Elevated TMAO levels linked to higher diabetes risk, study finds

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Diabetes News

Type 2 Diabetes,Diabetes Mellitus,Diet

A recent Nutrients study links elevated trimethylamine N-oxide (TMAO) levels with an increased risk of type 2 diabetes, highlighting the role of diet in diabetes prevention.

By Dr. Liji Thomas, MDJun 4 2024Reviewed by Benedette Cuffari, M.Sc. A recent study published in the journal Nutrients investigates how the incidence of diabetes is associated with altered trimethylamine N-oxide levels.

TMAO is a microbial metabolite with significant biological roles in cardiovascular health, inflammatory responses, renal function, platelet activation, and lipid metabolism. The primary dietary sources of TMAO include marine fish like cod and haddock, as well as shellfish. Choline, phosphatidylcholine, and L-carnitine, typically found in protein-rich foods like meat and eggs, are also precursor molecules for TMAO.

About the study The current study utilized longitudinal data obtained between 2019 and 2021 in the rural part of Fuxin County in China’s Liaoning Province. 1,515 individuals were included in the study, all of whom were 35 years of age or older, resided in Fuxin County for at least five years, and did not have diabetes at baseline.

Between 2019 and 2021, 81 new T2DM diagnoses were made, which amounts to an incidence rate of 5.35%. At baseline, the median TMAO levels between the T2DM cases and controls were 4.09 μmol/L and 5.08 μmol/L, respectively. Choline levels were associated with a higher T2DM risk. The third and fourth quartiles of serum choline, which reflected the lowest reduction in serum choline levels, were associated with a higher T2DM risk as compared with the first quartile or greatest reduction in serum choline levels.

Conclusions The study findings corroborate previous studies in China and Saudi Arabia, as well as other experimental studies, reporting that TMAO contributes to the development of T2DM. Several biological pathways may be affected by high TMAO levels, including Fox01 and protein kinase R-like ER kinase pathways, as well as bile acid synthesis, which subsequently reduces glucose sensitivity.

 

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