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Cholecystitis

Cholecystitis

Cholecystitis is inflammation of the gallbladder, most commonly caused by obstruction of the cystic duct. This blockage prevents bile from draining, leading to gallbladder distension, inflammation, and potentially serious complications. This condition may present acutely or chronically and can happen with or without gallstones.EtiologyAbout 95% of cholecystitis cases are calculous, caused by gallstones blocking the cystic duct, leading to bile accumulation and inflammation of the gallbladder...

Lipid Absorption

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Dietary triglycerides from chyme in the duodenum are mixed with bile salts produced by the liver to emulsify fats. As a result, large droplets are broken down into smaller ones, increasing the surface area for enzymatic action. Once emulsified, pancreatic lipases hydrolyze the triglycerides into free fatty acids and monoglycerides.
These breakdown products bind with bile salts and lecithin to form micelles, which quickly pass between microvilli to come in close contact with the apical...

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Related Experiment Video

Updated: May 15, 2026

Assessing Whole-Body Lipid-Handling Capacity in Mice

Assessing Whole-Body Lipid-Handling Capacity in Mice

Published on: November 24, 2020

Cholecystokinin elevates mouse plasma lipids.

Lichun Zhou¹, Hong Yang, Xinghua Lin

¹Department of Physiology, Meharry Medical College, Nashville, TN, USA.

|January 10, 2013

Summary

Cholecystokinin (CCK) significantly increases plasma cholesterol and triglycerides in mice by promoting biliary lipid reabsorption from the intestine. This peptide hormone

Area of Science:

Biochemistry
Endocrinology
Gastroenterology

Background:

Cholecystokinin (CCK) is a peptide hormone regulating digestion and fat absorption.
Bile acid and cholesterol excretion normally eliminates cholesterol, but CCK's role in plasma lipid levels is unclear.

Purpose of the Study:

To investigate the effect of CCK on plasma cholesterol and triglyceride levels in mice.
To elucidate the mechanisms underlying CCK-induced hyperlipidemia.

Main Methods:

Intravenous injection of a CCK analog ([Thr28, Nle31]-CCK) in low-density lipoprotein receptor knockout (LDLR(-/-)) and wild-type mice.
Analysis of plasma lipid and apolipoprotein levels.
Intervention with bile duct ligation, CCK receptor antagonist (proglumide), and NPC1L1 inhibitor (ezetimibe).

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Main Results:

CCK significantly increased plasma triglycerides and cholesterol in LDLR(-/-) mice.
CCK caused smaller, non-significant increases in wild-type mice.
CCK-induced hypercholesterolemia involved alterations in VLDL, LDL, and HDL, with increased apoB48, apoB100, apoE, and apoAI.
Bile duct ligation, proglumide, and ezetimibe treatments attenuated the hyperlipidemic effect of CCK.

Conclusions:

CCK administration increases plasma cholesterol and triglycerides.
These effects are mediated by enhanced reabsorption of biliary lipids from the intestine.
CCK plays a role in regulating lipid metabolism beyond its known digestive functions.