Age-related obesity is a heritage of the evolutionary past.

In the process of human aging, an increase in the total amount of fat is observed mainly due to accumulation of lipids in non-adipose tissues. Insulin resistance, provoked by the intracellular accumulation of triglycerides, is often associated with development of such age-related diseases as atherosclerosis, type 2 diabetes, cancer, osteoporosis, and also with systemic inflammation and lipo- and glucose toxicity. Accumulation of lipids and lipophilic compounds is a biological phenomenon common for both prokaryotes and eukaryotes. Initially, it arose as an adaptation to starvation and shortage of nitrogen-containing nutrients, but later it converted into a depot of membrane material, needed on recommencement of cell division. In rodents and humans, the accumulation of non-metabolized fat in non-adipose tissues can be regarded as an adaptation to changes in the internal medium on a certain stage of ontogenesis as a result of age-related dysfunction of adipose tissue.