Is Diabetes a Model for Gene-environment Interaction in Premature Senescence?

Abstract

A vast majority of human diseases or disorders are invariably associated with the complex regulations and functions of genes. These also involved in the integration of environmental signals for cells to modulate the functional output of the genome. The ageing process reflects the overall presentation of an organism and the interaction of its genes with the environment. Ageing results from a plethora of processes, which potentially include factors such as diabetes, immune system decline, oxidative damage, rates of apoptosis, and telomere shortening. Persons detected with shorter telomere lengths usually present with accelerated biological ageing, especially those with diabetes mellitus, glucose intolerance, and hypertension. Adverse social factors may be contributory to a worse prognosis for subjects with diabetes mellitus as regards early ageing.The deduction is that diabetes is inextricably linked with "premature ageing". There is appreciable variation in the rate of progression of ageing in humans. A simple biological model may not be sufficient to observe both the clinical and theoretical modalities to understand the mechanisms of gene-environment interaction for diabetes mellitus and premature ageing. The potential clinical and gerontological implications of this study are to configure the  population at risk for developing premature ageing among diabetic patients in order to develop early therapeutic strategies and curtail financial costs to prevent untoward sequelae.

Keywords: Diabetes; model; gene; environment; premature ageing; senescence, therapy, costs.