Abstract
Decreased peripheral utilization of glucose is an important pathogenic mechanism in diabetes. Although it is universally acknowledged that insulin resistance plays a major role in the reduction of glucose consumption by peripheral tissues, and many defects have been described in the function of insulin receptors (see chapter by Olefsky), indirect clinical and in vivo experimental observations suggest that hyperglycemia per se may participate in inducing and/or maintaining a reduced glucose uptake (summarized in chapter by De Fronzo). The idea occurred to us some years ago that a certain analogy may exist between the downregulation of hormone receptors by augmented hormone concentrations, and the reduction of glucose uptake by hyperglycemia. The extraordinary redundancy of compensatory events that operate in vivo make the testing of such a hypothesis near-impossible. We therefore chose to work in vitro, and because muscle is the main glucose consumer of the periphery, we focused on in vitro muscle preparations and myocyte lines.
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Sasson, S., Ashhab, Y., Melloul, D., Cerasi, E. (1993). Autoregulation of Glucose Transport: Effects of Glucose on Glucose Transporter Expression and Cellular Location in Muscle. In: Östenson, C.G., Efendić, S., Vranic, M. (eds) New Concepts in the Pathogenesis of NIDDM. Advances in Experimental Medicine and Biology, vol 334. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-2910-1_9
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DOI: https://doi.org/10.1007/978-1-4615-2910-1_9
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