The Effect of Different l-Carnitine Administration Routes on the Development of Atherosclerosis in ApoE Knockout Mice.
Level 5 - mechanism / opinion, no new human data
Preclinical animal experiment in ApoE knockout mice
PubMed 29178259 · doi:10.1002/mnfr.201700299
What was done
Male ApoE -/- mice on a high-fat diet (HFD) were randomized into three groups (n = 15 per group): HFD alone, HFD plus oral 1.3% L-carnitine (LC), and HFD plus subcutaneous LC. Investigators measured circulating Ly6C hi monocytes, atherosclerotic plaque area, plasma concentrations of LC, γ-butyrobetaine (γBB), and trimethylamine-N-oxide (TMAO), along with gut microbiota composition.
What was found
Compared to HFD control and HFD with subcutaneous LC, oral LC significantly increased circulating Ly6C hi monocytes, atherosclerotic plaque area, and plasma levels of γBB and TMAO (p < 0.001). Subcutaneous LC produced higher plasma LC levels than other groups without increasing TMAO or plaque area. Plaque area positively correlated with γBB, TMAO, and Ly6C hi monocytes (p < 0.01). TMAO positively correlated with Bacteroidetes and negatively correlated with Firmicutes at the phylum level. Exact absolute values were not reported in the abstract.
Why it matters
This study demonstrates that the pro-atherosclerotic effect of L-carnitine in this model depends on gut microbial metabolism to TMAO via the oral route, whereas parenteral delivery bypasses this pathway.
Limits
The experiment was limited to male ApoE -/- mice fed a high-fat diet, which may not replicate human physiology or dietary contexts. Absolute numerical outcomes and intervention duration were omitted from the abstract.
Cited by
- supports Oral L-carnitine has low absorption bioavailability and oral supplementation increases trimethylamine N-oxide (TMAO).