TITLE:
The acceleration of aging and Alzheimer’s disease through the biological mechanisms behind obesity and type II diabetes
AUTHORS:
Ian James Martins, Wei Ling Florence Lim, Andrea C. Wilson, Simon M. Laws, Ralph Nigel Martins
KEYWORDS:
Telomere; Sirtuin 1; Lifestyle; Nutrition; Diabetes; Obesity; Alzheimer’s Disease
JOURNAL NAME:
Health,
Vol.5 No.5,
May
27,
2013
ABSTRACT:
The incidence of diabetes is
predicted to increase to 21% by 2050. Currently, one third of US adults are
obese and over 11% of these individuals have diabetes. Due to the growing
need for therapeutic intervention to control and/or stabilize this increase in
the incidence of diabetes in Western communities, gaining a comprehensive
understanding of the association between obesity and Type 2 diabetes has become
increasingly important to diabetes research. The increased cell senescence
associated with diabetes has been associated with the limited ability of
cells to divide, with indication of telomere shortening and genomic instability
of the cells. Obese individuals have shorter telomeres suggesting an inverse
relationship between adiposity and telomere length. The implication that Type
2 diabetes has on biological aging is of particular interest since telomere
shortening in obesity and diabetes has been associated with an early risk for
dementia and even progression to Alzheimer’s disease (AD). Lifestyle, nutrition
and longevity are closely related and cellular senescence has been associated
with telomere shortening and connected to longevity. Diet, cholesterol lowering
drugs and exercise that control food intake and glucose tolerance in aging and
diabetic individuals, via connections between liver circadian clocks and the suprachiasmatic nucleus in the brain, also have been shown to alter telomere
lengths. Lifestyle interventions, such as diets low in fat and exercise,
target the rise in obesity and associated telomere shortening by delaying or preventing the onset of Type 2 diabetes. The
implementation of these anti-aging therapies early in life may prevent calorie overload and activation of calorie sensitive
genes such as Sirtuin 1 (Sirt1). This may maintain telomere length and the control of obesity, which is linked to cardiovascular disease, diabetes and
accelerates aging and AD.