Disease relevance of Vitamin D3

• Cholesta-5,8-dien-3 beta-ol (8-dehydrocholesterol) and cholesta-5,7-dien-3 beta-ol (7-dehydrocholesterol) were isolated from the fecal neutral sterol fraction from homozygotes with Smith-Lemli-Opitz syndrome [1].

High impact information on Vitamin D3

• DHCR KO mast cells, but not wild-type mast cells, accumulated DHC in lipid rafts [2].
• Incubation of cholesta-5,7-dien-3 beta-ol with rat liver microsomes in the presence of ADP/Fe2+ and NADPH gave rise to a number of oxygenated sterols [3].
• Subsequent Northern blotting studies confirmed that the expression of p75NTR is associated with the upregulation of cholesterol biosynthetic enzymes including 3-hydroxy-3-methylglutaryl CoA reductase (HMG CoA reductase), farnesyl-diphosphate synthase, and 7-dehydro-cholesterol reductase [4].
• Since oxysterols can participate in the regulation of cholesterol homeostasis, we examined the possibility that they are formed from these dehydrocholesterol intermediates [5].
• The RSH/Smith-Lemli-Opitz syndrome (RSH/SLOS) is an autosomal recessive malformation syndrome associated with increased levels of 7-dehydro-cholesterol (7-DHC) and a defect of cholesterol biosynthesis at the level of 3 beta-hydroxy-steroid-delta7-reductase (7-DHC reductase) [6].

Anatomical context of Vitamin D3

• Moreover, only males with a greater T-cell immune response had higher proportions of two steroids (ergosterol and dehydrocholesterol) in their femoral secretions, which might suggest that the signal is honest and costly to produce [7].
• Thus, abnormally elevated amniotic fluid dehydrocholesterol concentrations are an accurate predictor of fetal Smith-Lemli-Opitz syndrome [8].

References