Signaling pathways that regulate adaptive β‐cell proliferation for the treatment of diabetes

There are distinct signaling pathways that evoke adaptive β-cell proliferation between acute and chronic insulin resistance models. Those signals are, at least in part, mediated through humoral factors from the liver under chronic insulin resistance or fat under acute insulin resistance. AbstractThe decline in β-cell mass due to the failure of β-cell compensation is one cause of the development of type 2 diabetes. Therefore, elucidation of the mechanism by which an adaptive increase in β-cell mass occursin  vivo will lead to the development of a cure for diabetes. Insulin and insulin receptor (IR)-mediated signaling pathways play an important role in the mechanism that increases β-cell mass by compensatory β-cell proliferation in response to chronic insulin resistance. However, whether IR is required for compensatory β-cell proliferation remains controversial in some situations. It might be possible that IR acts as a scaffold for the signaling complex independent of its ligand. It has also been reported that the forkhead box protein M1/polo-like kinase 1/centromere protein A pathway plays a central role in adaptive β-cell proliferation during diet-induced obesity, hyperglycemia, pregnancy, aging and acute insulin resistance. We recently reported that the cro ss-talk of islets with fat tissue, in addition to the liver, through humoral factors is involved in adaptive β-cell proliferation. This accommodative response of β-cell proliferation through adipocytes...
Source: Journal of Diabetes Investigation - Category: Endocrinology Authors: Tags: Mini Review Source Type: research