Published online Sep 15, 2022. doi: 10.4239/wjd.v13.i9.765
Peer-review started: April 29, 2022
First decision: May 29, 2022
Revised: June 9, 2022
Accepted: August 25, 2022
Article in press: August 25, 2022
Published online: September 15, 2022
Processing time: 133 Days and 13.4 Hours
The pancreatic islet microcirculation adapts its metabolism to cope with limited oxygen availability and nutrient delivery. In diabetes, the balance between oxygen delivery and consumption is impaired. Insulin has been proven to exert complex actions promoting the maintenance of homeostasis of the pancreas under glucotoxicity.
We tried to provide new insight into the relationship between pancreatic microcirculatory oxygen profile and microvascular endothelial mitochondrial metabolism.
To test the hypothesis that insulin administration can improve the integrated pancreatic microcirculatory oxygen profile and bioenergetics.
A three-dimensional framework was generated to visualize the pancreatic microcirculatory oxygen profile. The microcirculatory partial oxygen pressure (PO2), relative hemoglobin (rHb) and hemoglobin oxygen saturation (SO2) were evaluated in nondiabetic, type 1 diabetes mellitus (T1DM), and insulin-treated mice. An Extracellular Flux Analyzer was used to detect the real-time changes in bioenergetics by measuring the oxygen consumption rate and extracellular acidification rate in islet microvascular endothelial cells (IMECs).
Insulin administration ameliorated the glucotoxicity-induced decreases in microcirculatory oxygen parameters (PO2, rHb, and SO2) and improved the mitochondrial ultrastructural abnormalities in IMECs. Insulin-treated IMECs exhibited significantly greater basal respiration than glucotoxicity-exposed IMECs. An energy map revealed increased energetic metabolism in insulin-treated IMECs, with significantly increased ATP production, non-mitochondrial respiration, and oxidative metabolism. Significant negative correlations were revealed between microcirculatory SO2 and bioenergetic parameters.
Glucotoxicity deteriorates the integrated pancreatic microcirculatory oxygen profile and bioenergetics, but this deterioration can be reversed by insulin administration.
Our understanding of the physiology and pathology of the pancreas islet microvascular endothelial cell in T1DM has been continually enhanced with the advancement of microcirculatory technology in parallel with rapidly developing bioenergetics that allows us to increase resolution and precision in our investigations.