The chick data of Marvin et al. corroborate the report by Schneider and Mercola. They show that inhibition of Wnt signaling in chick embryos promotes heart formation in the anterior lateral mesoderm while Wnt signaling on the opposite side, the posterior lateral mesoderm, promotes blood development. Though obesity is a well-known risk factor for Type II diabetes, the molecular basis of the link has remained unclear. Research done by Barbara Kahn, professor of medicine at Beth Israel Deaconess Medical Center, and colleagues now shows that glucose uptake by adipose tissue is important for maintaining the body's ability to respond to insulin. Their results also point to a mechanism by which an abnormality in adipocytes may trigger insulin resistance and ultimately diabetes.
Skeletal muscle is the primary tissue for insulin-stimulated glucose uptake.
Yet in obesity and Type II diabetes, expression of the primary insulin-stimulated glucose transporter, GLUT4, is normal in muscle but reduced in adipose tissue. This paradox led Kahn and colleagues to ask what role adipose-expressed GLUT4 may play in the development of insulin resistance. The group generated mice whose GLUT4 gene was selectively disrupted in adipose tissue. The mice are insulin resistant and glucose intolerant. As predicted, skeletal muscle from these mice was capable of normal glucose uptake ex vivo.