Abstract

Adipose tissue regulates many important physiological processes, and its dysfunction such as insulin resistance (IR) in type 2 diabetes is closely related to its disordered metabolic profile. However, the potential mechanism is still unclear1. To this end, non-targeted combined with targeted metabolimics based on ultra performance liquid chromatography coupled with mass spectrometry systems were used to assess the metabolic profile of subcutaneous adipose tissue between db/ + and db/db diabetic mice. Sixty-seven metabolites were identified that contributing to the discrimination of normal and diabetic mice. Among these differential metabolites, the abnormal metabolic profile of free fatty acids is mainly manifested in the significant decrease of propanoic acid (C3), myristic acid (C14:0), palmitic acid (C16:0), stearic acid (C18:0) and arachidic acid (C20:0). In addition, several metabolites in TCA cycle were increased significantly in adipose tissue which were associated with compensatory increase of energy metabolism in mitochondria under hyperglycemia2. The present results suggest that abnormal energy metabolism in mitochondria may be a potential mechanism of adipose tissue dysfunction and insulin resistance in diabetic mice.

References

1. Bickerton, A., et al. Adipose tissue fatty acid metabolism in insulin-resistant men. Diabetologia 51, 1466-1474 (2008).
2. Schmid, G.M., et al. Effect of high‐fat diet on the expression of proteins in muscle, adipose tissues, and liver of C57BL/6 mice. Proteomics 4, 2270-2282 (2004).