The bile acid TUDCA reduces age-related hyperinsulinemia in mice.

- Posted by

This article is about TUDCA and type 2 diabetes, but is likely of interest to our readers who are primarily interested in neurodegenerative publications.

TUDCA most likely has a positive effect on ALS patients. About half of ALS (and Alzheimer's) patients have insulin resistance. Insulin resistance is a disease state in which cells do not respond normally to the hormone insulin. In other words, cells starve, and motor neurons and fast muscle cells suffer first, and then the stress response begins, and so does protein aggregation. Eventually, type 2 diabetes occurs.

Aging is associated with glucose metabolism disturbances, such as insulin resistance and hyperinsulinemia, which contribute to the increased prevalence of type 2 diabetes and its complications in the elderly population. In this sense, some bile acids have emerged as new therapeutic targets to treat type 2 diabetes, as well as associated metabolic disorders.

The taurine conjugated bile acid, tauroursodeoxycholic acid improves glucose homeostasis in T2D, obesity, and Alzheimer's disease mice model. However, its effects in aged mice have not been explored yet.
Here, the authors evaluated the actions of TUDCA upon glucose-insulin homeostasis in aged C57BL/6 male mice treated with 300 mg/kg of TUDCA or its vehicle.

TUDCA attenuated hyperinsulinemia and improved glucose homeostasis in aged mice, by enhancing liver insulin-degrading enzyme expression and insulin clearance.

Furthermore, the improvement in glucose-insulin homeostasis in these mice was accompanied by a reduction in adiposity, associated with adipocyte hypertrophy, and lipids accumulation in the liver.

TUDCA-treated aged mice also displayed increased energy expenditure and metabolic flexibility, as well as a better cognitive ability.
Taken together, authors' data highlight TUDCA as an interesting target for the attenuation of age-related hyperinsulinemia and its deleterious effects on metabolism.

Read the original article on Pubmed

Please, help us continue to provide valuable information: