To be clear, type 2 diabetes is a self-inflicted harm for the majority of sufferers, caused by too much food and too much fat tissue carried over the years. It is a condition that can be turned back even in comparatively late stages by nothing more than weight loss and a much reduced diet. Nonetheless it is a prevalent condition and a great deal of research effort is focused on finding more sophisticated methods of treatment.
Here researchers consider the role of cellular senescence in the loss of active pancreatic beta cells involved in the condition: to what degree is type 2 diabetes age-related because of the trend towards increasing weight gain and lack of exercise versus the rising numbers of senescent cells in older tissues? Cells become senescent, removing themselves from the cell cycle, in response to damage or tissue conditions and a signaling environment that implies damage lies ahead. Senescent cells accumulate with age and are a meaningful contribution to the aging process, playing a role in the pathology of many age-related conditions. Given the trials showing that lifestyle choices can reverse type 2 diabetes, however, I am skeptical that cellular senescence is an important factor in most of the cases seen these days:
The incidence of type 2 diabetes significantly increases with age. The relevance of this association is dramatically magnified by the concomitant global aging of the population, but the underlying mechanisms remain to be fully elucidated. Here, some recent advances in this field are reviewed at the level of both the pathophysiology of glucose homeostasis and the cellular senescence of pancreatic islets. Overall, recent results highlight the crucial role of beta-cell dysfunction in the age-related impairment of pancreatic endocrine function.
Alterations of glucose homeostasis increase with age and represent leading causes of morbidity and mortality, mainly linked to both the complications associated with type 2 diabetes and the increased risk for several other age-related diseases. The classical pathophysiological factors responsible for this age-related failure of glucose homeostasis (insulin resistance and decreased secretory capability of beta cells) are quite well characterized, but new mechanisms have recently been revealed. Central to this new development is the key concept that loss or dysfunction of pancreatic beta cells plays a crucial role in the pathogenesis of type 2 diabetes. Since the predominant mechanism of beta-cell generation seems to be self-renewal, the senescence-associated cell cycle dysregulation and the consequent proliferative arrest assume a particular relevance.