P diabetes
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The Role of Selenoprotein P and PPARγ2 Polymorphism in Type 2 Diabetes
Elevated Selenoprotein P Levels in Type 2 Diabetes and Prediabetes
Selenoprotein P and Insulin Resistance
Recent research has highlighted the significant role of selenoprotein P (SeP), a hepatokine, in the regulation of glucose metabolism and insulin sensitivity. Elevated serum SeP levels have been observed in patients with type 2 diabetes and prediabetes compared to those with normal glucose tolerance. This suggests that SeP may contribute to the pathogenesis of insulin resistance, a key feature of type 2 diabetes.
Cardiometabolic Risk Factors
The study further demonstrated that higher SeP levels are associated with various cardiometabolic risk factors, including increased body mass index (BMI), waist circumference, systolic blood pressure, triglycerides, glucose, hemoglobin A1c, and insulin resistance. These associations were significant even after adjusting for age and gender, indicating a robust link between SeP and these risk factors.
Inflammation and Atherosclerosis
In addition to its role in insulin resistance, SeP levels were independently associated with markers of inflammation, such as high-sensitivity C-reactive protein, and atherosclerosis, as measured by carotid intima-media thickness. This underscores the potential of SeP as a biomarker for both metabolic and cardiovascular complications in diabetes.
PPARγ2 P12A Polymorphism and Albuminuria in Type 2 Diabetes
Genetic Influence on Diabetic Nephropathy
The PPARγ2 P12A polymorphism, particularly the A12 variant, has been studied for its impact on insulin resistance and diabetic nephropathy. While the A12 variant is known to reduce the risk of insulin resistance, its effect on albuminuria, a common complication in type 2 diabetes, has been less clear.
Meta-Analysis Findings
A comprehensive meta-analysis, including nine studies with a total of 2376 cases and 4188 controls, revealed that the A12 variant is significantly associated with a reduced risk of albuminuria in patients with type 2 diabetes. The overall odds ratio (OR) for this association was 0.694, indicating a protective effect of the A12 variant against albuminuria.
Methodological Considerations
The meta-analysis also highlighted significant heterogeneity in the genetic effect, which was attributed to differences in urine collection methods and albuminuria definitions across studies. Notably, the protective effect of the A12 variant was more pronounced in studies that measured albumin excretion rate rather than albumin concentration in a single urine sample.
Conclusion
The findings from these studies underscore the complex interplay between genetic and biochemical factors in the pathogenesis and complications of type 2 diabetes. Elevated selenoprotein P levels are linked to insulin resistance, inflammation, and atherosclerosis, while the PPARγ2 P12A polymorphism, particularly the A12 variant, offers a protective effect against albuminuria. These insights could pave the way for more targeted therapeutic strategies and risk assessment tools in managing type 2 diabetes and its complications.
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