Cholecystokinin elevates mouse plasma lipids.
Cholecystokinin (CCK) is a peptide hormone that induces bile release into the intestinal lumen which in turn aids in fat digestion and absorption in the intestine. While excretion of bile acids and cholesterol into the feces eliminates cholesterol from the body, this report examined the effect of CC...
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| Format: | Article |
| Language: | English |
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Public Library of Science (PLoS)
2012-01-01
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| Series: | PLoS ONE |
| Online Access: | http://europepmc.org/articles/PMC3533889?pdf=render |
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| author | Lichun Zhou Hong Yang Xinghua Lin Emmanuel U Okoro Zhongmao Guo |
| author_facet | Lichun Zhou Hong Yang Xinghua Lin Emmanuel U Okoro Zhongmao Guo |
| author_sort | Lichun Zhou |
| collection | DOAJ |
| description | Cholecystokinin (CCK) is a peptide hormone that induces bile release into the intestinal lumen which in turn aids in fat digestion and absorption in the intestine. While excretion of bile acids and cholesterol into the feces eliminates cholesterol from the body, this report examined the effect of CCK on increasing plasma cholesterol and triglycerides in mice. Our data demonstrated that intravenous injection of [Thr28, Nle31]-CCK at a dose of 50 ng/kg significantly increased plasma triglyceride and cholesterol levels by 22 and 31%, respectively, in fasting low-density lipoprotein receptor knockout (LDLR(-/-)) mice. The same dose of [Thr28, Nle31]-CCK induced 6 and 13% increases in plasma triglyceride and cholesterol, respectively, in wild-type mice. However, these particular before and after CCK treatment values did not achieve statistical significance. Oral feeding of olive oil further elevated plasma triglycerides, but did not alter plasma cholesterol levels in CCK-treated mice. The increased plasma cholesterol in CCK-treated mice was distributed in very-low, low and high density lipoproteins (VLDL, LDL and HDL) with less of an increase in HDL. Correspondingly, the plasma apolipoprotein (apo) B48, B100, apoE and apoAI levels were significantly higher in the CCK-treated mice than in untreated control mice. Ligation of the bile duct, blocking CCK receptors with proglumide or inhibition of Niemann-Pick C1 Like 1 transporter with ezetimibe reduced the hypercholesterolemic effect of [Thr28, Nle31]-CCK in LDLR(-/-) mice. These findings suggest that CCK-increased plasma cholesterol and triglycerides as a result of the reabsorption of biliary lipids from the intestine. |
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| format | Article |
| id | doaj.art-1d5bd01548614c03968f6dfb421b0b35 |
| institution | Directory Open Access Journal |
| issn | 1932-6203 |
| language | English |
| last_indexed | 2024-12-19T22:05:29Z |
| publishDate | 2012-01-01 |
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| series | PLoS ONE |
| spelling | doaj.art-1d5bd01548614c03968f6dfb421b0b352022-12-21T20:04:02ZengPublic Library of Science (PLoS)PLoS ONE1932-62032012-01-01712e5101110.1371/journal.pone.0051011Cholecystokinin elevates mouse plasma lipids.Lichun ZhouHong YangXinghua LinEmmanuel U OkoroZhongmao GuoCholecystokinin (CCK) is a peptide hormone that induces bile release into the intestinal lumen which in turn aids in fat digestion and absorption in the intestine. While excretion of bile acids and cholesterol into the feces eliminates cholesterol from the body, this report examined the effect of CCK on increasing plasma cholesterol and triglycerides in mice. Our data demonstrated that intravenous injection of [Thr28, Nle31]-CCK at a dose of 50 ng/kg significantly increased plasma triglyceride and cholesterol levels by 22 and 31%, respectively, in fasting low-density lipoprotein receptor knockout (LDLR(-/-)) mice. The same dose of [Thr28, Nle31]-CCK induced 6 and 13% increases in plasma triglyceride and cholesterol, respectively, in wild-type mice. However, these particular before and after CCK treatment values did not achieve statistical significance. Oral feeding of olive oil further elevated plasma triglycerides, but did not alter plasma cholesterol levels in CCK-treated mice. The increased plasma cholesterol in CCK-treated mice was distributed in very-low, low and high density lipoproteins (VLDL, LDL and HDL) with less of an increase in HDL. Correspondingly, the plasma apolipoprotein (apo) B48, B100, apoE and apoAI levels were significantly higher in the CCK-treated mice than in untreated control mice. Ligation of the bile duct, blocking CCK receptors with proglumide or inhibition of Niemann-Pick C1 Like 1 transporter with ezetimibe reduced the hypercholesterolemic effect of [Thr28, Nle31]-CCK in LDLR(-/-) mice. These findings suggest that CCK-increased plasma cholesterol and triglycerides as a result of the reabsorption of biliary lipids from the intestine.http://europepmc.org/articles/PMC3533889?pdf=render |
| spellingShingle | Lichun Zhou Hong Yang Xinghua Lin Emmanuel U Okoro Zhongmao Guo Cholecystokinin elevates mouse plasma lipids. PLoS ONE |
| title | Cholecystokinin elevates mouse plasma lipids. |
| title_full | Cholecystokinin elevates mouse plasma lipids. |
| title_fullStr | Cholecystokinin elevates mouse plasma lipids. |
| title_full_unstemmed | Cholecystokinin elevates mouse plasma lipids. |
| title_short | Cholecystokinin elevates mouse plasma lipids. |
| title_sort | cholecystokinin elevates mouse plasma lipids |
| url | http://europepmc.org/articles/PMC3533889?pdf=render |
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