A research project led by the University of California-Davis in the United States, and involving a research group at the University of Córdoba Department of Cell Biology, Physiology and Immunolog, has succeeded in palliating this lesion in mice by removing protein tyrosine phosphatase 1Bfrom renal podocytes, cells involved in forming the barrier which filters substances from the bloodstream; this barrier is a vital element in the kidney filtration system.
Recent studies have shown that protein tyrosine phosphatase 1B “blocks” the cell systems that react to insulin, and thus limits cell glucose uptake; when its action is inhibited, cell sugar levels increase and blood sugar levels are reduced to less harmful levels.
This new research has taken a new step in that direction. Earlier studies had used mice in which the protein was inhibited or eliminated from the whole organism, whereas the new research uses mice in which the protein is eliminated only from podocytes, the kidney cells involved in blood filtration.So far, findings have been highly promising. Mice subjected to this process displayed greater glucose tolerance and improved insulin sensitivity, thus alleviating some consequences of diabetes.
A major conclusion of the study, according to one of the paper's authors, professor of Cell Biology José Manuel Villalba, is that the protein that they have succeeded in eliminating "is crucial in regulating the glucose metabolism. In certain circumstances, such as hyperglycemia, exclusive inhibition of the protein in podocytes will benefit the whole organism”. Although, as Villalba remarks, "there is still a lot of work to be done", this research could contribute to the development of more selective drugs.The protein concerned is present throughout the body, and has a number of key functions; total inhibition could therefore have negative consequences. However, if a drug could be developed which inhibited the protein mainly in these kidney cells, kidney disease - one of the most serious complications of diabetes - could be tackled more effectively.
References:
Protein tyrosine phosphatase 1B deficiency in podocytes mitigates hyperglycemia-induced renal injury. Ito, Y; Hsu, MF; Bettaieb, A; Koike, S; Mello, A; Calvo-Rubio, M; Villalba, JM; Haj, FG. Metabolism.Volume 76, November 2017, Pages 56-69