Calories and gastric emptying: a regulatory capacity with implications for feeding

McHugh, Paul R.; Moran, Timothy H.

doi:10.1152/ajpregu.1979.236.5.r254

Cited by 142 publications

(121 citation statements)

References 15 publications

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“…The lower gastric retentions observed for the saline and water test meals compared to the rehydrating solution reflected the influences of osmotic concentration and of the calorie content of the meals upon gastric emptying, as reported in other studies (24)(25)(26)(27)(28). During the 72-h period of water deprivation, greater gastric retention of the water and rehydrating solution meals were observed in the dehydrated group.…”

Section: Discussionsupporting

confidence: 81%

Gastric emptying of liquids in rats dehydrated by water deprivation

Baracat

Collares

1997

Braz J Med Biol Res

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The gastric emptying of liquids was investigated in male Wistar rats (8 to 10 weeks old, 210-300 g) dehydrated by water deprivation. In this model of dehydration, weight loss, hematocrit and plasma density were significantly higher in the dehydrated animals than in the control groups after 48 and 72 h of water deprivation (P<0.05). Three test meals (saline (N = 10), water (N = 10) and a WHO rehydrating solution containing in one liter 90 mEq sodium, 20 mEq potassium, 80 mEq chloride and 30 mEq citrate (N = 10)) were used to study gastric emptying following water deprivation for 24, 48 and 72 h. After 72 h, gastric emptying of the water (39.4% retention) and rehydrating solution (49.2% retention) test meals was significantly retarded compared to the corresponding control groups (P<0.05, Mann-Whitney test). The 72-h period of deprivation was used to study the recovery from dehydration, and water was supplied for 60 or 120 min after 67 h of deprivation. Body weight loss, hematocrit and plasma density tended to return to normal when water was offered for 120 min. In the animals supplied with water for 60 min, there was a recovery in the gastric emptying of water while the gastric emptying of the rehydrating solution was still retarded (53.1% retention; P<0.02, KruskalWallis test). In the group supplied with water for 120 min, the gastric emptying of the rehydrating (51.7% retention) and gluco-saline (46.0% retention) solutions tended to be retarded (P = 0.04, Kruskal-Wallis test). In this model of dehydration caused by water deprivation, with little alteration in the body electrolyte content, gastric emptying of the rehydrating solution was retarded after rehydration with water. We conclude that the mechanisms whereby receptors in the duodenal mucosa can modify gastric motility are altered during dehydration caused by water deprivation. Correspondence

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Section: Discussionsupporting

confidence: 81%

Gastric emptying of liquids in rats dehydrated by water deprivation

Baracat

Collares

1997

Braz J Med Biol Res

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“…On the basis of prior experiments in monkeys, dogs, and humans (9,18,20), we predicted that normal regulation of gastric emptying would ensure virtually constant duodenal loads of glucose so that meal volumes and glucose concentrations could be manipulated to determine how different concentrations of glucose entering the duodenum might also affect postprandial hypotension. A secondary aim was to examine the effects of drink volume on the glycemic response to oral glucose.…”

mentioning

confidence: 99%

Effects of drink volume and glucose load on gastric emptying and postprandial blood pressure in healthy older subjects

Jones

O’Donovan

Russo

et al. 2005

American Journal of Physiology-Gastrointestinal and Liver Physi

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. Effects of drink volume and glucose load on gastric emptying and postprandial blood pressure in healthy older subjects. Am J Physiol Gastrointest Liver Physiol 289: G240 -G248, 2005. First published March 17, 2005 doi:10.1152/ajpgi.00030.2005.-Postprandial hypotension (PPH) occurs frequently in the elderly; the magnitude of the fall in blood pressure (BP) is related to the rate of glucose entry into the duodenum during intraduodenal glucose infusion and spontaneous gastric emptying (GE). It is unclear if glucose concentration affects the hypotensive response. Gastric distension may attenuate PPH; therefore, meal volume could influence the BP response. We aimed to determine the effects of 1) drink volume, 2) glucose concentration, and 3) glucose content on the BP and heart rate (HR) responses to oral glucose. Ten subjects (73.9 Ϯ 1.2 yr) had measurements of BP, GE, and blood glucose on 4 days after 1) 25 g glucose in 200 ml (12.5%), 2) 75 g glucose in 200 ml (37.5%), 3) 25 g glucose in 600 ml (4%), and 4) 75 g glucose in 600 ml (12.5%). GE, BP, HR, and blood glucose were measured for 180 min. After all drinks, duodenal glucose loads were similar in the first 60 min. Regardless of concentration, 600-ml (but not 200-ml) drinks initially increased BP, and in the first 30 min, systolic BP correlated (P Ͻ 0.01) with volume in both the proximal and total stomach. At the same concentration (12.5%), systolic BP fell more (P ϭ 0.02) at the smaller volume; at the same volumes, there were no effects of concentration on BP. There was no difference in the glycemic response to drinks of identical glucose content. We conclude that 1) ingestion of glucose at a higher volume attenuates and 2) under constant duodenal load, glucose concentration (4 -37%) does not affect the fall in BP. postprandial hypotension; gastric emptying; elderly POSTPRANDIAL HYPOTENSION, leading to syncope and falls, is an important clinical problem, particularly in the elderly and patients with autonomic dysfunction (7,12,14,19). The mechanisms responsible for postprandial hypotension are poorly defined, and current treatments are less than optimal (7,12,14,19). The magnitude of the postprandial fall in blood pressure is known to be dependent on meal compositioningestion of carbohydrate, particularly glucose, has the greatest effect on blood pressure (27), whereas the effects of fat and protein appear to be much less (10).Changes in splanchnic blood flow, sympathetic nerve activity, and release of gastrointestinal peptides are all thought to play a role in postprandial hypotension (7,12,14,19). Onset of the fall in blood pressure is evident soon after a meal, with a maximum response at 30 -60 min (14). While oral ingestion of glucose leads to a fall in blood pressure, intravenous infusion of glucose has little, if any, effect (13) indicating that the response is mediated from the gastrointestinal tract. We have reported that in both healthy older subjects and patients with type 2 diabetes managed by diet alone, the hypotensive and heart rate responses t...

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“…GASTRIC EMPTYING IS ONE MECHANISM involved in the regulation of food intake (33,43). A delay in gastric emptying limits the rate of absorption by reducing the rate of nutrient delivery to the small intestine (5,15,58) and is associated with suppression of food intake (43).…”

mentioning

confidence: 99%

5-HT₃receptors participate in CCK-induced suppression of food intake by delaying gastric emptying

Hayes¹,

Moore²,

Shah³

et al. 2004

American Journal of Physiology-Regulatory, Integrative and Comp

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Hayes, Matthew R., Rachael L. Moore, Samit M. Shah, and Mihai Covasa. 5-HT 3 receptors participate in CCK-induced suppression of food intake by delaying gastric emptying. Am J Physiol Regul Integr Comp Physiol 287: R817-R823, 2004. First published June 10, 2004 10.1152/ajpregu.00295.2004.-Serotonin type 3 (5-HT 3) receptors have been shown to participate in the negative-feedback control of food intake. We previously reported that cholecystokinin (CCK)-induced suppression of food intake is partly mediated through 5-HT 3 receptors when rats were tested on a preferred liquid diet, but whether such an effect occurs when they are tested on a solid maintenance diet is unknown. In the present study, we examined the effects of ondansetron, a selective 5-HT 3 antagonist, on CCK-induced suppression of solid chow intake. Intraperitoneal administration of ondansetron significantly attenuated 30-and 60-min CCK-induced reduction of food intake, with suppression being completely reversed by 120 min. It is not known whether 5-HT 3 receptors directly mediate CCK-induced satiation or whether their participation depends on CCK acting as part of a feedback cascade to inhibit ongoing intake. Because CCKinduced inhibition of sham feeding does not depend on additive gastric/postgastric-feedback signals, we examined the ability of ondansetron to reverse CCK-induced satiation in sham-feeding rats.Ondansetron did not attenuate reduction of sham feeding by CCK, suggesting that ondansetron does not directly antagonize CCK-satiation signals. CCK suppresses real feeding through a delay in gastric emptying. Ondansetron could attenuate CCK-induced reduction of food intake by reversing CCK-induced inhibition of gastric emptying. We found that blockade of 5-HT3 receptors attenuates CCK-induced inhibition of gastric emptying of a solid meal, as well as saline and glucose loads. We conclude that 5-HT 3 receptors mediate CCKinduced satiation through indirect mechanisms as part of a feedback cascade involving inhibition of gastric emptying. ondansetron; serotonin; osmotic; glucose; satiety GASTRIC EMPTYING IS ONE MECHANISM involved in the regulation of food intake (33, 43). A delay in gastric emptying limits the rate of absorption by reducing the rate of nutrient delivery to the small intestine (5, 15, 58) and is associated with suppression of food intake (43). Inhibition of gastric emptying is mediated by peripheral vagal and sympathetic nerves and by the release of a variety of peptides and neurotransmitters (43,54). Cholecystokinin (CCK) and serotonin [5-hydroxytryptamine (5-HT)] are two humoral signals thought to exert control on gastric emptying and are released in response to nutrients entering the duodenum (6,28,30,43,49,60). Both of these satiety signals bind to receptors on terminals of vagal afferent fibers, resulting in a delay in gastric emptying (4, 24, 49).Considerable evidence indicates that the serotonergic system participates in the negative-feedback control of food intake (for review see Ref. 25). Systemic serotonergic activity h...

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Calories and gastric emptying: a regulatory capacity with implications for feeding

Cited by 142 publications

References 15 publications

Gastric emptying of liquids in rats dehydrated by water deprivation

Gastric emptying of liquids in rats dehydrated by water deprivation

Effects of drink volume and glucose load on gastric emptying and postprandial blood pressure in healthy older subjects

5-HT₃receptors participate in CCK-induced suppression of food intake by delaying gastric emptying

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Calories and gastric emptying: a regulatory capacity with implications for feeding

Cited by 142 publications

References 15 publications

Gastric emptying of liquids in rats dehydrated by water deprivation

Gastric emptying of liquids in rats dehydrated by water deprivation

Effects of drink volume and glucose load on gastric emptying and postprandial blood pressure in healthy older subjects

5-HT3receptors participate in CCK-induced suppression of food intake by delaying gastric emptying

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5-HT₃receptors participate in CCK-induced suppression of food intake by delaying gastric emptying