The global prevalence of T2DM has been rising rapidly in recent decades. Obesity, as a well-recognized modifiable risk factor for T2DM, has long been evaluated using traditional indices such as BMI and WC. However, BMI and WC have limitations in accurately assessing T2DM risk in populations with different weight levels [13]. In this context, novel obesity indices that integrate multiple anthropometric parameters have gained increasing attention, among which WWI has emerged as a promising indicator due to its combination of WC and weight, theoretically overcoming the shortcomings of traditional indices.

This cross-sectional study involving a total of 747 participants found a positive correlation between WWI and the prevalence of T2DM. This indicates that individuals with higher WWI are more likely to develop T2DM, and the risk of T2DM significantly increases when WWI is greater than 10.4 cm/√kg. This study also showed that WWI is not related to gender, marital status, or residents’ basic disease conditions, including dyslipidemia and hypertension. Furthermore, the logistic regression analysis of WWI with BMI, WHR, and age stratification suggests that WWI has more advantages in the risk of elevated blood sugar than BMI and WHR at different ages. These observations indicate that an increase in WWI is an independent risk factor for T2DM, emphasizing the importance of WWI for the prevention and management of T2DM.

Currently, there is a lack of research on the association between WWI and T2DM. Some scholars have proven that elevated WWI is closely related to several diseases, such as abdominal aortic calcification, osteoporosis, heart failure, and stroke [14,15,16]. This study found a positive correlation between WWI and T2DM, indicating that WWI can be an important predictor of T2DM.

Obesity is one of the important risk factors for increasing the incidence of T2DM [17,18,19,20]. Even without other metabolic abnormalities, the risk of T2DM in obese people is still higher than in non-obese people [21,22,23,24]. BMI and WC are traditional indicators of obesity. A retrospective analysis pointed out that in the past 30 years, the BMI of adults in our country has increased by 1.8 kg/m2, the prevalence of obesity has increased 8 times, and the prevalence of T2DM has increased 14 times [25]. Bragg et al. followed up 482,589 Chinese people aged 30 to 79 for 9 years and found that the high waist circumference at baseline was positively correlated with the incidence rate of T2DM [26]. However, a 12.1-year follow-up of 37,733 non-diabetic patients in Spain by Huerta and others showed that BMI and WC have no obvious advantages in predicting the incidence of T2DM [27]. The fundamental reason for the controversy may be partly attributed to the fact that BMI and WC do not distinguish between fat mass and muscle mass. WWI combines the advantages of WC while weakening the relationship with BMI, suggesting that central obesity is unrelated to weight. Recent studies have shown that WWI is the strongest predictor of many diseases, superior to BMI and WC [13, 28]. The ROC analysis demonstrated that WWI outperforms BMI in predicting adverse outcomes in MetS [29].WWI overcomes the inherent flaws of BMI (inability to distinguish fat/muscle) and WC (ignorance of weight context) by integrating central fat distribution and weight normalization. Its stronger predictive power for CVD, T2DM, and related complications is consistent with this study; WWI can be an independent risk factor for T2DM. WWI is simple to calculate, economical and practical, and performs well in predicting disease risk, making it suitable for promotion and application at the grassroots level.

The positive correlation between WWI and T2DM may be related to the following points. First, an increase in WWI may reflect the accumulation of body fat, causing insulin resistance and hyperinsulinemia, reducing the utilization of glucose by muscles and other tissues, thereby reducing glucose tolerance and increasing the incidence of T2DM [30]. Secondly, high body fat reduces the control of blood sugar by DPP-4 inhibitors, increases DPP-4 levels, and accelerates the occurrence of T2DM [31]. Then, an increase in WWI may reflect dysfunction of adipose tissue, thereby promoting the production and release of various pro-inflammatory cytokines. Obesity-related immune activation can induce systemic insulin resistance leading to an increase in T2DM. Finally, at the genetic level, it has been found that in patients with central obesity, the levels of intronic miRNA, miR-676, are upregulated, released from the liver increases, enhancing the phosphorylation of C-Jun terminal kinase and inhibiting the phosphorylation of IRS-1’s Ser307 in the body, thereby causing insulin resistance and increasing the risk of T2DM [32].