作者: C.Royce Rasmussen , Bruce E. Maryanoff , Gene F. Tutwiler
DOI: 10.1016/S0065-7743(08)61284-1
关键词: Aldose reductase 、 Endocrinology 、 Blood sugar 、 Glucagon 、 Internal medicine 、 Carnitine 、 Diabetes mellitus 、 Insulin receptor 、 Preproinsulin 、 Insulin 、 Biology
摘要: Publisher Summary Lowering of blood sugar alone may not prevent the chronic complications diabetes. As a result, research has also focused on correction their underlying metabolic abnormalities. Inhibitors aldose reductase (AR) are being pursued because high, localized concentrations sorbitol believed to cause cataracts, retinopathies, and neuropathies. Review literatures diabetes mellitus presented between 1977 1980 discussed in chapter. Obese non-ketosis-prone (Type II; NIDD) often show resistance actions endogenous insulin. Weight loss only 10-15X improves insulin responsiveness and, thereby, glucose tolerance. Research messenger RNA (mRNA) revealed involvement larger polytepkide, preproinsulin, biosynthesis at ribosomal level. Because recombinant DNA methods allow molecular manipulation large proteins, by gene modification/expression, hormone analogs can be produced with amino acid substitutions, deletions, and/or additions. The chapter focuses insulin, glucagon, somatostatin mellitus. Based carbohydrates function receptor, many saccharide derivatives have been examined for agonist antagonist properties. Under conditions high lipid mobilization, products free fatty (FFA) oxidation depress muscle-glucose utilization maintain maximal rates gluconeogenesis. Inhibition FFA affected various mechanisms. Recent studies indicated that metabolite β-pentenoic inhibits 3-ketoacyl-CoA thiolase, one terminal enzymatic steps mitochondria1 p-oxidation, thus contradicting an explanation inhibitory effect pentenoic is its sequestration CoA carnitine as esters.