Inhibition of external pancreatic secretion by intracolonic and intraileal infusions in the cat.

Harper, A. A.; Hood, Ashley J.; Mushens, J; Smy, J R

doi:10.1113/jphysiol.1979.sp012863

Cited by 54 publications

(13 citation statements)

References 16 publications

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“…It is well known that infusion of fat into the terminal ileum or proximal colon leads to an inhibition of exocrine pancreatic secretion in man [4,7] dog [18], cat [5] and rat [6]. A hormonal nature of this inhibitory mechanism was postulated by Demo1 and Sarles [6] who found that pancreatic enzyme inhibition persisted in cross-circulation experiments.…”

Section: Discussionmentioning

confidence: 99%

“…A hormonal nature of this inhibitory mechanism was postulated by Demo1 and Sarles [6] who found that pancreatic enzyme inhibition persisted in cross-circulation experiments. Later, Harper and colleagues [5,19] extracted a peptide-like substance from the feline ileal and colonic mucosa that inhibited CCK stimulated gallbladder contraction. They coined the expression 'pancreotone', since this material inhibited pancreatic exocrine secretion stimulated both by secretin and CCK.…”

Section: Discussionmentioning

confidence: 99%

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Effect of jejunal infusion of different caloric loads on pancreatic enzyme secretion and gastro‐intestinal hormone response in man

Pfeiffer

Vidon

Feurle

et al. 1993

Eur J Clin Investigation

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It has recently been demonstrated that the infusion of a high caloric load (3.3 kcal min-1 = 14.0 kJ min-1) into human upper jejunum inhibited pancreatic enzyme and bile salt secretion. The aim of the present study was to investigate whether this phenomenon was mediated by gastrointestinal hormones which interfere with pancreatic secretion. In six healthy volunteers, jejunal infusion of 1.3 kcal min-1 (5.5 kJ min-1) did not modify secretion of lipase and chymotrypsin to any significant extent compared with saline infusion, but the rate of 3.3 kcal min-1 (14.0 kJ min-1) resulted in an inhibition. Somatostatin and pancreatic polypeptide, which are known to inhibit exocrine pancreatic secretion, remained unchanged during jejunal nutrient infusion. The inhibition of pancreatic enzyme secretion was observed in temporal relationship with an increase of the stimulators of pancreatic exocrine secretion such as secretin, neurotensin, and CCK. The existence of an hitherto undefined inhibitor and a feedback mechanism is postulated.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Effect of jejunal infusion of different caloric loads on pancreatic enzyme secretion and gastro‐intestinal hormone response in man

Pfeiffer

Vidon

Feurle

et al. 1993

Eur J Clin Investigation

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“…Unchanged postprandial responses of these enzymes after both acute and chronic cholestyramine administration, may suggest that inhibitory mechanisms on trypsin and amylase secretion may operate under these conditons. The CCK effect may be antagonized by inhibitory factors present in the gut, named either pancreatone [39] or anti-CCK [40]. A possible candi-date is neurotensin, which has been shown to inhibit trypsin output in man [41].…”

Section: Discussionmentioning

confidence: 99%

Effect of cholestyramine on plasma cholecystokinin and pancreatic polypeptide levels, and exocrine pancreatic secretion

Koop

Fellgiebel

Koop

et al. 1988

Eur J Clin Investigation

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Abstract. The effect of acute and long-term administration of cholestyramine, a non-absorbable bile salt binding resin, on exocrine pancreatic secretion, plasma-cholecystokinin (CCK) and plasma-pancreatic polypeptide (PP) was investigated in 10 healthy volunteers. Oral ingestion of 12 g cholestyramine augmented the stimulatory effect of a liquid test meal on plasma-CCK (3.5-fold) and plasma-PP (2-fold). During prolonged treatment with 3 x 12 g cholestyramine daily for 4 weeks, the most pronounced increase in basal hormone levels was observed after 1 day, but progressively decreased during treatment and had normalized after 4 weeks. However, the stimulated plasma-CCK output was still significantly elevated after cessation of treatment, compared with pretreatment values. After acute and chronic cholestyramine administration only stimulated lipase secretion was elevated, whereas trypsin and amylase remained unchanged. It is suggested that removal of bile salts enhances CCK and thereby PP release and pancreatic lipase secretion.

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“…The distal intestine is known to play an important role in the control of gastrointestinal function. Nutrient (especially lipid) delivered to the ileum results in the inhibition of gastric emptying (21), decreased intestinal motility and transit (30), and decreased pancreatic secretion (14). Ileal nutrient also inhibits food intake (25,33).…”

Section: Pyymentioning

confidence: 99%

Gastrointestinal Satiety Signals IV. Apolipoprotein A-IV

Tso¹,

Sun²,

Liu³

2004

American Journal of Physiology-Gastrointestinal and Liver Physi

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The focus of this article is to review evidence that apolipoprotein A-IV (apo A-IV) acts as a satiety factor. Additionally, information regarding the general involvement of apo A-IV in the regulation of food intake and body weight is stated. Apo A-IV is a glycoprotein synthesized by the human intestine. In rodents, both the small intestine and liver secrete apo A-IV, but the small intestine is the major organ responsible for circulating apo A-IV. There is now solid evidence that the hypothalamus, especially the arcuate nucleus, is another active site of apo A-IV expression. Intestinal apo A-IV synthesis is markedly stimulated by fat absorption and does not appear to be mediated by the uptake or reesterification of fatty acids to form triglycerides. Rather, the local formation of chylomicrons acts as a signal for the induction of intestinal apo A-IV synthesis. Intestinal apo A-IV synthesis is also enhanced by a factor from the ileum, probably peptide tyrosine-tyrosine (PYY). The inhibition of food intake by apo A-IV is mediated centrally. The stimulation of intestinal synthesis and secretion of apo A-IV by lipid absorption are rapid; thus apo A-IV likely plays a role in the short-term regulation of food intake. Other evidence suggests that apo A-IV may also be involved in the long-term regulation of food intake and body weight, as it is regulated by both leptin and insulin. Chronic ingestion of a high-fat diet blunts the intestinal as well as the hypothalamic apo A-IV response to lipid feeding. It also suppresses apo A-IV gene expression in the hypothalamus. Whereas it is tempting to speculate that apo A-IV may play a role in diet-induced obesity, we believe the confirmation of such a proposal awaits further experimental evidence.

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Inhibition of external pancreatic secretion by intracolonic and intraileal infusions in the cat.

Cited by 54 publications

References 16 publications

Effect of jejunal infusion of different caloric loads on pancreatic enzyme secretion and gastro‐intestinal hormone response in man

Effect of jejunal infusion of different caloric loads on pancreatic enzyme secretion and gastro‐intestinal hormone response in man

Effect of cholestyramine on plasma cholecystokinin and pancreatic polypeptide levels, and exocrine pancreatic secretion

Gastrointestinal Satiety Signals IV. Apolipoprotein A-IV

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