Endocrine Abstracts

Background: C-peptide therapy ameliorates sensory nerve function in T1DM neuropathy. Prolonged GLUT-4 translocation and delayed counter regulation can induce hypoglycemia. GLUT-2 protein is the primary hepatic liver transporter related to hepatic glucose regulation it also plays a role on glucose sensing by pancreatic beta cells, via hepatoportal sensors controlling the autonomic nervous system and stimulates glucagon secretion.

Objective: To discuss the role of isoforms GLUT 2, GLUT 4 and C peptide in the control of diabetes based on analyses of published scientific literatures.

Methods: Review of relevant preclinical and published clinical trial literature on GLUT 2, GLUT 4 and C peptide was completed. Results are analyzed in relation to its role in T1DM or T2DM. Authorship and journal citation observed.

Results: A randomized and placebo controlled study on C-peptide with 139 participants with mean age of 30.6 years. Eighty six percent has neurological impairment. C peptide treatment for 6 months among T1DM participants. GLUT 2 serves as a specific molecule which is required on glucose metabolism and play a role on pancreatic beta cell glucose sensing mechanism. Analyses of cultured hepatocytes treated with high glucose (25 mmol/L) shows that glucose plays a major role in GLUT2 gene upregulation. Comparison of T1DM mice versus normal control mice and the effect of exercise in GLUT 4 shows in mean ± SE, that T1DM group demonstrates a sudden dipping of glucose with exercise stimulus at hour 3 post prandial versus the control on steady state all throughout hour 5.

Conclusions: C-peptide treatment improves sensory nerve function in early stage type 1 diabetic neuropathy. GLUT2 plays a role in primary hepatic regulation and pancreatic beta cells. Exercise induced hypoglycemia in T1DM by prolonging GLUT 4 translocation.