Interorgan Crosstalk Contributing toβ-Cell Dysfunction.
Type 2 diabetes mellitus (T2DM) results from pancreaticβ-cell failure in the setting of insulin resistance. In the early stages of this disease, pancreaticβ-cells meet increased insulin demand by both enhancing insulin-secretory capacity and increasingβ-cell mass. As the disease progresses,β-cells fail to maintain these compensatory responses. This involves both extrinsic signals and mediators intrinsic toβ-cells, which adversely affectβ-cells by impairing insulin secretion, decreasing proliferative capacities, and ultimately causing apoptosis. In recent years, it has increasingly been recognized that changes in circulating levels of various factors from other organs play roles inβ-cell dysfunction and cellular loss. In this review, we discuss current knowledge of interorgan communications underlyingβ-cell failure during the progression of T2DM.
Division of Endocrinology, Metabolism, Hematological Science and Therapeutics, Yamaguchi University Graduate School of Medicine, Ube, Yamaguchi, Japan.
Katsuya
0000-0001-9802-0584
K
Tanabe
Division of Endocrinology, Metabolism, Hematological Science and Therapeutics, Yamaguchi University Graduate School of Medicine, Ube, Yamaguchi, Japan.
Kikuko
K
Amo-Shiinoki
Division of Endocrinology, Metabolism, Hematological Science and Therapeutics, Yamaguchi University Graduate School of Medicine, Ube, Yamaguchi, Japan.
Masayuki
M
Hatanaka
Division of Endocrinology, Metabolism, Hematological Science and Therapeutics, Yamaguchi University Graduate School of Medicine, Ube, Yamaguchi, Japan.
Yukio
Y
Tanizawa
D017667:Adipocytes / Q000378:metabolism; D000273:Adipose Tissue / Q000378:metabolism*; D000818:Animals; D003924:Diabetes Mellitus, Type 2 / Q000378:metabolism*; D006801:Humans; D007328:Insulin / Q000378:metabolism*; D007333:Insulin Resistance / Q000502:physiology*; D000078790:Insulin Secretion; D050417:Insulin-Secreting Cells / Q000378:metabolism*
D007328:Insulin