Mimicking   gastric  bypass glucotonic effect: the role of atypical PKC activation and GLUT1
Bariatric surgery has demonstrated a significant therapeutic impact in reducing obesity and achieving euglycemia in diabetic patientspatients with diabetes. We previously demonstrated that iIntestinal glucotonic transformation, defined as increased intestinal serum glucose uptake and secretion into the lumen, has anplays a vital  important role in bypass surgeryies. Altered transcriptomes were evaluated in variable intestinal glucotonic models and big-data artificial  intelligence AI-based drug discovery systems. We found noted  that protein kinase C (PKC) activation mimics the intestinal transcriptome changes alterations observed in during intestinal glucotonic transformation. Among PKC subfamilies, atypical PKC promotes GLUT1- mediated  intestinal glucotonic transformation without inducing oncogenic proliferation. Intestinal aPKC activation through via the transposon expression vector induces serum glucose uptake into intestinal tissue and excretion into the lumeinal space. . Prostratin, a non-tumorigenic phorbol ester, was found observed to activate aPKC and induce a similar glucotonic effect. Taken together, our study results highlightCollectively, we identified  a a new chemical compound and target molecular pathways  that may provide a distinct and effective approach to to treating diabetes . Overall design: To find the DEGs after PRKCZ overexpression, 3 mouse intestine samples with PRKCZ overexpression and 3 control mouse intestine samples were analysed.