Review
Copyright ©The Author(s) 2020.
World J Diabetes. May 15, 2020; 11(5): 165-181
Published online May 15, 2020. doi: 10.4239/wjd.v11.i5.165
Figure 1
Figure 1 Slice through a bilayer membrane containing an intrinsic protein viewed in two different conformational states, r and t. At right, the cross-sectional area profile A(z) of each of the two states is plotted as a function of depth z within the membrane of thickness h. This figure is a reprint from Cantor’s work[36]. Reproduced with permission from Lateral pressures in cell membranes: a mechanism for modulation of protein function. Copyright 1997 American Chemical Society.
Figure 2
Figure 2 Although the results of genome-wide screen for type 2 diabetes susceptibility genes are still under debate, a refined working hypothesis proposes that the primary effect of the involved genes generates an increased flux of mitochondrial intermembrane-space protons through UCP1 into the matrix, which causes an increase of extra heat. This process initiates the slow-down principle. UCP: Uncoupling protein; FFA: Free fatty acid; GLUT: Glucose transporter.