Scientists have explained why overeating and obesity leads to premature aging

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Discovering the link between obesity, aging, telomere length and metabolic disease is the subject of a joint research team at the University of Texas Health Science Center at Houston (UTHealth).

Telomeres act as protective caps on the ends of chromosomes , to prevent replication errors during cell division. Each time a chromosome replicates, the telomeres shorten. When telomeres become too short, the cell can no longer safely replicate its chromosomes and stops or senesces. This reduction was associated with the aging process and the development of degenerative diseases.

“Recent studies have also shown a link between metabolic diseases caused by obesity, such as type 2 diabetes, and the accumulation of senescent cells that have entered a state of irreversible arrest,” said lead author Mykhailo Kolonin at UTHealth McGovern School of Medicine. – “Cell aging can be caused by telomere shortening due to excessive division of stem cells.”

It is unclear how overnutrition and obesity are mechanistically related to cellular senescence. The authors hypothesized that overfeeding, which causes stem cell overproliferation and telomere depletion, predisposes adipose (fat) cells to premature aging and tissue dysfunction.

Telomeric shortening is prevented by telomerase, an enzyme that repairs telomeres at each division. cells The group created mice with telomerase genetically inactivated in the stem cells that give rise to adipocytes, the lipid-storing cells of adipose tissue. Modeling clinical observations, these mice underwent replicative senescence in adipose tissue, further progression on a high-calorie diet, and development of type 2 diabetes.

To further assess the translational relevance of these results, the team analyzed biopsies from patients who had undergone bariatric surgery. Shorter telomeres were observed in patients who were more resistant to the weight-loss effects of treatment and had a history of metabolic dysfunction.

Together, these results provide a new look at the mechanistic links between aging, obesity-induced diet and metabolic disorders.