Alterations in gastric secretion following hypothalamic lesions producing hyperphagia

1965 ◽  
Vol 209 (2) ◽  
pp. 319-323 ◽  
Author(s):  
Peter T. Ridley ◽  
Frank P. Brooks
Keyword(s):  
Food Intake ◽  
Gastric Secretion ◽  
Neural Control ◽  
Neural Mechanisms ◽  
Gastric Fistula ◽  
Central Regulation ◽  
Pepsin Secretion ◽  
Insulin Hypoglycemia ◽  
Hypothalamic Lesions

Fasting gastric secretion and secretion during insulin hypoglycemia were collected from hypothalamic hyperphagic rats equipped with chronic gastric fistula in an attempt to correlate the hypothalamic neural mechanisms controlling food intake with gastric secretion. The interdigestive or basal fasting secretion of rats rendered hyperphagic by stereotaxic ablation of the ventromedial nuclei was significantly increased in volume, acid concentration and output, and pepsin output when compared with control and sham-operated rats and rats with hypothalamic lesions without hyperphagia. Hypothalamic hyperphagic rats did not show a significant increase in gastric secretion during insulin hypoglycemia, whereas the other groups did. The levels of hypoglycemia induced by insulin were comparable in all groups. These studies suggest an important role of the ventromedial nuclei in the central regulation of acid and pepsin secretion, and also relate the hypothalamic neural control of gastric secretion to that of food intake. The results also indicate that this nucleus is involved either as a "center" or pathway in the augmentation of gastric secretion by insulin hypoglycemia.

Effects of bombesin on food intake and gastric acid secretion in cats

1989 ◽  
Vol 256 (1) ◽  
pp. R181-R186
Author(s):  
A. Bado ◽  
M. J. Lewin ◽  
M. Dubrasquet
Keyword(s):  
Gastric Emptying ◽  
Food Intake ◽  
Gastric Secretion ◽  
Acid Secretion ◽  
Gastric Fistula ◽  
Single Class ◽  
Heidenhain Pouch ◽  
Daily Food Intake ◽  
Feeding Experiments ◽  
Daily Food

The brain and gut peptide bombesin has been reported both to stimulate gastric secretion and to induce satiety. To understand how the peripheral administration of bombesin affects food intake and whether gastric mechanisms are involved, a comparative study of the doses of bombesin active on gastric secretion, gastric emptying, and food intake was undertaken in cats provided with a gastric fistula and a denervated Heidenhain pouch. The smallest dose of intravenous bombesin that stimulated significantly basal acid secretion (20 pmol.kg-1.h-1) by the gastric fistula also enhanced meal-stimulated acid secretion by the Heidenhain pouch (+138%, P less than 0.01), delayed gastric emptying of a liquid protein meal (-30%, P less than 0.01), and suppressed food intake when the test meal was allowed to reach the stomach (-15%, P less than 0.01). Conversely, in sham-feeding experiments, the same dose of bombesin increased food intake (+35%, P less than 0.01). In full-day experiments conducted in nonfasted cats, bombesin decreased both the food intake in the 4-h period after the infusion and the daily food intake, whereas octapeptide cholecystokinin induced a transient satiety but did not decrease daily food intake. These results indicate that in cats the interaction of bombesin with "pregastric" mechanisms is not sufficient to induce satiety and that a relation could exist between the effects of bombesin on gastric secretion, emptying, and food intake. A single class of receptors might be involved in these peripheral effects of bombesin.

Vagal Gastric Secretory Nerves in the Rat Demonstrated With Insulin

1957 ◽  
Vol 191 (2) ◽  
pp. 262-264 ◽  
Author(s):  
Ardelle Lane ◽  
A. C. Ivy ◽  
E. K. Ivy
Keyword(s):  
Gastric Secretion ◽  
Secretory Response ◽  
Gastric Fistula ◽  
Vagus Nerves ◽  
Insulin Hypoglycemia

It was found in four tests on each of 12 rats with a chronic gastric fistula and accustomed to the experimental procedures that insulin hypoglycemia short of convulsions stimulated gastric secretion when the vagus nerves were intact. In five tests on each of seven rats, it was found that section of the vagi abolished the secretory response to insulin hypoglycemia. This evidence is interpreted as establishing the presence of gastric secretory nerves in the vagi of the rat.

scholarly journals Glial Modulation of Energy Balance: The Dorsal Vagal Complex Is No Exception

2022 ◽  
Vol 23 (2) ◽  
pp. 960
Author(s):  
Jean-Denis Troadec ◽  
Stéphanie Gaigé ◽  
Manon Barbot ◽  
Bruno Lebrun ◽  
Rym Barbouche ◽  
...  
Keyword(s):  
Energy Balance ◽  
Food Intake ◽  
Glial Cells ◽  
Present Review ◽  
Dorsal Vagal Complex ◽  
Central Regulation ◽  
The World ◽  
Nutritional Imbalance ◽  
Nutritional Balance

The avoidance of being overweight or obese is a daily challenge for a growing number of people. The growing proportion of people suffering from a nutritional imbalance in many parts of the world exemplifies this challenge and emphasizes the need for a better understanding of the mechanisms that regulate nutritional balance. Until recently, research on the central regulation of food intake primarily focused on neuronal signaling, with little attention paid to the role of glial cells. Over the last few decades, our understanding of glial cells has changed dramatically. These cells are increasingly regarded as important neuronal partners, contributing not just to cerebral homeostasis, but also to cerebral signaling. Our understanding of the central regulation of energy balance is part of this (r)evolution. Evidence is accumulating that glial cells play a dynamic role in the modulation of energy balance. In the present review, we summarize recent data indicating that the multifaceted glial compartment of the brainstem dorsal vagal complex (DVC) should be considered in research aimed at identifying feeding-related processes operating at this level.

Effects of KCl and insulin on benzimidazole-inhibited canine gastric secretion

1983 ◽  
Vol 245 (6) ◽  
pp. G739-G744
Author(s):  
B. I. Hirschowitz ◽  
J. Fong
Keyword(s):  
Gastric Secretion ◽  
Parietal Cell ◽  
Acid Output ◽  
Gastric Fistula ◽  
Large Decrease ◽  
Pepsin Secretion ◽  
K Secretion ◽  
Inhibited Acid ◽  
K Concentration ◽  
Bethanechol Chloride

The final step in acid secretion is believed to result from the H+-K+-ATPase-mediated exchange of H+ in the parietal cell, with K+ in the lumen. To study the K+ secretion we used Picoprazole and insulin separately and together to inhibit gastric secretion stimulated in gastric fistula dogs with histamine (100 micrograms X kg-1 X h-1). Picoprazole, a substituted benzimidazole (750 mg/kg), reduced gastric H+ concentration and volume with a rise in K+ concentration [( K+]) to 20–25 meq/l. Insulin alone inhibited acid output to the same extent as Picoprazole but with a marked fall in [K+]. Insulin (0.6 U/kg) given with Picoprazole did not alter inhibition of H+ but prevented the large decrease in gastric juice [K+]. An injection of KCl (1 meq/kg) 1 h after Picoprazole did not alter the effects of the inhibitor. Pepsin secretion after insulin was delayed by Picoprazole, whereas during bethanechol chloride infusion (80 micrograms X kg-1 X h-1) pepsin output was reduced for a shorter period and to a lesser extent than acid. We concluded that insulin affects gastric H+ and K+ secretion by a mechanism not related to H+-K+-ATPase and that Picoprazole affects pepsin secretion probably indirectly via its effect on the parietal cell, where its action is quite consistent with an effect limited to inhibition of the H+-K+-ATPase of the parietal cell.

The gastrointestinal peptides and nutrition

1983 ◽  
Vol 61 (4) ◽  
pp. 282-289 ◽  
Author(s):  
J. C. Brown ◽  
C. H. S. McIntosh ◽  
R. A. Pederson
Keyword(s):  
Gastric Emptying ◽  
Food Intake ◽  
Acid Secretion ◽  
Water Movement ◽  
Gut Hormones ◽  
Gastric Inhibitory Polypeptide ◽  
Pepsin Secretion ◽  
Aqueous Component ◽  
Satiety Hormone

Gastrointestinal (GI) peptides have been identified in endocrine cells and nerve fibres throughout the GI tract. They play both a direct and indirect role in the regulation of food intake, digestion, and absorption. The rate at which food is absorbed is dependent upon the rates of gastric emptying, intestinal transit, membrane transport, and enzymatic degradation. The control of pepsin secretion is intimately linked to that of acid secretion and stimulatory peptides, e.g., gastrin and bombesin. Inhibitors of acid secretion such as gastric inhibitory polypeptide (GIP), vasoactive intestinal peptide (VIP), secretin, and glucagon also control pepsin secretion. Powerful inhibitory reflexes, both nervous and hormonal, operate from the duodenum to slow gastric emptying and the most compelling evidence exists for the involvement of neurally released VIP. However, a unifying concept for the role of peptides in the control of intestinal motility is lacking. It is well established that the enzyme component of pancreatic secretion is controlled by the peptide cholecystokinin (CCK) and the aqueous component by secretin. Nutrient absorption can be affected by the endocrine pancreas and by somatostatin. Control of luminal enzyme secretion is increased by CCK, secretin, GIP, VIP, glucagon, and gastrin. Peptides influence the rate and direction of electrolyte and attendant water movement. The secretory actions of VIP are well documented. Peptides, again notably VIP, probably influence digestion and absorption via blood flow changes. Evidence has accumulated that gut hormones stimulate insulin release from the pancreas. The peptide, GIP, has been demonstrated to be a hormone involved in this mechanism and has been hypothesized to be a causal agent in disease states involving hyperinsulinemta, e.g., obesity and maturity onset diabetes. The hypothalamus is recognized to be the major regulatory area for appetite. It receives rich peptidergic innervation as well as being influenced by exogenous peptides. CCK has been shown to inhibit food intake. The presence of this peptide in the brain as well as the gut has led to the suggestion that it is a satiety hormone. However, problems with experimental design render equivocal the role of CCK and other peptides in the control of food intake.

Rapid alterations of hypothalamic and hippocampal bombesin-like peptide levels with feeding status

1993 ◽  
Vol 265 (2) ◽  
pp. R420-R425 ◽  
Author(s):  
Z. Merali ◽  
C. C. Kateb
Keyword(s):  
Food Intake ◽  
Food Deprivation ◽  
Time Course ◽  
Physiological Role ◽  
Ingestive Behavior ◽  
Central Regulation ◽  
Food Ingestion ◽  
Ad Libitum ◽  
Access To Food

It has been suggested that bombesin (BN)-like peptides may play a physiological role in the control of food intake. We studied the time course of changes in the levels of central BN-like peptides during a meal. Four groups of animals were used: rats that were food (but not water) deprived for 12-h period (preprandial group) and then given access to food for either 10 min (partially satiated group) or 35 min (postprandial group). The fourth group constituted nondeprived controls (ad libitum fed group). BN-like immunoreactivity (BLI) of the hypothalamus, hippocampus, and medulla was determined using a radioimmunoassay. Our data revealed that at the hypothalamus, the BLI content dropped significantly after food deprivation (preprandially), and returned to the ad libitum fed control levels after the meal (postprandially). At the hippocampus, food deprivation did not affect the BLI levels; however, food ingestion significantly elevated the BLI content within 35 min. The medullary BLI levels failed to alter in relation to the feeding status. The observed rapid alterations suggest that the hypothalamic response to food intake is satiety linked and hence lend support to the contention that BN-like peptides play a physiological role in the central regulation of ingestive behavior. The alterations noted at the hippocampus implicate physiological role of BN-like peptides in other meal-associated processes (such as memory).

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