Gall bladder contraction

The presence of lipids in the GI tract stimulates gall bladder contracts and biliary and pancreatic secretions, including bile salts, phospholipids, and cholesterol. These products, along with the gastric shear movement, form a crude emulsion, which promotes the solubilization of the coadministered lipophilic drug. Exogenous surface-active agents incorporated into the formulation may further stimulate the solubilization of the lipophilic compound. 

Ivy AC, Oldberg E. Hormone mechanism for gall-bladder contraction and evacuation. Am. J. Physiol. 1928 86 599-613. 

A species difference should be pointed out CCK does not provoke gall bladder contraction in rats, since rats do not have gall bladders. The rat liver, however, does release bile salt into the duodenum. The rat probably lacks a gall bladder because it tends to nibble its food slowly over the course of a night. The dog, on the other hand, "wolfs" its food and needs a big supply of bile salts to contend with the sudden entry of fat into the gut. 

Bile, pH 7.8-8.6, is produced continuously in humans. Hepatic bile is concentrated and stored in the gall bladder between meals. It is ejected from the gall bladder and flows into the duodenum when food enters the intestine. The main constituents of bile are bile salts, bilirubin, end products of hemoglobin breakdown, the electrolytes sodium, chloride, and bicarbonate, cholesterol, phospholipids, and lecithin. The gall bladder contracts within 30 min after eating due to liberation of cholecystokinin. The most effective stimulus to this is food high in fat. 

Cholecystokinin (Table 2a) with main effect to stimulate gall bladder contraction and secretion has been implicated in the growth of gut tumors as already reported [53,54] and pituitary tumors [75]. 

Commercial preMrations of cholecystokinin stimulated peristalsis in the colon of man and gall bladder, stomach, and small intestine in the dog.° In dogs, secretion of natural cholecystokinin stimulated by. jejunal perfusion with 0.1 N HCl did not produce an increase in small intestinal motility but did produce gall bladder contraction. ... 

PP occurs in endocrine cells in the pancreatic islets (Alumets et al., 1978), and the peptide inhibits pancreatic exocrine secretion and gall bladder contraction (Schwartz,... 

Plasma bile acids (total bile acids, TBAs) have been recommended as an alternative measurement to plasma bilirubin because TBAs can indicate biliary functionality in terms of the response to food intake. TBA values are dependent upon a number of factors, including stomach emptying gall bladder contraction, where it exists intestinal motility intestinal absorption hepatic uptake and hepatic excretion. The enterohepatic circulation amplifies deficiencies in the hepatic transport system this results in reduced secretion of bile acids into the bile. Studies with dogs have shown that timed postprandial measurements have greater diagnostic value than fasting or random samples (Center et al. 1991 Jensen and Poulsen 1992), but the collection of timed postprandial samples is more difficult. 

Stimulates secretion of pancreatic enzymes and gall bladder contraction where present, inhibits gastric emptying... 

As early as in 1856 the observation was made by Claude Bernard that introduction of hydrochloric acid into the duodenum causes the flow of bile. In the nineteen-twenties, Ivy and his coworkers proved the presence of cholecystokinin in intestinal extracts, but the gall bladder contracting hormone was isolated, from hog intestines, only several decades later, by the efforts of J.E. Jorpes and V. Mutt (Plate 23) [2] who concluded their study with the elucidation of the structure [115]. The 33-residue sequence of cholecystokinin (CCK, porcine). 

Brown AM, Bradshaw MJ, Richardson R et al (1987) Pathogenesis of the impaired gall bladder contraction of coeliac disease. Gut 28 1426-1432... 

In 1943, Harper and Paper (bottom right) demonstrated that extracts of the mucosa of the upper intestine contained a substance that, on intravenous administration, stimulated the pancreas to secrete enzymes (amylase) as opposed to secretin, which stimulated water and bicarbonate secretion. In addition, no effect on volume output was noted. The British researchers proposed the name pancreozymin to describe the former (background). Thereafter, in 1966, the peptide chemists Jorpes and Mutt demonstrated that CCK and pancreozymin shared the same chemical structure and that the two biologic effects-of gall bladder contraction and pancreatic enzyme secretion—were induced by this agent. 

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