Maximus Peto’s Commentary
This group reported on some interesting effects of *oral* trehalose on the development of atherosclerosis in ApoE knockout mice. Trehalose administration also apparently reduced the accumulation of lipids in the liver, and all of these effects appeared to be LDL and HDL-independent.
The Influence of Trehalose on Atherosclerosis and Hepatic Steatosis in Apolipoprotein E Knockout Mice.
Int J Mol Sci. 2019 Mar 28;20(7). pii: E1552.
Stachowicz A, Wiśniewska A, Kuś K, Kiepura A, Gębska A, Gajda M, Białas M, Totoń-Żurańska J, Stachyra K, Suski M, Jawień J, Korbut R, Olszanecki R
PubMed publication date (edat): 3/31/2019
Atherosclerosis and nonalcoholic fatty liver disease (NAFLD) are frequent causes of death in the Western countries. Recently, it has been shown that autophagy dysfunction plays an important role in the pathogenesis of both atherosclerosis and NAFLD; thus, activators of autophagy might be useful for novel therapeutic interventions. Trehalose-a naturally occuring disaccharide present in plants, bacteria, fungi, insects, and certain types of shrimps-is a known inducer of autophagy. However, according to the literature, its anti-atherosclerotic and anti-steatotic potential seem to depend on the experimental setting. The aim of our study was to comprehensively describe the influence of a prolonged treatment with orally administered trehalose on the development of atherosclerotic lesions and hepatic steatosis in apolipoprotein E knockout (apoE-/-) mice in an experimental set up reflecting both moderate and severe proatherogenic conditions: male apoE-/- mice on a chow diet (CD) and female apoE-/- mice fed with a high-fat diet (HFD). We found that exogenous trehalose inhibited atherosclerosis and attenuated hepatic steatosis in apoE-/- mice. Such effects of trehalose were not associated with changes of plasma cholesterol, low-density lipoproteins (LDL), or high-density lipoproteins (HDL). Moreover, the anti-steatotic action of trehalose in the liver was associated with the induction of autophagy. The exact molecular mechanisms of both the anti-atherosclerotic action of trehalose and its inhibitory effect on liver steatosis require further clarification.
Free Full-Text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6479548/