The attrition of telomeres is believed to be a key event not only in mammalian aging, but also in disturbed nutrient sensing, which could lead to numerous metabolic dysfunctions. The current debate focuses mainly on the question whether telomere shortening, e.g., as a heritable trait, may act as a cause or rather represents a consequence of such chronic diseases. This review discusses the damaging events that ultimately may lead or contribute to telomere shortening and can be associated with metabolic diseases.
Keywords: diabetes; leucocyte telomere length; metabolic diseases; obesity telomere shortening.