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Abstract
Recent data underscore the importance of intertissue communication in the maintenance of normal glucose homeostasis. Important signals are conveyed by hormones, cytokines, and fuel substrates and are sensed through a variety of cellular mechanisms. The ability of tissues to sense and adapt to changes in metabolic status and fuel availability is altered in insulin-resistant states including type 2 diabetes. Here we review the roles of glucose and its metabolites as signaling molecules and the diverse physiologic mechanisms for glucose sensing.
Authors
Mark A. Herman, Barbara B. Kahn
Figure 4
The adipocyte as a glucose sensor.
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Physiologic downregulation of GLUT4 in the fasted state, pathologic downregulation in insulin-resistant states, or genetic knockout result in diminished glucose flux. The diminished glucose flux is sensed by the adipocyte, resulting in increased RBP4 secretion. Additionally, the diminished glucose flux may limit the ability to generate glycerol-3-phosphate via glycolysis. The adipocyte becomes reliant on glyceroneogenesis for glycerol-3-phosphate production, which may be limiting for fatty acid re-esterification and contribute to increased fatty acid release. G3P, glycerol-3-phosphate; PEP, phosphoenolpyruvate.
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ISSN: 0021-9738 (print), 1558-8238 (online)