Since most humans with NASH are obese and insulin resistant, this represents an important difference in how
MCD diets model human NASH.
When both CD and
MCD diets were fed to rats for 7 weeks, the MCD diet group had higher scores of liver inflammation and steatosis than the CD group.
Importantly, unlike human or other diet - induced rodent models of NAFLD, rodents fed
MCD diets lose weight (due to a vastly lower caloric intake) and do not become insulin resistant (9, 19).
In a follow - up study, Pickens et al. showed that despite inducing the same overall level of hepatic fat accumulation, fructose was more effective than glucose at inducing hepatocellular injury in mice fed
MCD diets for 21 days (16).
When fed for equal lengths of time, HFD feeding results in 10-fold lower liver fat levels compared to what accumulates on
an MCD diet (20).
MCD diet - induced NASH is reversible in rats by switching to a diet with suffcient methionine and choline (15).
The mechanisms involved with liver fat accumulation on CD diets may be different from those at work during
MCD diet feeding (11).
Sucrose is an important component of
the MCD diet, since replacing it with corn starch greatly reduces liver fat accumulation, inflammation and injury, likely through reductions in sucrose - induced de novo lipogenesis and triglyceride synthesis (17).
The MCD diet prevents the body from manufacturing choline from methionine, vitamin B12, and folate, so MCD diets severely reduce choline levels; and without choline VLDL particles are not produced.
Not exact matches
And if you go there every week like I do, then you are going to want to give it a little thought rather than let
McD decide your family's
diet.