Dihydrocholesterol

Dihydrocholesterol-induced gallstones in the rabbit: evidence that bile acids cause gallbladder epithelial injury.[Pubmed: 383127]

Br J Exp Pathol. 1979 Jun;60(3):231-8.

Rabbits fed a diet containing 0.75% Dihydrocholesterol for 7 days develop bile acid allodeoxycholic (ADCA) and deoxycholic acid (DCA) stones in the gallbladder.
METHODS AND RESULTS:
In this model, inflammatory changes in the gallbladder mucosa are often observed even before stones are formed. Within 3 days of the lithogenic diet, abnormalities of platelet function were detectable. Platelet aggregation upon addition of adenosine diphosphate (ADP) was impaired. At the same time the red cells became crenated and developed thorny spicules (echinocytes). This morphological changes was associated with intracellular dehydration and excessive loss of potassium. These changes coincided with a rise in serum ADCA and DCA and preceded a slow rise in serum cholesterol. In vitro incubation studies also suggested that the bile acids had probably caused membrane injury to the platelets and red cells.
CONCLUSIONS:
It is concluded that changes in the bile ADCA and DCA probably induce gallbladder epithelial injury in this model of experimental cholelithiasis.

Plasma cholesterol-lowering activity of dietary dihydrocholesterol in hypercholesterolemia hamsters.[Pubmed: 26184696 ]

Atherosclerosis. 2015 Sep;242(1):77-86.

Cholesterol analogs have been used to treat hypercholesterolemia. The present study was to examine the effect of Dihydrocholesterol (DC) on plasma total cholesterol (TC) compared with that of β-sitosterol (SI) in hamsters fed a high cholesterol diet.
METHODS AND RESULTS:
Forty-five male hamsters were randomly divided into 6 groups, fed either a non-cholesterol diet (NCD) or one of five high-cholesterol diets without addition of DC and SI (HCD) or with addition of 0.2% DC (DA), 0.3% DC (DB), 0.2% SI (SA), and 0.3% SI (SB), respectively, for 6 weeks. Results showed that DC added into diet at a dose of 0.2% could reduce plasma TC by 21%, comparable to that of SI (19%). At a higher dose of 0.3%, DC reduced plasma TC by 15%, less effective than SI (32%). Both DC and SI could increase the excretion of fecal sterols, however, DC was more effective in increasing the excretion of neutral sterols but it was less effective in increasing the excretion of acidic sterols compared with SI. Results on the incorporation of sterols in micellar solutions clearly demonstrated both DC and SI could displace the cholesterol from micelles with the former being more effective than the latter.
CONCLUSIONS:
DC was equally effective in reducing plasma cholesterol as SI at a low dose. Plasma TC-lowering activity of DC was mediated by inhibiting the cholesterol absorption and increasing the fecal sterol excretion.