Fig. 5.

Loss of intestinal CTα reduces dietary cholesterol absorption. A: Cholesterol in fecal samples from female control and CTα^IKO mice (n = 5 per group). Male control and CTα^IKO received an oral dose of [³H]cholesterol (2 µCi) with 6 mg of unlabeled cholesterol in 150 µl of olive oil and an intravenous injection of [¹⁴C]cholesterol (1 µCi) mixed in Intralipid^®. Blood and feces were collected at 24, 48, and 72 h after cholesterol administration (n = 4 per group). B: Plasma [³H]-labeled at 24, 48, and 72 h. C: Cumulative counts in fecal [³H]-labeled neutral sterols over 72 h. D: Plasma [¹⁴C]-labeled at 24, 48, and 72 h. E: Cumulative counts in fecal [¹⁴C]-labeled neutral sterols over 72 h. Cumulative [³H]-labeled in bile salts (F) and cumulative [¹⁴C]-labeled in bile salts (G) over 72 h. Nonesterified cholesterol (H), cholesterol esters (I), and mRNA abundance of cholesterol synthetic genes (J) in the jejunum of control and CTα^IKO mice refed the HFD (n = 4 or 5 per group). Values are means ± SEM. * P < 0.05; **** P < 0.0001. Cyp51, cytochrome P450, family 51; Fdft1, farnesyl-diphosphate farnesyltransferase 1; Fdps, farnesyl diphosphate synthase; Hmgcr, 3-hydroxy-3-methylglutaryl-CoA reductase; Hmgcs, 3-hydroxy-3-methylglutaryl-CoA synthase; Lss, lanosterol synthase; Mvk, mevalonate kinase; Nsdhl, NAD(P)-dependent steroid dehydrogenase-like; Sqle, squalene epoxidase.