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 Galardin price credible.\n\nMethod: 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.\n\nResults: 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 selleck products than reported decreases, and the model predicts
no decrease whatsoever in glucosexinsulin, 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 BAY 80-6946 concentration by muscle contraction during exercise.\n\nConclusions: 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.”
“The predictions of two source-to-dose models are evaluated with observed data collected in a village polluted by an operating secondary lead smelter. Both models were built up from several sub-models linked together and run using Monte-Carlo simulation. The first model system provides the distribution of the media-specific lead concentrations (air, soil, fruit, vegetables, and blood) in the whole area investigated. The second model provides an estimate of the concentration of exposure of specific individuals living in the study area.