Abstract
One of the most common pathologies in aging humans is the development of glucose metabolism dysfunction. The high incidence of metabolic dysfunction, in particular type 2 diabetes mellitus, is a significant health and economic burden on the aging population. However, the mechanisms that regulate this age-related physiological decline, and thus potential preventative treatments, remain elusive. Even after accounting for age-related changes in adiposity, lean mass, blood lipids, etc., aging is an independent factor for reduced glucose tolerance and increased insulin resistance. Oxidative stress has been shown to have significant detrimental impacts on the regulation of glucose homeostasis in vitro and in vivo. Furthermore, oxidative stress has been shown to be modulated by age and diet in several model systems. This review provides an overview of these data and addresses whether increases in oxidative stress with aging may be a primary determinant of age-related metabolic dysfunction.
Highlights
The aging process is associated with functional declines in nearly every physiological parameter measured to date [1]
Development of insulin resistance in skeletal muscle, white adipose tissue, and liver is generally thought to be the primary etiology of glucose metabolism dysfunction
If oxidative stress is a significant contributor to this process, it would be predicted that elevated levels of oxidative stress/damage in these tissues would be associated with 1) metabolic dysfunction and 2) increasing age
Summary
The aging process is associated with functional declines in nearly every physiological parameter measured to date [1]. Development of insulin resistance in skeletal muscle, white adipose tissue, and liver is generally thought to be the primary etiology of glucose metabolism dysfunction. If oxidative stress is a significant contributor to this process, it would be predicted that elevated levels of oxidative stress/damage in these tissues would be associated with 1) metabolic dysfunction and 2) increasing age. If oxidative stress is a significant cause of glucose intolerance/insulin resistance, antioxidant treatments would be predicted to prevent metabolic dysfunction. Several genetic models of increased antioxidant expression have been shown to protect from obesity-induced insulin resistance; overexpression of Mn-superoxide dismutase, catalase ( in mitochondria; mCAT) and peroxiredoxin 3 have all been shown to preserve glucose homeostasis with high fat feeding [42,101,102]. New insights into the mechanisms by which oxidative stress negatively affects glucose metabolism may provide new antioxidants, or treatment regimes, that can prevent agerelated metabolic dysfunction
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