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We have used this atlas to describe how islet GPCRs interact with their endogenous ligands, regulate islet hormone secretion, and interact with drugs known to target GPCRs, with a focus on drug/receptor interactions that may affect insulin secretion.
The observed changes may affect insulin sensitivity and glucose metabolism in these subjects.
Large scale association studies [9], [10], [14] suggested that two common MTNR1B SNPs rs1387153 and rs10830963 (r2 = 0.7 in Europeans) may affect insulin secretion and glucose homeostasis.
Nonetheless, we cannot rule out the possibility that an effect of E2 on α-cells may affect insulin release [23] [25].
Plasma melatonin follows an opposite circadian rhythm to plasma insulin and glucose, rising by night and falling by day, which suggests that melatonin may affect insulin release and glucose level via its islet-specific receptor [18].
Alternatively, coffee may affect insulin and glucose signalling.
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Furthermore, impairment of glucose transporter 4 (GLUT4) expression and GLUT4 translocation and/or insulin signaling may affect insulin-stimulated glucose uptake, also resulting in insulin resistance and type 2 diabetes mellitus (T2DM) [3].
These alterations may subsequently affect insulin secretion or insulin resistance.
Current-generation PIs may not affect insulin secretion (24).
Serum potassium, which may also affect insulin release, was not measured during the clamp test.
Both polymorphisms may, however, affect insulin levels (Xita et al., 2005).
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