Purpose: The purpose of this study was to evaluate the efficiency of multiple abdominal fat indices as measured via ultrasonography for predicting the presence and severity of carotid artery atherosclerosis and to compare the predictive capacity of ultrasonographic measurements to that of anthropometric measurements. Methods: A total of 92 patients were included in this study. All participants underwent clinical and laboratory assessments, and anthropometric measurements were obtained. Ultrasound examinations were performed to measure the values of all abdominal fat indices and the intimamedia thickness, as well as to detect the presence of atherosclerotic plaques. Univariate and multivariate logistic regression analyses were performed. Results: In the multivariate analysis, significant associations were detected between carotid artery atherosclerosis and posterior right perinephric fat thickness (PRPFT) (hazard ratio [HR], 15.23; P<0.001), preperitoneal fat thickness (PPFT) (HR, 4.31; P=0.003), visceral adipose tissue volume (VAT) (HR, 7.61; P<0.001), visceral fat thickness (VFT) (HR, 8.84; P<0.001), the ratio of VFT to subcutaneous fat thickness (VFT/SCFT) (HR, 9.39; P<0.001), and waist-to-height ratio (WHtR) (HR, 2.65; P=0.046). In the multivariate analysis, significant associations were also detected between carotid artery plaque and PRPFT (HR, 7.09; P<0.001), the abdominal wall fat index (AFI) (HR, 3.58; P=0.010), and VFT/SCFT (HR, 4.17; P=0.006). Conclusion Many abdominal fat indices as measured by ultrasound were found to be strong predictors of carotid artery atherosclerosis, including PRPFT, VFT/SCFT, VFT, VAT, PPFT, and WHtR. Moreover, PRPFT, VFT/SCFT, and AFI were identified as strong predictors of the presence of carotid artery plaque.

Diabetes mellitus is associated with inadequate bone health and quality and heightened susceptibility to fractures, even in patients with normal or elevated bone mineral density. Elevated advanced glycation end-products (AGEs) and a suppressed incretin pathway are among the mechanisms through which diabetes affects the bone. Accordingly, the present review aimed to investigate the effects of antidiabetic medications on bone quality, primarily through AGEs and the incretin pathway. Google Scholar, Cochrane Library, and PubMed were used to examine related studies until February 2024. Antidiabetic medications influence AGEs and the incretin pathway directly or indirectly. Certain antidiabetic drugs including metformin, glucagon-like peptide-1 receptor agonists (GLP-1RA), dipeptidyl-peptidase-4 (DDP-4) inhibitors, α-glucosidase inhibitors (AGIs), sodium-glucose co-transporter-2 inhibitors, and thiazolidinediones (TZDs), directly affect AGEs through multiple mechanisms. These mechanisms include decreasing the formation of AGEs and the expression of AGEs receptor (RAGE) in tissue and increasing serum soluble RAGE levels, resulting in the reduced action of AGEs. Similarly, metformin, GLP-1RA, DDP-4 inhibitors, AGIs, and TZDs may enhance incretin hormones directly by increasing their production or suppressing their metabolism. Additionally, these medications could influence AGEs and the incretin pathway indirectly by enhancing glycemic control. In contrast, sulfonylureas have not demonstrated any obvious effects on AGEs or the incretin pathway. Considering their favorable effects on AGEs and the incretin pathway, a suitable selection of antidiabetic drugs may facilitate more protective effects on the bone in diabetic patients.