Mapping Type 2 Diabetes Metabolism


Type 2 Diabetes (T2D) is the most common type of diabetes, currently affecting 90% of people with this systematic metabolic disease. In diabetic individuals, glucose is released in the stomach and absorbed into the bloodstream. There are sufficient levels of insulin produced, but cells fail to intake glucose, therefore, high levels of glucose circulate in the organism along with the bloodstream. It is well known that these excessive levels of circulating glucose have a negative metabolic impact, particularly in eye, kidneys, heart and nerves (see section A in figure 1).

Although diabetes is a systemic metabolic disease, surprisingly, there is not any extensive characterization of how this disease affects the different organs of the body which could be potentially damaged by these high levels of glucose. This means, the deterioration caused could be underestimated and consequently, certain organs and function under-monitored in patients.

It would be too difficult to obtain biopsies from all the organs in enough people, therefore, we used the best animal model to map the metabolic changes caused by T2D. This animal model is the db/db mouse model (Figure 1, section B).

Figure 1. Main changes occurring in Type 2 Diabetes.

The results obtained in this study identified over 60 metabolites (small molecules with specific functions such as singling, fuel or structure) altered in diabetic individuals. Interestingly, out of the 19 organs or biofluids studied, the most metabolically affected by diabetes were kidneys, spleen and eyes. Some of these organs, such as spleen, have been traditionally neglected in diabetes research. This study highlights the need to devote more attention to these forgotten organs and offers a comprehensive list of biomarkers to monitor diabetes and progress in new therapies.

This is study is now available open access. Please, click here to read more.

By Marina Mora-Ortiz

Full citation: Mora-Ortiz, M., Nuñez Ramos, P., Oregioni, A. et al. Metabolomics (2019) 15: 89. https://doi.org/10.1007/s11306-019-1548-8