Abstract
Several studies have demonstrated that renal glucose reabsorption is increased in patients with type 2 diabetes. However, the increased renal glucose reabsorption may contribute to the progression of hyperglycemia. Therefore, promoting urine glucose excretion (UGE) by suppression of renal glucose reabsorption is an attractive approach for the treatment of diabetes. Insulin resistance is identified as a major characteristic in the pathogenesis of type 2 diabetes. Thus, our aim was to evaluate the association of UGE with serum insulin levels and insulin resistance in subjects with glucose abnormalities, including prediabetes and newly diagnosed diabetes (NDD). The present study included 1129 subjects, 826 individuals with prediabetes and 303 individuals with NDD. Urine samples were collected within 2 h of oral glucose loading for the measurement of glucose. Fasting serum insulin was measured. Homeostatic model assessment of insulin resistance (HOMA-IR) was assessed. Multiple linear regression analysis and multivariate logistic regression analysis were performed to determine the association of UGE with insulin levels and HOMA-IR. A negative association between serum insulin levels and UGE was observed. The relationship remained significant after adjustment for potential confounders, including age, gender, blood pressure and glucose (β = -5.271, 95% CI: -9.775 to -0.767, p = 0.022). Furthermore, multivariable logistic regression model showed that increased insulin levels were associated with a decreased risk for high UGE after multivariable adjustment. In addition, similar correlation was also observed between HOMA-IR and UGE. HOMA-IR was negatively correlated with UGE after controlling for potential confounders. Moreover, an independent inverse relationship between HOMA-IR and the risk of high UGE was found (OR = 0.85, 95% CI: 0.78–0.93, p < 0.001). In conclusion, insulin levels and HOMA-IR were negatively correlated with UGE after adjusting for potential confounders. Subjects with increased insulin levels or IR were at a decreased risk of high UGE independent of blood glucose. The study suggests that insulin might affect UGE through other ways, in addition to the direct blood glucose-lowering effect, thereby resulting in reduced UGE.
Highlights
The kidney plays a central role in glucose homeostasis, largely through glucose reabsorption (Gerich, 2010; DeFronzo et al, 2012)
No significant differences in age, heart rate (HR), insulin, Homeostatic model assessment of insulin resistance (HOMA-IR), HDLc, low-density lipoprotein-cholesterol (LDL-c), creatinine, and blood urea nitrogen (BUN) were found between the two groups
We found that serum insulin levels were negatively associated with urine glucose excretion (UGE)
Summary
The kidney plays a central role in glucose homeostasis, largely through glucose reabsorption (Gerich, 2010; DeFronzo et al, 2012). Accumulating evidences have demonstrated that renal glucose reabsorption is increased in patients with type 2 diabetes mellitus since enhanced SGLT2 expression (DeFronzo et al, 2013; Osaki et al, 2016). Increased glucose reabsorption may contribute to the progression of hyperglycemia. Promoting urine glucose excretion (UGE) by inhibition of renal glucose reabsorption has been recognized as an effective strategy for the treatment of diabetes (Ferrannini, 2017). Assessing the significance of UGE in clinical practice, such as glycemic control and diabetes screening, has become a noteworthy field (Lu et al, 2011; Yang et al, 2015; Chen et al, 2018a)
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