
Obesity is one of the most important public health problems due to its association with many diseases, including type 2 diabetes mellitus, hypertension, dyslipidemia, and metabolic syndrome [1-4]. Metabolic syndrome is characterized by insulin resistance (IR), as studies have mainly noted IR in subjects with individual metabolic syndrome components, such as abdominal obesity, hypertension, and dyslipidemia [5-7]. The populations with obesity maintain normal glucose level since a preserved ability to secrete insulin [8]. However, if IR increases, the ability to secrete insulin decreases, as IR is one of the factors in the de-differentiation and death of beta cells [9, 10].
Recently, research on metabolic syndrome and IR is currently being conducted all over the world. However, there are few studies on the relationship between beta cell function and metabolic syndrome in Korea, and research findings on the association between beta cell function and metabolic syndrome components were not consistent according to countries and ethnic groups, healthy subjects and subjects with chronic disease (e.g., obesity, diabetes) [11-15]. The prevalence of metabolic syndrome and obesity in the Republic of Korea has been increasing due to the Westernized diet [16]. Therefore, the present study aimed to investigate the relationship between metabolic syndrome and the increased levels of its components and the HOMA-
This study was based on data from the fifth KNHANES (2010), which is the most recent data that measured insulin among the KNHANES. The KNHANES is a cross-sectional survey conducted nationwide by the Division of Korean National Health and Welfare. The fifth KNHANES (2010) was performed from January 2010 to December 2010. In the fifth KNHANES (2010), 8,958 individuals over 1 year of age were sampled for the survey. Among the 6,665 subjects who participated in the fifth KNHANES (2010), we limited the analyses to adults aged over 20 years. We excluded 4,805 subjects who were in no-obesity group (3,941 subjects, body mass index [BMI] <25.0 kg/m2) or for whom data were missing for an important analytic variables, such as the insulin, fasting blood glucose (FBG), and various blood chemistry tests (864 subjects). Finally, 1,860 subjects were included in the statistical analysis. The KNHANES study was approved by the Institutional Review Board of the Centers for Disease Control and Prevention in Korea (IRB No, 2010-02CON-21-C). All participants in the survey signed an informed written consent form.
Anthropometric measurements included height, weight, waist circumference (WC), and BMI as well as final measurements of diastolic blood pressure (DBP) and systolic blood pressure (SBP). Blood chemistry included measurement of total cholesterol (TC), triglycerides (TGs), high-density lipoprotein cholesterol (HDL-C), FBG, and 25-hydroxyvitamin D [25(OH)D].
The HOMA-
Metabolic syndrome was defined using the diagnostic criteria of the revised National Cholesterol Education Program Adult Treatment Panel III [20], including TGs, HDL-C, BP, FBG, and WC. TGs over 150 mg/dL for dyslipidemia were set as the criteria for elevated TGs. The criteria for reduced HDL-C were HDL-C of less than 50 mg/dL and 40 mg/dL for females and males, respectively. FBG over 100 mg/dL were set as the criteria for elevated FBG. DBP over 85 mmHg or SBP over 130 mmHg were set as the criteria for elevated BP. The criteria for abdominal obesity were WC of over 80 cm and 90 cm for females and males, respectively [21]. The presence of defined abnormalities in any three of these five measures constitutes a diagnosis of metabolic syndrome. The metabolic syndrome (MSS) indicates the presence of elevated FBG, elevated TGs, and reduced HDL-C, abdominal obesity, and elevated BP. Subjects without any of the five risk factors received an MSS of 0, while those with one, two, three, or four or more of the risk factors received an MSS of 1, 2, 3, and ≥4, respectively [22].
The collected data were statistically analyzed using SPSS statistics 20 (SPSS Inc., Chicago, IL, USA). The distributions of the subjects characteristics were converted into percentages (%), and the successive data were presented as averages with standard deviations (M±SD). Clinical characteristics grouped by men or women were analyzed using chi-square and an independent t-test. The average difference in the HOMA-IR and HOMA-
The clinical characteristics of the research participants are shown in Table 1. In the males, the HOMA-IR and HOMA-
General characteristics of research subjects
N (%), Mean±SD (N=1,860)
Variables | Category | Males (N=934) | Females (N=926) | |
---|---|---|---|---|
Age | 20∼29 | 79 (8.5) | 59 (6.2) | <0.001 |
30∼39 | 214 (22.9) | 125 (13.5) | ||
40∼49 | 227 (24.3) | 151 (16.3) | ||
50∼59 | 173 (18.5) | 226 (24.4) | ||
≥60 | 241 (25.8) | 367 (39.6) | ||
Metabolic syndrome | MSS <3 | 512 (54.8) | 476 (51.4) | 0.150 |
MSS ≥3 | 422 (45.2) | 450 (48.6) | ||
Metabolic syndrome score | 0 | 80 (8.6) | 27 (2.9) | <0.001 |
1 | 172 (18.4) | 176 (19.0) | ||
2 | 260 (27.8) | 273 (29.5) | ||
3 | 248 (26.6) | 250 (27.0) | ||
≥4 | 174 (18.6) | 200 (21.6) | ||
WC (cm) | 91.86±6.68 | 88.57±7.64 | <0.001 | |
BMI (kg/m2) | 27.15±2.11 | 27.59±2.41 | <0.001 | |
SBP (mmHg) | 122.83±15.43 | 124.47±17.70 | 0.033 | |
DBP (mmHg) | 79.96±10.39 | 76.88±10.19 | <0.001 | |
HOMA-IR | 3.20±1.86 | 3.23±1.99 | 0.750 | |
HOMA- |
129.55±69.85 | 139.65±79.13 | 0.004 | |
TC (mg/dL) | 195.19±37.18 | 200.20±39.48 | 0.005 | |
TG (mg/dL) | 190.30±152.14 | 142.55±84.56 | <0.001 | |
HDL-C (mg/dL) | 42.57±8.78 | 47.34±10.16 | <0.001 | |
25(OH)D (ng/dL) | 19.25±6.27 | 17.00±6.29 | <0.001 | |
FBG (mg/dL) | 104.06±26.96 | 100.65±20.94 | 0.002 |
Abbreviations: WC, waist circumference; BMI, body mass index; SBP, systolic blood pressure; DBP, diastolic blood pressure; HOMA-IR, homeostasis model assessment of insulin resistance; HOMA-
Comparisons of the HOMA-IR and HOMA-
Comparisons of the HOMA-IR and HOMA-
Mean±SD (N=1,860)
Variable | Category | Obesity subjects [BMI ≥25.0 kg/m2] | |||
---|---|---|---|---|---|
HOMA-IR | HOMA-B | ||||
WC (cm) | Reference |
2.66±1.17 | <0.001 | 126.72±62.83 | 0.003 |
Abdominal obesity |
3.41±2.10 | 137.35±78.38 | |||
BP (mmHg) | Reference |
3.13±2.12 | 0.054 | 141.20±73.21 | <0.001 |
Elevated blood pressure |
3.30±1.72 | 127.91±75.43 | |||
TGs (mg/dL) | Reference |
2.97±1.77 | <0.001 | 132.36±65.51 | 0.169 |
Elevated triglycerides |
3.60±2.08 | 137.45±86.19 | |||
HDL-C (mg/dL) | Reference |
3.01±1.71 | <0.001 | 131.32±66.84 | 0.030 |
Reduced HDL-C |
3.56±2.20 | 139.53±85.70 | |||
FBG (mg/dL) | ReferenceI | 2.62±1.16 | <0.001 | 158.04±77.92 | <0.001 |
Elevated FPG |
4.13±2.45 | 97.86±50.92 |
Abbreviations: aReference is defined as WC <90 cm in males or <80 cm in females, bAbdominal obesity is defined as WC >90 cm in males or >80 cm in females, cReference is defined as SBP <130 mmHg or DBP <85 mmHg, dElevated blood pressure is defined as SBP >130 mmHg or DBP >85 mmHg, eReference is defined as TGs <150 mg/dL, fElevated triglycerides is defined as TGs >150 mg/dL, gReference is defined as HDL-C >40 mg/dL in males or >50 mg/dL in females, hReduced HDL-C is defined as HDL-C <40 mg/dL in males or <50 mg/dL in females, iReference is defined as FBG <100 mg/dL, jElevated FBG is defined as FBG >100 mg/dL.
Comparisons of the HOMA-IR and HOMA-
Comparisons of the HOMA-IR levels according to metabolic syndrome and metabolic syndrome scores in obesity subjects
(N=1,860)
HOMA-IR (M±SD) non-adjusted (95%, CI) |
HOMA-IR (M±SE) adjusted |
|||
---|---|---|---|---|
MSS 0 | 2.14±0.81 (1.99∼2.30) | <0.001 | 2.41±0.17 (2.06∼2.75) | <0.001 |
1 | 2.40±0.95 (2.30∼2.50) | 2.55±0.01 (2.36∼2.74) | ||
2 | 3.00±1.81 (2.85∼3.15) | 2.99±0.08 (2.84∼3.14) | ||
3 | 3.48±1.80 (3.32∼3.64) | 3.41±0.08 (3.26∼3.57) | ||
≥4 | 4.24±2.53 (3.98∼4.49) | 4.12±0.09 (3.93∼4.29) | ||
Non-mets | 2.69±1.50 (2.61∼2.79) | <0.001 | 2.65±0.07 (2.51∼2.79) | <0.001 |
Mets | 3.80±2.17 (3.66∼3.94) | 3.76±0.06 (3.64∼3.88) |
Abbreviations: MSS, metabolic syndrome score; Non-Mets, non-metabolic syndrome; Mets, metabolic syndrome.
*Adjusted for age, gender, BMI, TC, and 25(OH)D.
Comparisons of the HOMA-
(N=1,860)
HOMA- non-adjusted (95%, CI) |
HOMA- adjusted |
|||
---|---|---|---|---|
MSS 0 | 145.82±54.39 (135.39∼156.24) | <0.001 | 146.19±7.12 (132.22∼160.16) | <0.001 |
1 | 142.82±70.55 (135.38∼150.26) | 141.83±3.92 (134.14∼149.51) | ||
2 | 142.66±66.44 (137.01∼148.32) | 141.09±3.09 (135.02∼147.15) | ||
3 | 129.33±70.99 (122.46∼136.19) | 130.44±3.22 (124.12∼136.76) | ||
≥4 | 119.15±86.69 (110.34∼127.97) | 120.73±3.79 (113.30∼128.16) | ||
Non-mets | 143.06±66.69 (139.09∼147.25) | <0.001 | 143.03±2.96 (137.23∼148.83) | <0.001 |
Mets | 124.96±81.94 (119.35∼130.27) | 125.59±2.52 (120.64∼130.53) |
Abbreviation: See Table 3.
*Adjusted for age, gender, BMI, TC, and 25(OH)D.
The present study investigated the association between metabolic syndrome and its components and HOMA-
Many previous studies have shown that IR is associated with metabolic syndrome and its components. Yin et al [23] reported that all of the metabolic syndrome components were associated with the HOMA-IR of Chinese children and teenagers (
Studies on the association between beta cell function and metabolic syndrome components are not so much, and previous results were not consistent according to healthy subjects and subjects with disease, country and ethnicity [13, 28, 29]. Imamura et al [28] conducted the association between the risk factors of type 2 diabetes mellitus (T2DM) and IR and beta cell function in the Cardiovascular Health Study and they suggested that HOMA-
Obesity is the one of the factors responsible for T2DM. However, in order to develop into hyperglycemia, the human body must fail to produce sufficient insulin, and this is associated with the beta cells that secrete insulin. Even in the populations with obesity, in the absence of IR, beta cells are activated for insulin secretion when blood glucose increases [30, 31]. However, the beta cell function or mass is significantly reduced in subjects with IR, such as T2DM and metabolic syndrome [32, 33]. In previous studies [34, 35], decreases in pancreatic beta cell mass were mainly seen in subjects with IR, implying that it is caused by an increase in beta cell apoptosis or necrosis or autophagy in the state of IR. Metabolic syndrome is characterized by IR [5], and the risk factors of metabolic syndrome are the strongly associated with oxidative stress or the elevated circulating concentration of free fatty acids [36], Oxidative stress increases in response to the increased production of reactive oxygen species, which is increased by the decrease of antioxidant enzymes. In particular, endoplasmic reticulum stress is caused by prolonged high lipid molecules or insulin production, such as free fatty acids [9]. The de-differentiation and death of pancreatic beta cells are caused by IR [11], oxidative stress [37], and increased endoplasmic reticulum stress [38].
In conclusions, the relationship between the HOMA-
본 연구는 대한민국 비만 성인에서 대사증후군과 대사증후군 구성요소의 증가와 인슐린저항성(homeostasis model assessment of insulin resistance, HOMA-IR) 및 베타세포기능(homeostasis model assessment of beta cell function, HOMA-
This paper was supported by Wonkwang Health Science University in 2020.
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Yoon H, Professor.