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   <subfield code="a">Stapleton</subfield>
   <subfield code="D">S. R.</subfield>
   <subfield code="u">Department of Chemistry, Western Michigan University, Kalamazoo (Michigan 49008, USA), Fax +1 616 387 2909, e-mail: stapleton@wmich.edu, US</subfield>
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   <subfield code="a">Selenium: an insulin mimetic</subfield>
   <subfield code="h">[Elektronische Daten]</subfield>
   <subfield code="c">[S. R. Stapleton]</subfield>
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   <subfield code="a">Abstract.: Insulin or agents that can mimic its action (insulin mimetics) are necessary to promote the entry of glucose into tissues where the glucose can either be converted into energy or stored for later use. In recent years, selenium has been shown to mediate a number of insulin-like actions both in vivo and in vitro. These insulin-like actions include stimulating glucose uptake and regulating metabolic processes such as glycolysis, gluconeogenesis, fatty acid synthesis and the pentose phosphate pathway. The mechanism by which selenium is capable of mimicking insulin is not clear; however, reports indicate that selenium does activate key proteins involved in the insulin-signal cascade. Various proteins in the insulin-signal cascade have been shown to be necessary for different insulin-regulated events, and presumably data will be forthcoming soon that illustrate this similarly for selenium. This review compares the action of selenium to that of insulin and discusses the available evidence in support of selenium as an insulin mimetic.</subfield>
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   <subfield code="a">Birkhäuser Verlag Basel,, 2000</subfield>
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   <subfield code="a">Key words. Selenium</subfield>
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   <subfield code="a">insulin-mimetic</subfield>
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   <subfield code="u">Department of Chemistry, Western Michigan University, Kalamazoo (Michigan 49008, USA), Fax +1 616 387 2909, e-mail: stapleton@wmich.edu, US</subfield>
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