Search PubMed⌕ Search

Biomedical subjects

V L Go

Publications and source records attributed to V L Go.

At least 325 records · Page 18Linked to original sources
PubMed1970

Pancreozymin bioassay in man based on pancreatic enzyme secretion: potency of specific amino acids and other digestive products.

The ability of products of digestion to stimulate pancreozymin secretion in man was investigated using a bioassay procedure, based on duodenal perfusion, which quantified the total outputs of pancreatic enzymes evoked by intraduodenal stimuli under steady-state conditions. Patterns of response resulting from physiologic intraduodenal concentrations of test material were basal output (with isotonic saline), washout of enzymes (with dextrose, micellar fatty acid, and amino acids), and sustained output of enzymes (with amino acids and micellar fatty acid). The sustained secretion of pancreatic enzymes found during the 2nd hr of perfusion and subsequently was characteristic of pancreozymin-induced secretion. The enzyme output in response to a mixture of essential and nonessential amino acids was significantly higher than that evoked by micellar fatty acid and was comparable with that resulting from the maximally tolerated dose of pancreozymin given by vein. Perfusion with essential amino acids caused enzyme outputs comparable to those induced by perfusion with the original amino acid mixture, whereas perfusion with nonessential amino acids had no effect. When the essential amino acids were tested individually, only phenylalanine, methionine, and valine caused significant increases in pancreatic enzyme output; the effect of tryptophan was indeterminate. However, the pancreatic enzyme output was less in response to these three essential amino acids than to mixtures containing all of them.

Adult↗
PubMedDate not supplied

Pathogenesis of steatorrhea in primary biliary cirrhosis.

To investigate the pathophysiology of steatorrhea in primary biliary cirrhosis, the severity of steatorrhea, small bowel histology and function, cholestasis, exocrine pancreatic secretion and liver histology were studied. Twenty-four primary biliary cirrhotic patients had a quantitative stool fat collection, serum bilirubin and alkaline phosphatase and liver biopsies. From this group, ten had further studies: a small bowel biopsy (n = 7); a D-xylose test (n = 9); measurement of pancreatiobiliary concentrations and outputs after intravenous cholecystokinin (n = 10); essential amino acid perfusion of the duodenum (n = 9), and eating a test meal (n = 7). D-xylose absorption was normal, and only one patient had a minimal small bowel mucosal abnormality. Pancreatic lipase outputs in response to cholecystokinin were low in two primary biliary cirrhotic patients, but were greater than 10% of normal. Postprandial lipase outputs were normal except in one patient who had abnormal duodenal acidification. Mean enzyme outputs in primary biliary cirrhotic patients were normal in response to essential amino acid perfusion; but 6 had low lipase and 5 had low trypsin outputs which were associated with decreased bile acid outputs (p less than 0.03). Severity of steatorrhea was associated with reduced bile acid outputs and concentrations (r = 0.82; p less than 0.0001), degree of cholestasis (serum bilirubin; r = 0.88; p less than 0.001) and advanced histologic stages (p less than 0.005). Severe intraluminal bile acid deficiency combined with a submaximal intraluminal stimulus (essential amino acids) may be associated with decreased exocrine pancreatic secretion in primary biliary cirrhosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Alkaline Phosphatase↗
PubMedDate not supplied

In vitro, release of cholecystokinin from hypothalamus and frontal cortex of Sprague-Dawley, Zucker lean (Fa/-) and obese (fa/fa) rats.

Cholecystokinin (CCK) has been suggested as a putative satiety factor, whose site of action is in the hypothalamus. The genetically obese (fa/fa) Zucker rat has been proposed as a model of human obesity. Though hypothalamic tissue levels of CCK did not vary between the fa/fa rat and age-matched lean littermates (25.5 +/- 5.7 vs. 27.6 +/- 5.2 pmoles/g tissue) we sought to determine if the releasability of hypothalamic and cortical CCK was the same in lean and obese rats. The in vitro superfusion paradigm was used to study the release of CCK and substance P (sP) from hypothalamus, and CCK and vasoactive intestinal polypeptide (VIP) from frontal cortex. The potassium stimulated release of CCK from obese rat hypothalamic tissue was significantly higher than from lean rat hypothalamus (3.62 +/- 0.3 vs. 1.91 +/- 0.3 fmole equivalents CCK-8/mg tissue/10 min). Similarly, sP release was exaggerated in obese rats in a parallel fashion (5.56 +/- 0.44 vs. 2.761 +/- 0.46 fmoles/mg tissue/10 min). However, the potassium stimulated release of CCK and VIP from cortical tissue was the same in all three groups of rats. The obese Zucker rat thus, may have an anomalous release of CCK and sP from the hypothalamus, but not from the frontal cortex, an area not presumably associated with satiety.

Animals↗