Pathophysiological Similarities of GDM and T2DM
During normal pregnancy, women experience increased adiposity and weight gain, which begin near mid-pregnancy and progress throughout the third trimester [13]. In this period, insulin resistance ensues as a consequence of multiple factors, including increased production of placental growth hormone, estrogen, and tumor necrosis factor α [14, 15]. Pregnant women with normal glucose tolerance can increase their β-cell insulin secretion in response to this increased insulin resistance during pregnancy. Although the mechanism of increased β-cell insulin secretion during pregnancy is not fully understood, it is reported that prolactin, which increases during pregnancy, can repress islet menin levels and stimulate β-cell proliferation in mice [16]. In addition, recent reports suggest that β-cell serotonin signaling is also a major determinant of β-cell mass during pregnancy [17]. It has been suggested from several clinical studies that GDM women have limited insulin secretion capacity that cannot compensate for the increased insulin resistance [13]. Similar to GDM, T2DM is also characterized by relative deficiency in insulin secretion in the face of increased insulin resistance. Various factors, including increased age, obesity, high-fat diet, and sedentary lifestyle, can induce insulin resistance, and those who do not have sufficient β-cell insulin secretory capacity are more likely to develop T2DM [13]. Therefore, it is said that a large proportion of GDM women are experiencing future T2DM in advance.