Gastrin and glucoregulation in T2DM

What is it about?

Management of T2DM, despite new treatment options is still demanding. Newer and safer drugs are available, but their use is sometimes limited by treatment costs. Identifying responders from nonresponders for a certain type of therapy would reduce a period of unsuccessful treatment and minimize health care costs. Incretin therapies, mainly glucagon-like peptide (GLP)-1 receptor agonists (GLP-1RA) increase insulin and lower glucagon response as well as slow down glucose absorption by acting on gastric emptying. However, problem with incretin-based therapy is distinguishing responders from non-responders and currently lack of specific predictors of treatment response. Experimental data demonstrated that activation of GLP-1 and gastrin signaling induces beta cell neogenesis, leading to glucose-dependent insulin secretion. Several studies showed better glycemic control in patients with type 2 diabetes (DMT2) co-treated with proton pump inhibitors (PPI) and incretin based therapy agents. Higher gastrin levels in patients with diabetes prior to initiation of treatment with incretin mimetics could suggest a better potential for reversible human beta-cell reprogramming with concomitant incretin therapy. Therefore, baseline levels of endogenous gastrin could be used as a predictor of response to GLP-1 therapy. In addition, treatment with PPI could also raise gastrin levels and in patients treated with GLP-1RA, lead to better glycemic control.

Featured Image

Why is it important?

Number of people sufferng from T2DM is globally increasing. Despite the available agents, patients often do not reach glycemic targets and develop chronic complications which increase morbidity and mortalitiy. It is important to find proper agents to which patients would respond in order to reverse or stop the unfavorable progress of diabetes