Here's a study in which they measured a decrease in endogenous cholesterol synthesis after various amounts of dietary cholesterol: Dietary Cholesterol Feeding Suppresses Human Cholesterol Synthesis Measured by Deuterium Incorporation and Urinary Mevalonic Acid Levels (Arteriosclerosis, Thrombosis, and Vascular Biology, 1996):
The objective of this study was to measure the response of cholesterol
biosynthesis in subjects to three different amounts of dietary
cholesterol: 50 (low), 350 (medium), and 650 (high) mg cholesterol per
2800 kcal. Individuals with low (n=7), normal (n=12), and elevated
(n=11) plasma cholesterol concentrations consumed in random order
solid-food test diets (15%, 55%, and 30% of energy as protein,
carbohydrate, and fat, respectively) at each dietary cholesterol
level. The three diets were consumed for 4 weeks each, and each
dietary phase was separated by a 4-week washout period. During the
final week of each diet, 0.7 g D2O was given per kilogram of body
water and deuterium incorporation into the erythrocyte cholesterol
pool was measured for 24 hours. Urinary mevalonate levels were also
determined in samples obtained during two consecutive 24-hour periods.
Both techniques provided measurements of whole-body cholesterol
biosynthesis. In all subjects the cholesterol synthesis rate as
measured by deuterium incorporation was significantly lower (P<.05)
after the transition from low- to medium- and low- to high-cholesterol
diets. Urinary mevalonate excretion decreased after the change from
the medium- to high- (P<.05) and low- to high- (P<.01) cholesterol
diets. Although correspondence between the two methods was poor, they
both indicated some suppression of cholesterol synthesis by dietary
cholesterol. The response of cholesterogenesis to different amounts of
dietary cholesterol was related to the rate of synthesis under
depressed conditions of the low-cholesterol diet. These findings
indicate modest downregulation of synthesis in response to dietary
cholesterol in humans, independent of plasma cholesterol levels.
Metabolic responses to increased dietary cholesterol potentially
include reduced endogenous synthesis, decreased absorption, and
increased biliary excretion of cholesterol.
In some people, who are cholesterol hyperresponders, dietary cholesterol does not effectively suppress endogenous cholesterol synthesis, so it results in elevated blood cholesterol levels (Comprehensive Biotechnology, 2011). In one study, a decrease in dietary cholesterol intake resulted in a decrease of blood cholesterol in hyperresponders but not in hyporesponders: Endogenous cholesterol synthesis, fecal steroid excretion and serum lanosterol in subjects with high or low response of serum cholesterol to dietary cholesterol (Clinical Nutrition, 1986):
In this study we addressed the question whether hypo- and
hyper-responders to dietary cholesterol differ with regard to the
flexibility of endogenous cholesterol synthesis after changes in
cholesterol intake. Whole-body cholesterol synthesis was measured as
faecal excretion of neutral steroids and bile acids minus cholesterol
intake. In addition, we determined serum concentrations of lanosterol,
a precursor of cholesterol and a possible indicator of cholesterol
biosynthetic activity. The study was carried out with 2 hyper- and 4
hypo-responders; these subjects had shown a consistently high or low
response of serum cholesterol to a decrease in dietary cholesterol in
two previous experiments.
The subjects received controlled high- (on average 697 mg of
cholesterol per day) and low-cholesterol (109 mg/day) diets for
periods of 4 weeks in succession; cholesterol was the only dietary
variable. The two hyper-responders again showed a significant decrease
in serum cholesterol. There was essentially no decrease in serum
cholesterol in three of the four hypo-responders. The decrease in
cholesterol intake caused an increase in cholesterol synthesis in five
out of the six subjects.
In conclusion, in most people, dietary intake of cholesterol does not increase blood cholesterol levels because of decreased absorption and endogenous synthesis and increased excretion of cholesterol.