The most common bariatric surgery, Roux-en-Y gastric bypass, leads to glycemia normalization in most patients long before there is any appreciable weight loss. This effect is too large to be attributed purely to caloric restriction, so a number of other mechanisms have been proposed. The most popular hypothesis is enhanced production of an incretin, active glucagon-like peptide-1 (GLP-1), in the lower intestine. We therefore set out to test this hypothesis with a model which is simple enough to be robust and credible. Our method involves (1) setting up a set of time-dependent equations for the concentrations of the most relevant species, (2) considering an “adiabatic” (or quasi-equilibrium) state in which the concentrations are slowly varying compared to reaction rates (and which in the present case is a postprandial state), and (3) solving for the dependent concentrations (of e.g. insulin and glucose) as an independent concentration (of e.g. GLP-1) is varied. Even in the most favorable scenario, with maximal values for (i) the increase in active GLP-1 concentration and (ii) the effect of GLP-1 on insulin production, enhancement of GLP-1 alone cannot account for the observations. I.e., the largest possible decrease in glucose predicted by the model is smaller than reported decreases, and the model predicts no decrease whatsoever in glucose ×insulin, in contrast to large observed decreases in homeostatic model assessment insulin resistance (HOMA-IR). On the other hand, both effects can be accounted for if the surgery leads to a substantial increase in some substance that opens an alternative insulin-independent pathway for glucose transport into muscle cells, which perhaps uses the same intracellular pool of GLUT-4 that is employed in an established insulin-independent pathway stimulated by muscle contraction during exercise. Glycemia normalization following Roux-en-Y gastric bypass is undoubtedly caused by a variety of mechanisms, which may include caloric restriction, enhanced GLP-1, and perhaps others proposed in earlier papers on this subject. However, the present results suggest that another possible mechanism should be added to the list of candidates: enhanced production in the lower intestine of a substance which opens an alternative insulin-independent pathway for glucose transport.

A simple formula is obtained for coupling electrons in a complex system to the electromagnetic field. It includes the effect of intra-atomic excitations and nuclear motion, and can be applied in, e.g., first-principles-based simulations of the coupled dynamics of electrons and nuclei in materials and molecules responding to ultrashort laser pulses. Some additional aspects of nonadiabatic dynamical simulations are also discussed, including the potential of “reduced Ehrenfest” simulations for treating problems where standard Ehrenfest simulations will fail.

Using a new formalism that modifies a tight-binding Hamiltonian to include interaction with a time-dependent electromagnetic field, we have obtained an analytical expression for the second-order susceptibility. This expression has been used to calculate the energy dependence of ${\chi }^{\mathrm{}\left(2\right)\mathrm{}}\left(\omega \right)$ for GaAs. The results are in agreement with previous calculations and with available experimental data.