Abstract
Fundamental pancreatic β-cell function is to produce and secrete insulin in response to blood glucose levels. However, when β-cells are chronically exposed to hyperglycemia in type 2 diabetes mellitus (T2DM), insulin biosynthesis and secretion are decreased together with reduced expression of insulin transcription factors. Glucagon-like peptide-1 (GLP-1) plays a crucial role in pancreatic β-cells; GLP-1 binds to the GLP-1 receptor (GLP-1R) in the β-cell membrane and thereby enhances insulin secretion, suppresses apoptotic cell death and increase proliferation of β-cells. However, GLP-1R expression in β-cells is reduced under diabetic conditions and thus the GLP-1R activator (GLP-1RA) shows more favorable effects on β-cells at an early stage of T2DM compared to an advanced stage. On the other hand, it has been drawing much attention to the idea that GLP-1 signaling is important in arterial cells; GLP-1 increases nitric oxide, which leads to facilitation of vascular relaxation and suppression of arteriosclerosis. However, GLP-1R expression in arterial cells is also reduced under diabetic conditions and thus GLP-1RA shows more protective effects on arteriosclerosis at an early stage of T2DM. Furthermore, it has been reported recently that administration of GLP-1RA leads to the reduction of cardiovascular events in various large-scale clinical trials. Therefore, we think that it would be better to start GLP-1RA at an early stage of T2DM for the prevention of arteriosclerosis and protection of β-cells against glucose toxicity in routine medical care.
Highlights
The number of patients with type 2 diabetes mellitus (T2DM) has been increasing all over the world and T2DM is recognized as one of the most prevalent and serious metabolic diseases
It was shown that GLP-1R activator (GLP-1RA) treatment normalized blood pressure, cardiac hypertrophy, vascular fibrosis, endothelial dysfunction, oxidative stress and vascular inflammation in an endothelial GLP-1 receptor (GLP-1R)-dependent manner [65]. We think that these novel findings are strong evidence showing that endothelial GLP-1R expression is GLP-1R is expressed in various cell types, it was not clearly elucidated how GLP-1RA can retard the progression of arteriosclerosis
We described the usability of GLP-1RA based on the molecular mechanism for β-cell glucose toxicity and for the development of arteriosclerosis
Summary
The number of patients with type 2 diabetes mellitus (T2DM) has been increasing all over the world and T2DM is recognized as one of the most prevalent and serious metabolic diseases. It is well known that incretins, glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) have pleiotropic effects on a variety of tissues including. It is well known that incretins, glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) have pleiotropic effects on a variety of tissues including pancreatic β-cells, artery, heart, liver, neuron and adipose tissues. The glucagon-like peptide-1 peptide-1 receptor agonist (GLP-1RA) and dipeptidyl peptidase-IV (DPP-IV) inhibitor are receptor agonist (GLP-1RA) and dipeptidyl peptidase-IV (DPP-IV) inhibitor are very often very often used in subjects with type 2 diabetes mellitus (T2DM). The DPP-IV inhibitor suppresses suppresses activity of DPP-IV, which is a splitting enzyme of incretin and increases serum activity of DPP-IV, which is a splitting enzyme of incretin and increases serum levels of levels of GLP-1 and GIP Both incretins stimulate insulin secretion in a glucose-dependent.
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