PubMed · 10907979
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C M Terpening. 2000. The FDA: protector or puppet?. https://doi.org/10.1592/phco.20.9.860.35196
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Progressive beta-cell dysfunction and beta-cell failure are fundamental pathogenic features of type 2 diabetes. Ultimately, the development and continued progression of diabetes is a consequence of the failure of the beta-cell to overcome insulin resistance. Strategies that aim to prevent diabetes must, therefore, ultimately aim to stabilize the progressive decline of the beta-cell. Clinical study evidence from several sources now suggests that thiazolidinediones (TZDs) have profound effects on the beta-cell, such as improving insulin secretory capacity, preserving beta-cell mass and islet structure and protecting beta-cells from oxidative stress, as well as improving measures of beta-cell function, such as insulinogenic index and homeostasis model assessment of beta-cell function (HOMA-%B). Furthermore, intervention studies suggest that TZDs have the potential to delay, stabilize and possibly even prevent the onset on diabetes in high-risk individuals, and these effects appear to accompany improvements in beta-cell function. Here, we review the evidence, from in vitro studies to large intervention trials, for the effects of TZDs on beta-cell function and the consequences for glucose-lowering therapy.
Single crystals of the phenylcoumarin named mammeigin (or mammea A/AA cycle D) [systematic name: 5-hydroxy-8,8-dimethyl-6-(3-methylbutanoyl)-4-phenyl-2H,8H-pyrano[2,3-f]chromen-2-one], C25H24O5, were obtained in the course of a chemotaxonomic study of the Guttiferae family. Mammeigin was extracted from the fruits of Kilmeyera pumila. The structure reveals an infinite three-dimensional network stabilized by non-classical intermolecular hydrogen bonds.
The preparation and characterization of two vitamin E analogs-sydnonimine conjugates, delta-tocopheryloxycarbonyl-3-morpholinosydnonimine (2) and troloxoxycarbonyl-3-morpholinosydnonimine (3), in which the hydroxyl group of the tocopheryl moieties is linked via an enzymatically cleavable urethane group to the sydnone moiety is described. In the presence of porcine liver esterase, these tocopheryl-sydnonimine conjugates generated the expected antioxidant moieties, i.e., delta-tocopherol or Trolox, and were found to convert oxyhemoglobin to methemoglobin at 37 degrees C in 50 mM phosphate buffer at pH 7.4, thus providing evidence for nitric oxide release. Their potency as antioxidants was indirectly studied by associating the two products of the hydrolysis, SIN-1, and delta-tocopherol or Trolox. Our findings suggest that unlike the other members of the sydnonimine family these chromane-sydnonimine derivatives do not act as peroxynitrite donors, and require enzymatic bioactivation before nitric oxide or nitroxyl anion (NO(-)) can be released.