Abstract
Results from a recent study indicate that a higher level of oleic acid/stearic acid ratio was associated with metabolically unhealthy obesity. This was further validated in cross-sectional and interventional studies; however, this was not extensively studied in a non-obese population. We recruited 260 Japanese subjects with serum free fatty acid profiles undergoing anti-aging health examinations. The determinants for oleic acid/stearic acid ratio were investigated using multiple regression analyses. To compare different markers, the subjects were classified based on oleic acid/stearic acid ratio and the combination of oleic acid/stearic acid ratio and triglyceride levels. The oleic acid/stearic acid ratio exhibited a positive correlation with the logmatic transformed triglyceride/high-density lipoprotein cholesterol ratio and the fasting triglycerides-glucose index, both of which were used as markers for insulin resistance. Multiple regression analyses revealed that the triglyceride/high-density lipoprotein cholesterol ratio and fasting triglyceride-glucose index were positively associated with the oleic acid/stearic acid ratio. Most markers were the worst in the highest triglyceride group in both oleic acid/stearic acid groups. In addition, most markers were worse in high oleic acid/stearic acid ratio group than low group. In conclusion, oleic acid/stearic acid ratio might be a useful marker for insulin resistance in non-obese Japanese subjects.
Keywords: oleic acid to stearic acid ratio, triglyceride to high-density lipoprotein cholesterol ratio, triglyceride-glucose index, insulin resistance
Introduction
Results of a recent 10-year longitudinal Shanghai Diabetes Study (SHDS),(1) indicate that a higher baseline level of oleic acid/stearic acid (OA/SA), and lower levels of stearic acid/palmitic acid (SA/PA), and arachidonic acid/dihomo-γ-linolenic acid (AA/DGLA) ratios were associated with a higher rate of conversion between metabolic healthy obesity to metabolically unhealthy obesity conversion. This finding was validated in cross-sectional and interventional studies. It is speculated that, the ratios of [product free fatty acid (FFA)/precursor FFA] may better reflect the status of endogenous fatty acid metabolism, as compared to concentrations of individual FFAs.
Insulin-resistant states are associated with impaired vascular response to insulin, and endothelial dysfunction. Insulin resistance (IR) is related to many pathological conditions, including metabolic syndrome (MetS), atherosclerosis, hypertension, and diabetes mellitus, and therefore, it is crucial to measure IR. The hyperinsulinemic-euglycemic clamp remains the gold standard for IR and the homeostasis model assessment for IR (HOMA-IR) is the most widely used alternative to date.(2–4) However, due to cost, accessibility, reproducibility and replicability, these options are impractical in clinical practice.(2,4–7) In addition, fasting insulin levels are required to calculate HOMA-IR. However, they are not routinely measured in clinical settings.
It is indicated that the triglyceride (TG)/high-density lipoprotein cholesterol (HDL-C) ratio strongly correlates with IR,(8–10) and it appears to be a useful predictor for the development of diabetes,(11) coronary heart disease, and cardiovascular mortality.(12) The TG/HDL-C ratio has been shown to be a better screening index for MetS, as compared to HOMA-IR.(13) It is reported that, in Japanese adults, the lipid ratios of TG/HDL-C, Total-C/HDL-C, LDL-C/HDL-C, as well as TG and HDL-C, were associated with MetS and IR. The receiver operating characteristic curve analyses indicated that the best marker for these variables was TG/HDL-C ratio, in both men and women.(14) However, a very limited number of studies have investigated this ratio as an indicator of metabolic syndromes in specific populations.(14,15)
The fasting triglyceride-glucose (TyG) index, a product of the fasting levels of triglycerides and glucose, has presented promising results as a surrogate marker for the assessment of IR.(16–18)
This study was designed to investigate whether the OA/SA ratio is associated with IR. The study also investigates whether the OA/SA ratio measures metabolic abnormalities in non-obese Japanese adults.
Materials and Methods
Subjects
A total of 319 subjects, undergoing an anti-aging health examination at the Health Screening Center, Tokai University Tokyo Hospital in 2016, were included in this cross-sectional study. After excluding 28 subjects, for whom the serum FFA profiles were not analyzed, and 31 subjects with incomplete data, 260 subjects were included in the final analysis. Medical histories were obtained using self-administered questionnaires and through interviews conducted by nurses.
Measurements
Waist circumference (WC) was measured at the level of the umbilicus during slight expiration, with the participant in a standing position. Blood pressure (BP) was measured on the upper right arm using an automatic BP monitor (TM-2655P; A&D, Tokyo, Japan), while the participant was seated. Blood samples were collected in heparin-coated tubes early in the morning, following an overnight fast. The fasting plasma glucose (FPG) level was measured with an L-type Glu 2 kit, using the hexokinase/glucose-6-phosphate dehydrogenase method (Wako Pure Chemicals, Osaka, Japan). The low-density lipoprotein cholesterol (LDL-C), HDL-C, and TG levels, were measured using visible spectrophotometry (Determiner L LDL-C, Determiner L HDL-C and Determiner L TG II, respectively; Kyowa Medex, Tokyo, Japan). Uric acid (UA) levels were measured with an L-Type UA M kit, using the uricase-N-(3-sulfopropyl)-3-methoxy-5-methylaniline method (Wako Pure Chemicals). The serum FFA profile was measured using gas-chromatography. The TyG index was calculated as logmatic transformations (ln) [fasting triglycerides (mg/dl) × fasting glucose (mg/dl)/2].(16,17)
All subjects gave written informed consent to the use of their health records for analysis. This study was approved by the Ethics Committee of Tokai University (No. 11R-125) and was conducted in accordance with the Declaration of Helsinki.
Statistical analyses
Data are expressed as the mean ± SD or median (inter-quartile range). Normality was examined using the Kolmogorov–Smirnov test. The Bonferroni’s multiple comparison test was used to compare mean values across three or more groups. In order to compare various markers, the subjects were divided into three groups based on OA/SA ratios, and into six groups based on the combinations of OA/SA ratios and TG levels. Determinants of the OA/SA ratio were identified by multiple linear regression analysis. Two sets of variables were considered: one set for TG/HDL-C ratio [sex, age, body mass index (BMI), WC, systolic and diastolic BP, FPG, TG/HDL-C ratio, LDL-C, UA], and the other set for TyG index (sex, age, BMI, WC, systolic and diastolic BP, TyG index, HDL-C, LDL-C, UA). Determinants for the upper tertile of OA/SA were analyzed by multiple logistic regression analysis using the same variables used in the multiple linear regression analysis A stepwise procedure was used to select variables for multiple regression analyses. All statistical analyses were performed using SAS studio ver. 3.4 (SAS Institute, Cary, NC). All p values were two-tailed, and a p value of <0.05 was defined as statistically significant.
Results
All the characteristics evaluated in this study are represented in Table 1. Out of the 260 subjects, 105 (40.4%) were women. The mean age, BMI, FPG, median TG, mean TyG index, HDL-C levels, and median TG/HDL-C ratio were 53.9 years old, 22.4 kg/m2, 95.9 mg/dl, 84.0 mg/dl, 8.30, 64.4 mg/dl, and 1.31, respectively.
Table 1.
Characteristics of study subjects
| Men/women (n) | 155/105 |
| Age | 53.9 ± 14.0 |
| BMI (kg/m2) | 22.4 ± 3.1 |
| Waist circumference (cm) | 81.4 ± 9.2 |
| Systolic BP (mmHg) | 121.9 ± 16.7 |
| Diastolic BP (mmHg) | 77.8 ± 11.7 |
| FPG (mg/dl) | 95.9 ± 11.0 |
| TG (mg/dl) | 84.0 [56.0, 118.5] |
| TyG index | 8.30 ± 0.57 |
| HDL-C (mg/dl) | 64.4 ± 14.5 |
| TG/HDL-C ratio | 1.31 [0.81, 2.01] |
| LDL-C (mg/dl) | 120.1 ± 31.8 |
| non-HDL-C (mg/dl) | 140.8 ± 33.8 |
| UA (mg/dl) | 5.6 ± 1.3 |
| OA (µg/ml) | 578.6 ± 220.4 |
| SA (µg/ml) | 201.5 ± 56.2 |
| OA/SA ratio | 2.85 ± 0.60 |
Variables are given as mean ± SD or median [interquartile range]. BMI, body mass index; BP, blood pressure; FPG, fasting plasma glucose; TG, triglyceride; TyG index, triglyceride-glucose index; HDL-C, high-density lipoprotein cholesterol; LDL-C, low-density lipoprotein cholesterol; non-HDL-C, non high-density lipoprotein cholesterol; UA, uric acid; OA, oleic acid; SA, stearic acid.
Possible associations of TG/HDL-C ratio and TyG index, with OA/SA ratio were investigated using Pearson’s correlation coefficient. As shown in Fig. 1, OA/SA ratio exhibited a positive correlation with both, ln (TG/HDL-C ratio) [r = 0.735, 95% confidence interval (CI) 0.674–0.786, p<0.0001; Fig. 1A], and TyG index [r = 0.690, 95% CI 0.620–0.748, p<0.0001; Fig. 1B].
Fig. 1.
Scatter plots and regression lines for the comparisons of ln (TG/HDL-C) (A) or TyG index (B) and OA/SA ratio. Pearson’s correlation coefficient with 95% confidence intervals is indicated on the graph. ln (TG/HDL-C), logarithmic transformed triglyceride to high-density lipoprotein cholesterol ratio; TyG index, triglyceride-glucose index; OA/SA, oleic acid to stearic acid ratio.
Determinants of the OA/SA ratio were identified by multiple linear regression analysis (Table 2). Two sets of variables were considered: one set for TG/HDL-C ratio, the other set for TyG index. Among the variables included for TG/HDL-C ratio (sex, age, BMI, WC, systolic and diastolic BP, FPG, TG/HDL-C ratio, LDL-C, UA), two variables (TG/HDL-C ratio and UA) were selected using a stepwise procedure (Table 2A). Among the variables included for TyG index (sex, age, BMI, WC, systolic and diastolic BP, TyG index, HDL-C, LDL-C, UA), four variables (age, TyG index, HDL-C, LDL-C) were selected using a stepwise procedure (Table 2B). The analysis revealed that TG/HDL-C ratio, UA, and TyG index were positively associated with the OA/SA ratio, while age, HDL-C, and LDL-C were negatively associated with the OA/SA ratio (Table 2A and B).
Table 2.
Multiple linear regression analysis for the oleic acid to stearic acid ratio
| (A) TG/HDL-C | ||||
|---|---|---|---|---|
| RC | SRC | t | p | |
| TG/HDL-C | 0.23754 | 0.60277 | 12.14 | <0.0001 |
| UA | 0.05489 | 0.11845 | 2.39 | 0.0178 |
| (B) TyG index | ||||
| Age | –0.00575 | –0.13459 | –3.23 | 0.0014 |
| TyG index | 0.67627 | 0.64211 | 12.53 | <0.0001 |
| HDL-C | –0.00832 | –0.20131 | –4.09 | <0.0001 |
| LDL-C | –0.00340 | –0.18026 | –4.12 | <0.0001 |
Variable selection was made by a stepwise procedure. OA, oleic acid; SA, stearic acid; RC, regression coefficient; SRC, standardized regression coefficient; TG, triglyceride; HDL-C, high-density lipoprotein cholesterol; UA, uric acid; TyG index, triglyceride-glucose index; LDL-C, low-density lipoprotein cholesterol.
Determinants for the upper tertile of OA/SA were analyzed using a multiple logistic regression analysis (Table 3). When we analyzed the same variables in multiple linear regression analysis for TG/HDL-C ratio, three variables (age, TG/HDL-C ratio and UA) were selected using a stepwise procedure (Table 3A). For TyG index, two variables (age and TyG index) were selected using a stepwise procedure (Table 3B). The results of the analysis revealed that TG/HDL-C, UA, and TyG index were positively associated with the upper tertile of OA/SA ratio. Age was negatively associated with the upper tertile of OA/SA ratio.
Table 3.
Multiple logistic regression analysis for the upper tertile of oleic acid to stearic acid ratio
| (A) TG/HDL-C | |||||
|---|---|---|---|---|---|
| RC | SE | OR | 95% CI | p | |
| Age | –0.0327 | 0.0126 | 0.968 | 0.944–0.992 | 0.0092 |
| TG/HDL-C | 0.9415 | 0.1748 | 2.564 | 1.820–3.612 | <0.0001 |
| UA | 0.3358 | 0.1356 | 1.399 | 1.073–1.825 | 0.0133 |
| (B) TyG index | |||||
| Age | –0.0477 | 0.01400 | 0.953 | 0.928–0.980 | 0.0006 |
| TyG index | 3.1526 | 0.4338 | 23.396 | 9.997–54.755 | <0.0001 |
Variable selection was made by a stepwise procedure. TG, triglyceride; HDL-C, high-density lipoprotein cholesterol; RC, regression coefficient; SE, standard error; OR, odds ratio; CI, confidence interval; UA, uric acid; TyG index, triglyceride-glucose index.
To evaluate the impact of OA/SA ratio on various markers, the subjects were divided into three OA/SA groups. Table 4 represents the characteristics of study subjects stratified according to the OA/SA ratio. The BMI, WC, FPG, TG, TyG index, TG/HDL-C ratio, LDL-C, non-HDL-C, UA, OA, SA, and OA/SA ratio increased as the OA/SA ratio increased. On the contrary, HDL-C decreased as the OA/SA ratio increased.
Table 4.
Characteristics of study subjects stratified according to oleic acid to stearic acid ratio
| OA/SA ratio |
|||
|---|---|---|---|
| <2.50 (n = 83) | 2.50–3.04 (n = 88) | ≥3.04 (n = 89) | |
| Men/women (n) | 45/38 | 41/47 | 19/70 |
| Age | 55.7 ± 13.7 | 55.4 ± 15.1 | 50.8 ± 12.8 |
| BMI (kg/m2) | 21.2 ± 2.7 | 22.3 ± 3.1 | 23.6 ± 3.1**,# |
| Waist circumference (cm) | 78.1 ± 8.5 | 82.0 ± 9.5* | 84.0 ± 8.5**,## |
| Systolic BP (mmHg) | 122.4 ± 17.6 | 121.0 ± 17.2 | 122.3 ± 15.4 |
| Diastolic BP (mmHg) | 78.2 ± 12.8 | 76.8 ± 10.9 | 78.5 ± 11.4 |
| FPG (mg/dl) | 94.5 ± 11.7 | 96.0 ± 11.8 | 97.2 ± 9.2 |
| TG (mg/dl) | 56.0 [45.0, 72.0] | 79.5 [58.5, 107.5]** | 123.0 [96.0, 169.0]**,## |
| TyG index | 7.88 ± 0.38 | 8.26 ± 0.52** | 8.73 ± 0.45**,## |
| HDL-C (mg/dl) | 73.3 ± 13.5 | 63.8 ± 11.9** | 56.5 ± 13.0**,## |
| TG/HDL-C ratio | 0.77 [0.58, 1.08] | 1.28 [0.93, 1.82]** | 2.22 [1.50, 3.63]**,## |
| LDL-C (mg/dl) | 117.1 ± 29.0 | 119.7 ± 30.2 | 123.2 ± 35.7 |
| non-HDL-C (mg/dl) | 135.6 ± 30.2 | 139.9 ± 32.5 | 146.5 ± 37.4 |
| UA (mg/dl) | 5.2 ± 1.2 | 5.4 ± 1.4 | 6.1 ± 1.1**,## |
| OA (µg/ml) | 439.1 ± 88.7 | 550.9 ± 225.2** | 736.2 ± 203.1**,## |
| SA (µg/ml) | 194.3 ± 34.6 | 200.5 ± 78.1 | 209.3 ± 45.1 |
| OA/SA ratio | 2.26 ± 0.19 | 2.74 ± 0.16** | 3.50 ± 0.47**,## |
Variables are given as mean ± SD or median [inter-quartile range]. BMI, body mass index; BP, blood pressure; FPG, fasting plasma glucose; TG, triglyceride; TyG index, triglyceride-glucose index; HDL-C, high-density lipoprotein cholesterol; LDL-C, low-density lipoprotein cholesterol; non-HDL-C, non high-density lipoprotein cholesterol; UA, uric acid; OA, olic acid; SA, stearic acid. **p<0.01, *p<0.05 (<2.50 vs 2.50–3.04, <2.50 vs ≥3.04), ##p<0.01, #p<0.05 (2.50–3.04 vs ≥3.04) by Bonferroni’s multiple comparison test.
To further evaluate the impact of TG levels on various markers in OA/SA stratified groups, the study subjects were further divided into three TG groups. Table 5 represents the characteristics of study subjects stratified according to OA/SA ratio and TG levels. Most markers except for age were worst in the highest TG group in both OA/SA groups. In addition, most markers except for age, BP, FPG, LDL-C, non-HDL-C and SA were worse in OA/SA ratio ≥2.85 than <2.85.
Table 5.
Characteristics of study subjects stratified according to oleic acid to stearic acid ratio and triglyceride
| TG (mg/dl) | OA/SA ratio <2.85 |
OS/SA ratio ≥2.85 |
|||||
|---|---|---|---|---|---|---|---|
| <67 (n = 75) | 67–106 (n = 53) | ≥106 (n = 12) | <67 (n = 10) | 67–106 (n = 34) | ≥106 (n = 76) | ||
| Men/women (n) | 31/44 | 30/23 | 7/5 | 3/7 | 20/14 | 64/12 | |
| Age | 53.7 ± 15.8 | 57.4 ± 12.3 | 61.8 ± 12.8 | 47.8 ± 12.6 | 52.6 ± 14.0 | 51.9 ± 13.0 | |
| BMI (kg/m2) | 20.9 ± 2.9 | 22.4 ± 3.0 | 22.7 ± 2.1 | 20.1 ± 1.5 | 22.5 ± 2.8 | 24.1 ± 3.0**,# | |
| Waist circumference (cm) | 76.4 ± 8.6 | 82.3 ± 8.8** | 85.8 ± 8.7** | 72.4 ± 5.2 | 82.4 ± 8.0* | 86.0 ± 7.7** | |
| Systolic BP (mmHg) | 117.9 ± 18.3 | 122.7 ± 16.2 | 131.4 ± 12.7* | 112.8 ± 11.2 | 119.1 ± 18.8 | 125.8 ± 14.0 | |
| Diastolic BP (mmHg) | 75.2 ± 12.4 | 78.1 ± 11.0 | 81.5 ± 9.1 | 71.8 ± 6.3 | 75.3 ± 11.8 | 81.2 ± 11.4# | |
| FPG (mg/dl) | 92.3 ± 11.9 | 97.3 ± 9.5 | 98.7 ± 9.3 | 87.4 ± 6.7 | 97.2 ± 8.8* | 98.7 ± 11.2** | |
| TG (mg/dl) | 48.0 [42.0, 56.0] | 79.0 [71.0, 90.0]** | 119.0 [114.0, 126.0]**,## | 53.0 [48.0, 58.0] | 89.0 [75.0, 100.0] | 142.0 [121.0, 194.5]**,## | |
| TyG index | 7.67 ± 0.27 | 8.26 ± 0.17** | 8.83 ± 0.52**,## | 7.73 ± 0.16 | 8.33 ± 0.18** | 8.92 ± 0.31**,## | |
| HDL-C (mg/dl) | 73.9 ± 13.6 | 65.8 ± 12.0** | 65.0 ± 11.0 | 68.9 ± 13.6 | 62.0 ± 12.2 | 54.3 ± 11.7**,## | |
| TG/HDL-C ratio | 0.66 [0.49, 0.79] | 1.18 [1.05, 1.53]* | 1.86 [1.59, 2.16]**,## | 0.79 [0.67, 0.91] | 1.40 [1.21, 1.65] | 2.82 [2.01, 3.94]**,## | |
| LDL-C (mg/dl) | 109.4 ± 26.7 | 125.6 ± 27.9* | 129.8 ± 24.6* | 94.2 ± 29.6 | 119.4 ± 33.7 | 128.9 ± 35.2** | |
| non-HDL-C (mg/dl) | 125.9 ± 28.0 | 145.8 ± 26.7** | 160.8 ± 30.8** | 107.6 ± 27.4 | 135.8 ± 31.8 | 155.4 ± 36.2**,# | |
| UA (mg/dl) | 4.9 ± 1.2 | 5.4 ± 1.2 | 5.7 ± 1.5 | 5.2 ± 1.5 | 5.9 ± 1.1 | 6.2 ± 1.1 | |
| OA (µg/ml) | 408.1 ± 68.8 | 505.4 ± 60.7* | 755.3 ± 525.6**,## | 487.7 ± 61.1 | 574.2 ± 81.9 | 784.0 ± 186.7**,## | |
| SA (µg/ml) | 177.5 ± 30.3 | 201.6 ± 26.2 | 287.6 ± 181.6**,## | 161.2 ± 21.7 | 184.2 ± 23.7 | 224.7 ± 41.5**,## | |
| OA/SA ratio | 2.31 ± 0.26 | 2.51 ± 0.17** | 2.59 ± 0.19** | 3.04 ± 0.21 | 3.12 ± 0.22 | 3.50 ± 0.53**,## | |
Variables are given as means ± SD or median [inter-quartile range]. BMI, body mass index; BP, blood pressure; FPG, fasting plasma glucose; TG, triglyceride; TyG index, triglyceride-glucose index; HDL-C, high-density lipoprotein cholesterol; LDL-C, low-density lipoprotein cholesterol; non-HDL-C, non high-density lipoprotein cholesterol; UA, uric acid; OA, olic acid; SA, stearic acid. **p<0.01, *p<0.05 (TG <67 vs 67–106, <67 vs ≥106), ##p<0.01, #p<0.05 (TG 67–106 vs ≥106) by Bonferroni’s multiple comparison test.
Discussion
In this study, most markers except for age were worst in the highest TG group in both OA/SA groups. In addition, most markers except for age, BP, FPG, LDL-C, non-HDL-C, and SA were worse in OA/SA ratio ≥2.85 than <2.85. We showed that the measurement of OA/SA ratio may be a useful indicator of IR, and it may be used to evaluate MetS in non-obese subjects.
Chronically elevated FFA are believed to play a role in the pathogenesis of certain forms of type 2 diabetes by both, inhibiting insulin stimulated peripheral glucose uptake, and contributing to β-cell dysfunction.(19,20) This increases the subsequent risks of MetS, type 2 diabetes mellites, and CVD. Previous cross-sectional study has indicated that metabolically unhealthy obese subjects have increased levels of total FFA, as compared to metabolically healthy obese subjects.(21)
FAs are often grouped as saturated FA (SFA) or monounsaturated fatty acids, according to the biochemical structure. However, the FA within a structural group may not be metabolically equivalent. The P/S (polyunsaturated FA/SFA) ratio is a simple index that is typically used to represent the dietary FA composition of food, or as a biomarker of FA, in epidemiological studies.(22) A high proportion of n-3 FAs and low n-6 FAs in tissues may be beneficial to health, particularly with respect to CVD.(23) Recent report indicated that fish oil (rich in n-3 FA) supplementation combined with high-intensity interval training is superior to fish oil intervention because of its greater effects on glycemic control, IR, CVD risk, and fat mass.(24)
Measuring individual FFA is challenging due to the lack of easy, fast, and reliable methods to quantitate small fractions of FFA in circulation. Evidence indicates the various effects of individual FA, in human health and disease. For instance, olive oil, rich in OA, is supposed to present a modulatory effect in a wide range of physiological functions. Some studies also suggest that it has a beneficial effect in cancer, autoimmune and inflammatory diseases, and facilitates wound healing.(25) it was also reported that a diet rich in SA led to low levels of LDL-C and HDL-C.(26–28) However, few studies have used the product FFA/precursor FFA ratios to investigate the relationship between FFA and human health and disease. This ratio may reflect the function of elongase and desaturase during the endogenous FA metabolism and may be a better predictor for MetS than individual FAs. Further detailed studies on relationship between product FFA/precursor FFA and various disorders are required.
As the fasting immunoreactive insulin levels were not available, we used TG/HDL-C ratio and TyG index as surrogate markers of IR. We recently reported that, in healthy Japanese subjects, the TG/HDL-C ratio is associated with IR, components of MetS, exercise, physical activity, and smoking. However, it is not associated with alcohol intake.(29) The TyG index was well correlated with HOMA-IR (r = 0.41; p<0.001), and showed a strong positive association with TG/HDL-C (r = 0.84; p<0.001).(30) Another report suggested that the TyG index was correlated to the adiposity, metabolic, and atherosclerosis markers related to IR, and it presented a moderate degree of agreement with hyperglycemic clamp.(31)
The cross-sectional design of this study was its major limitation, as it hindered the determination of a causal relationship between the OA/SA ratio and IR. The data regarding fasting immunoreactive insulin levels is not available in this study, and therefore, the IR measured by TG/HDL-C and TyG index was not compared with the HOMA-IR. In addition, the information on dietary intake of FA was not available. All the participants in this study were middle-aged and Japanese; thus, we were not able to determine if the relationship between the OA/SA ratio and clinical markers reported here was affected by ethnicity. Finally, our dataset was small, and our findings may not apply to all Japanese individuals.
In conclusion, our results indicate that the OA/SA ratio might be a useful indicator for IR and may be used to measure metabolic abnormalities in non-obese Japanese adults.
Conflict of Interest
The authors(s) declared no potential conflict of interest with respect to the research, authority, and/or publication of this article.
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