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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 
 

Plasma triglycerides after oral glucose load specifically associate with metabolic risk markers in healthy type 2 diabetes offspring.

OBJECTIVE: To assess the potential of plasma triglycerides measured after glucose load as biomarker for insulin resistance and cardiovascular risk. METHODS: An oral glucose tolerance test (OGTT, n=91) was performed in healthy type 2 diabetes offspring. Plasma lipids, lipoproteins, glucose and hormones were quantified in fasting and post-challenge samples. RESULTS: During the OGTT total plasma triglycerides decreased in most subjects, however, they increased in some individuals and this increase was strongly associated with metabolic risk factors. Subjects with increasing triglycerides (n=18) were more obese and insulin resistant than those with the most pronounced triglyceride decrease (n=18), as indicated by higher HOMA-IR, BMI and waist circumference. Correlation analysis (n=91) demonstrated that the changes of total plasma and VLDL-associated triglycerides between 0h and 2h (Δ-TG, Δ-VLDL-T) were strongly associated with risk factors. Δ-TG, and especially Δ-VLDL-T, correlated better than fasting triglycerides with waist circumference, waist-to-hip ratio and fasting glucose. The correlations remained significant after adjustment for gender, age and HDL cholesterol. CONCLUSION: The observed increase of triglycerides after glucose load in subjects with signs of insulin resistance and obesity suggests that post-glucose triglyceride change is a potential novel biomarker for early detection of metabolic risk. The specific association of post-glucose triglyceride change with abdominal obesity and fasting glucose suggests a link to hepatic steatosis and insulin resistance.[1]

References

  1. Plasma triglycerides after oral glucose load specifically associate with metabolic risk markers in healthy type 2 diabetes offspring. Vossen, M., Tödter, K., Altenburg, C., Beisiegel, U., Scheja, L. Atherosclerosis (2011) [Pubmed]
 
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