ABSTRACT
Oxidative Stress ............................................................................................ 322 21.4 Antioxidants .................................................................................................. 324 21.5 Meal-Induced Insulin Sensitization .............................................................. 325 21.6 Absence of Meal-Induced Insulin Sensitization ........................................... 326
21.6.1 AMIS, Age, and Sucrose .................................................................. 328 21.7 HDIR Associated with Age Accelerated by Sucrose Supplement and
Attenuated by Samec .................................................................................... 328 21.8 Implications and Applications ...................................................................... 331 21.9 Summary Points ........................................................................................... 332 Acknowledgments .................................................................................................. 332 References .............................................................................................................. 332
Aging is commonly associated with insulin resistance, characterized by a progressive impairment in glucose uptake and utilization primarily in skeletal muscle. Redistribution of body mass from muscle to fat and progressive hyperglycemia, hyperlipidemia, hyperinsulinemia, and hypertension (the “metabolic syndrome”) often occur. Dysfunction of the central nervous system and the autonomic nervous system, including reduced parasympathetic and CNS cholinergic tone, are also
commonly seen with aging. We have recently suggested that the initiating metabolic defect that leads progressively to the metabolic syndrome, diabetes, and multiple organ failure is a postprandial defect in glucose sequestration that results in nutrient energy being shifted from normal storage as glycogen in skeletal muscle to production and storage of lipids and is typied by postprandial hyperglycemia, hyperinsulinemia, hyperlipidemia, and increased reactive oxidative stress.
