diabetes Dev Ctries (October–December 2015) 35(4):439–447
and TG level or eTGWC is cheap and easy, and these
values can be used as a significant marker of HT and
T2DM.
AO induced by high fat and high carbohydrate intake is a
major risk factor for the development of diabetes and cardio-
vascular disease [24, 25]. Contributors such as sedentary life-
style combined with diet rich in carbohydrate (rice), sugar, and
Western dietary pattern are toxic to the metabolism. In large-
scale human observational studies among various popula-
tions, white rice with a high glycemic index or glycemic load
was associated with increased risk of developing T2DM [26].
Any approaches aim at the management of the risk of HT,
T2DM, and CVD. AO patients will require a multifaceted
approach directly related with critical factors, including bal-
anced nutrition with more vegetables and fruits, less sugar,
rice, and more physical activity. Whole grain, one of Thai
dietary pattern, was ignored from Thai dietary intake. Con-
sumption of whole grains has been associated with reduced
Int J Diabetes Dev Ctries (October–December 2015) 35(4):439–447
blood pressure, body mass index, triglycerides, the risk of
diabetes, and with increased HDL-C [27].
Conclusion
It is suggested that AO may serve as the early phenotype-
associated sequel to eTG reach to eTGWC. The simultaneous
measurement and interpretation of waist circumference and
fasting TG could be used as inexpensive screening tools to
identify those at high risk of HT and T2DM. It is necessary to
have public health strategies to reduce AO in general popula-
tion which would be a significant approach to reduce the risk
of HT and T2DM.
Acknowledgments We sincerely thank the Mobile Unit for Health and
Occupation Development, Naresuan University, for financial support. We
also thank the Faculty of Allied Health Sciences for the facility support.
We would like to thank Asst. Prof. Dr. Ronald A. Markwardt, Burapha
University, for his critical reading and correction of the manuscript.
Conflict of interest No conflict of interest.
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