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Development and Validation of a Methodology for Establishing Obese Rat Models with Typical Fatty Pancreas
Published on: November 11, 2025
Diabese youngsters have 3.7 more chances in developing metabolic syndrome compared with the obese
A Galli-Tsinopoulou1, M G Grammatikopoulou, C Stylianou
1Medical School, Aristotle University of Thessaloniki - 4th Department of Pediatrics, General Hospital Papageorgiou, Thessaloniki, Greece. galtsin@otenet.gr
Background And Aims:
Diabesity, the coexistence of diabetes and obesity, is a new health epidemic. The present case-control study aimed in assessing the prevalence of metabolic syndrome (MS) between diabese and obese children and adolescents.
Methods And Results:
One-hundred and fifty-four obese children and adolescents aged 4-16 yr were recruited and divided in 2 groups: the diabese (no.=85) who were diagnosed with obesity and impaired glucose tolerance (IGT) and the obese (no.=69), who formed the controls group and did not demonstrate IGT. Von Willebrand factor (vWF), plasminogen activator inhibitor-1 (PAI-1), and uric-acid levels were measured. Being diabese increased the odds ratio (OR) for developing MS (OR: 3.714), demonstrating increased serum triglycerides (TG) (OR: 9.067) and low HDL-cholesterol (HDL-C) (OR: 1.405), developing hypertension (OR: 0.750) and acanthosis nigricans (OR: 2.882). In the total sample, low HDL-C was the most common MS criterion, diagnosed in 68% of the diabese and 62% of the obese subjects. Age and weight-adjustment of the continuous data demonstrated that the diabese subjects had higher fat mass index, blood pressure, and TG levels, however the obese exhibited lower HDLC concentrations. Principal component analysis demonstrated that among the inflammatory biomarkers PAI-1 and vWF contributed to the prevalence of MS.
Conclusion:
The present study is the first to demonstrate that the diabese youngsters have 3.7 times more chances in developing MS compared with the obese. From the examined atherosclerotic biomarkers, PAI-1 and vWF contributed to the prevalence of the syndrome and both indicate the initiation of endothelial dysfunction.
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