SEARCH · PubMed Health

Results for “Postprandial”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources

PubMed1979

Postprandial gastric function in pancreatic insufficiency.

Abnormalities in postprandial gastric function could contribute to the maldigestion of pancreatic insufficiency. To measure simultaneously postprandial gastric secretion and emptying and correlate these measurements with intraluminal duodenal changes, we performed intestinal intubation and duodenal perfusion during feeding of a solid-liquid test meal in 10 healthy controls and 10 patients with documented pancreatic insufficiency before and after replacement therapy. In pancreatic insufficiency, intraduodenal pH was significantly decreased late in the postprandial period while simultaneously measured duodenal acid loads were normal, confirming that reduced bicarbonate output rather than increased acid delivery was responsible for higher duodenal acidity in these patients. Significant (P less than 0.05) reductions in postprandial acid, pepsin, and total secretory outputs were noted in untreated patients only during the first postprandial hour. Absolute gastric emptying rates were lower in patients (P less than 0.05) than in healthy subjects, but fractional rates of emptying were similar. Fasting and postprandial hypergastrinaemia were consistently observed in the patients with pancreatic disease. There are postprandial disturbances of secretory function but no primary gastric motor defect in patients with exocrine pancreatic insufficiency.

Duodenum↗

PubMed1977

Postprandial plasma lysine as an indicator of dietary lysine adequacy in infants.

Postprandial plasma free amino acids were studied as an index of the level of dietary lysine. Fasting blood was obtained from 11 children who were then fed a meal in which wheat provided 100% of 0.4 g protein and 30% to 50% of 25 kcal/kg body weight. Blood samples were obtained 3 and 4 hours postprandially. Fasting blood samples were obtained from these same children after 9, 18 and 27 (n=6) days of consuming the same diet (2 g protein, 125 kcal/kg/day). Postprandial blood samples were taken from four additional children after consuming a meal containing 25 kcal and 0.75 g protein (0.5 g from wheat, 0.25 g casein)/kg. This meal was expected to provide adequate lysine while still maintaining lysine in lowest concentration among the essential amino acids relative to needs for protein synthesis. After consuming the unsupplemented wheat diet postprandial values showed a significant rise of total amino acids at 3 hours with a return to fasting levels at 4 hours. Total essential amino acids did not change at 3 or 4 hours. Lysine concentration was significantly lower at 3 and 4 hours. The ratio of lysine to total essential amino acids decreased at 3 and, more so, at 4 hours. In 3 of 4 children studied the postprandial decrease of plasma lysine and its molar fraction was not manifest after consuming wheat + casein. The fasting lysine concentration during continued wheat consumption showed no change at 9 days and then a progressive fall at 18 and 27 days. The results with wheat + casein lend support to the concept that a postprandial fall in the concentration of lysine and its molar fraction indicates not merely that lysine is present in lowest concentration but that it is present in inadequate concentration relative to needs for protein synthesis.

Amino Acids↗

PubMed2026

Supplementations of docosahexaenoic acid and blueberry suppress a high-fat breakfast-induced postprandial inflammation but only docosahexaenoic acid improves endothelial function in healthy adults: a randomized, double-blind, placebo-controlled crossover intervention study.

Blueberries and n - 3 polyunsaturated fatty acids each can provide protection against inflammation and cardiometabolic disorders. However, the underlying mechanisms are not fully understood. We hypothesized that blueberry and docosahexaenoic acid (DHA) can suppress high fat (HF) meal-induced postprandial inflammation and improve endothelial function. Sixty-two healthy participants (age: 26.8 ± 1.2 y; BMI: 22.1 ± 1.2 kg/m²) consumed an isoenergetic breakfast (850 kcal) containing 34.7 g mostly animal fat (36% kcal), 25.3 g protein, and 111 g carbohydrate, with or without either 42.2 g blueberry powder (BBP) or 1.76 g DHA in a randomized, double-blind, placebo-controlled crossover intervention study. Blood samples were collected before and 1 h, 3 h and 6 h after breakfast. Monocyte activation, proinflammatory gene expression, cytokine production and endothelial function were assessed. Compared with the placebo control, DHA supplementation suppressed the HF breakfast-induced: expression of IL-1β by 21.6% (P < .01) and prostaglandin-endoperoxide synthase 2 (PTGS2, i.e., cyclooxygenase 2) by 22.8% (P < .01) at 6 h; plasma IL-1β production by 40.1 to 49.8% (P < .01) at 1-6 h; lipoprotein lipase (LPL)-treated blood IL-1β production by 40.9% (P < .0001) at 6 h; and total cholesterol/HDL cholesterol ratio by 2.2% (P < .01) at 3 h and 3.5% (P < .0001) at 6 h. BBP supplementation suppressed LPL-treated blood IL-1β production by 23.1% (P < .05) at 6 h. BBP and DHA also induced postprandial increases in reactive hyperemia index (RHI) scores relative to the fasting baselines, with DHA producing a 13.3% increase compared with placebo at 6 h (P < .05). In conclusion, supplementation with BBP or DHA suppressed the HF meal-induced postprandial inflammation but only DHA improved postprandial endothelial function. This study was registered at clinicaltrails.gov (NCT02472171).

Blueberry↗

PubMed1979

Haemodynamic and electrocardiographic accompaniments of resting postprandial angina.

The early postprandial changes in 10 patients with angiographically proven coronary artery disease and history of postprandial angina were studied by the continuous recording on magnetic tape of the electrocardiogram and haemodynamic variables. The significant changes 20 minutes after a meal not followed by angina included increases in cardiac index and stroke index, with a decrease in systemic vascular resistance. When angina developed after a meal, there were significant increases in mean systemic arterial blood pressure, heart rate, pulmonary capillary wedge pressure, and systemic vascular resistance with decreases in stroke index at the onset of pain rather than at the onset of ischaemic electrocardiographic abnormalities. The first haemodynamic variable to change was pulmonary capillery wedge pressure which tended to increase coincident in time with the electrocardiographic abnormalities. In all cases, postprandial angina occurred within 25 minutes after a meal. In every instance, there was little or no change in the product of heart rate and systolic arterial blood pressure at the onset of the ischaemic electrocardiographic abnormalities at a time when the pulmonary capillary wedge pressure had begun to rise. Postprandial angina, like many cases of rest angina, may rise on the basis of a primary decrease in myocardial perfusion, the nature of which is unclear but merits further investigation.

Aged↗

PubMed2026

GIP contributes to postprandial regulation of splanchnic blood supply in humans with type 2 diabetes: a randomised, single-blinded, placebo-controlled, crossover study.

AIMS/HYPOTHESIS: In healthy lean humans, endogenous glucose-dependent insulinotropic polypeptide (GIP) contributes significantly to the postprandial increase in arteria mesenterica superior blood flow. The vascular biology related to activation of the GIP receptor is markedly impaired in individuals with type 2 diabetes and is sometimes absent. In this population, we investigated the role of endogenous GIP on postprandial splanchnic blood flow by using the GIP receptor antagonist, GIP(3-30)NH2. The primary outcome of this study was the changes in blood flow in arteria mesenterica superior during oral glucose with or without GIP receptor antagonist infusion. METHODS: Ten participants with type 2 diabetes (age 20-80 years, BMI 20-35 kg/m2, and HbA1c >48 mmol/mol and <75 mmol/mol) were investigated in a randomised, placebo-controlled, crossover study. On four separate occasions, participants received the following treatment: oral glucose + i.v. GIP(3-30)NH2; oral glucose + i.v. saline (154 mmol/l NaCl); oral water + i.v. GIP(3-30)NH2; oral water + i.v. saline. Participants were randomly assigned to intervention groups using (random.org). Participants were unaware of allocation, while investigators were aware. No additional allocation concealment procedures were used. During all four interventions, splanchnic blood flow was measured using phase-contrast MRI in the arteria mesenterica superior, truncus coeliacus and vena portae during oral glucose (75 g) or water ingestion. The study was conducted at Rigshospitalet, Copenhagen. Liver volume and oxygenation, as well as gallbladder volume, were assessed. Blood samples were collected and analysed for insulin, C-peptide, GIP, glucagon and glucose. RESULTS: Oral glucose alone increased mean blood flow in arteria mesenterica superior by 57% (95% CI 26, 88) and this was 15% (95% CI -2, 32) lower during concomitant GIP receptor antagonist infusion, p=0.012. Infusion of GIP receptor antagonist during oral glucose treatment did also result in lower insulin secretion, C-peptide and C-peptide/glucose ratio compared with saline infusion, whereas glucagon levels and plasma glucose were unaffected. Oral water did not affect any outcomes. CONCLUSIONS/INTERPRETATION: Endogenous GIP contributes to postprandially increased splanchnic blood flow in people with type 2 diabetes. TRIAL REGISTRATION: ClinicalTrials.gov NCT06426823 FUNDING: This work was supported by the Novo Nordisk Foundation.

Humans↗

PubMed2026

Effects of short-bout accumulated exercise on postprandial metabolism in adults: A systematic review and meta-analysis.

OBJECTIVE: To systematically evaluate the acute effects of short-bout accumulated exercise (SBAE) interrupting prolonged sedentary behaviour on postprandial glucose, insulin, and triglycerides in adults. METHODS: Systematic searches in PubMed, Web of Science, Embase, Cochrane Library, CINAHL, SPORTDiscus, and CNKI (inception to 10 December 2025) identified randomised crossover trials comparing SBAE (≤10 min/bout, inter-bout interval ≥30 min or adequate recovery) with continuous sedentary behaviour. Outcomes included postprandial glucose, insulin, and triglyceride AUCs. Standardised mean differences (SMD) were pooled using random-effects models. RESULTS: Thirty-one publications reporting data from 29 independent cohorts involving 573 unique participants (mean age 47.8 ± 20.3 years; 47.5% female; mean BMI 29.0 ± 5.1 kg/m²) were included. Compared with continuous sedentary behaviour, SBAE significantly reduced glucose AUC (SMD = -0.53, 95% CI: -0.71 to -0.34, P < 0.001) and insulin AUC (SMD = -0.58, 95% CI: -0.85 to -0.31, P < 0.001), but not triglyceride AUC (SMD = -0.17, 95% CI: -0.48 to 0.15, P = 0.306).Exploratory subgroup analyses showed statistically significant reductions in glucose and insulin for walking and for inter-bout intervals < 60 min, but not for standing alone or intervals ≥ 60 min. A statistically significant insulin-lowering effect was observed in obese individuals. CONCLUSION: SBAE acutely improves postprandial glucose and insulin control. Exploratory subgroup analyses showed statistically significant effects for walking and for inter-bout intervals < 60 min, but these comparisons are observational and no formal interaction test was conducted. These findings provide preliminary evidence for acute SBAE in sedentary populations, though long-term health effects and real-world generalisability require further investigation.

Adult↗

PubMed1978

Fasting and postprandial serum gastrin levels before and after highly selective gastric vagotomy, truncal vagotomy with pyloroplasty and truncal vagotomy with antrectomy: is there a cholinergic antral gastrin inhibitory and releasing mechanism?

Fasting serum gastrin levels and postprandial gastrin response were measured before and 1 month after highly selective vagotomy, truncal vagotomy with pyloroplasty and truncal vagotomy with antrectomy. The three groups of patients, 12 in each group, were closely matched for age, sex, maximum acid output and completeness of vagotomy. After highly selective and truncal vagotomy an identical and significant increase in fasting gastrin was observed, whereas after truncal vagotomy with antrectomy the pre- and postoperative fasting gastrin levels were not different. The net postprandial gastrin output over basal value was significantly increased after highly selective vagotomy, unchanged after truncal vagotomy and significantly lowered after truncal vagotomy with antrectomy. These results suggest the presence in the intact subject of a cholinergic inhibitory mechanism in the gastric body and fundus for the release of antral gastrin in the fasting and postprandial states and a possible cholinergic facilitatory mechanism for the release of antral gastrin after meals.

Clinical Trials as Topic↗

PubMed1979

Postprandial serum gastrin levels in patients with combined hypergastrinaemia and hyperchlorhydria.

We have determined the serum gastrin response to a standard test meal in 13 unoperated patients with combined fasting hypergastrinaemia (more than 150 ng/l) and basal hypersecretion of gastric acid (BAO more than 10 mmol/h). In 10 of 11 patients with proved of presumptive Zollinger-Ellison syndrome the peak postprandial rise in serum gastrin concentration was less than 50 per cent of basal value. The integrated gastrin response to feeding ranged from 71-9 to 211-8 mug/lX 150 min. In 2 patients with proved hypergastrinaemia of antral origin, however, serum gastrin rose to 223 per cent and 255 per cent respectively of basal value after ingestion of the meal. The integrated postprandial serum gastrin responses in these patients were 66-8 and 22-0 mug/lX 150 min. Two patiets with Zollinger-Ellison syndrome and total gastrectomy showed peak serum gastrin levels after feeding of 174 and 255 per cent of basal concentration. The integrated postprandial gastrin secretions were 365 and 366 mug/l X 150 min respectively. It is concluded that the serum gastrin response to feeding, when expressed as percentage change, may be helpful in the differential diagnosis of unoperated patients with fasting hypergastrinaemia and basal gastric acid hypersecretion.

Eating↗

PubMed1978

Plasma secretin concentrations in fasting and postprandial state in man.

Plasma immunoreactive secretin concentrations were determined in both healthy subjects and patients with duodenal ulcer. The modified radioimmunoassay method could detect significant increases in the plasma secretin concentrations when 0.05 N HCl was infused intraduodenally at a rate of 1.1 and 2.2 ml/min. The mean fasting plasma secretin concentration of 13 normal healthy subjects was 4.4 +/- 0.38 pg/ml which was significantly less (P less than 0.01) than that of 13 duodenal ulcer patients, 6.9 +/- 0.64 pg/ml. In both groups ingestion of a meat-containing meal resulted in significant increase in the plasma secretin concentrations. Recording of pH from proximal duodenum indicated that pH fell periodically below 4.5 during the postprandial period, indicating that only a short segment of proximal duodenum was exposed to acid after meal. The postprandial rise in plasma secretin levels was abolished when antral pH was raised 5.5 by intragastric infusion of 0.3 N NaHCO3 solution. These observations indicate that although fasting plasma secretin levels are low, the plasma secretin levels increase significantly after ingestion of a meal. This increase appears to be attributable to an increased amount of acid delivered to the proximal duodenum, and patients with duodenal ulcer were found to release more secretin during the postprandial period than normal subjects.

Adult↗

PubMed1976

Postprandial plasma triglyceride and cholesterol responses to a low-fat meal.

Postprandial plasma cholesterol and triglyceride (TG) levels were measured after the consumption of a relatively low-fat (35% of calories) diet in 41 subjects. Plasma cholesterol levels did not change appreciably during the postprandial state. In 34 subjects a biphasic plasma TG response curve was noted, with an initial peak occurring 1 to 3 hr after feeding and a secondary TG peak 4 to 7 hr after the meal. The primary peak was greater than 90%, accounted for by chylomicrons, whereas the secondary peak represented very low-density lipoproteins (greater than 82%). Furthermore, the heights of the primary and secondary peaks were closely correlated to the fasting TG level (r = 0.61 and 0.72, respectively) indicating that the fasting TG concentration is an important determinant of the postprandial TG response. Because low-fat (high-carbohydrate) diets are known to raise fasting TG levels in patients who do not have fasting hyperchylomicronemia, and because relatively few patients have chylomicrons in the fasting state, these data suggest that such diets may lead to day long increases in plasma TG levels in the majority of subjects.

Adult↗

PubMed1979

Plasma secretin concentrations in fasting and postprandial states in dog.

In four dogs with a modified Herrara pancreatic fistula and gastric cannula and three dogs with two duodenal cannulas, ingestion of a meat meal resulted in a significant and sustained increase in the mean plasma immunoreactive secretin concentrations, from mean fasting levels of less than 10 pg/ml to 25--55 pg/ml. This increase in the plasma secretin concentration coincided with a marked increase in pancreatic bicarbonate output and frequent decreases in the mean proximal duodenal pH to less than 4.5 from the range of 6.5 in the fasting state. Intravenous administration of cimetidine, 150 mg, produced a marked suppression of postprandial increases in both pancreatic bicarbonate output and plasma secretin concentration. Moreover, the postprandial duodenal pH rarely reached below 5.0 after cimetidine administration. These studies indicate that plasma secretin concentration does increase significantly after a meal. The postprandial increase in plasma secretin concentration appears to depend on the gastric acid delivered in the proximal duodenum. A possible physiological role of secretin in the pancreatic secretion after a meal is indicated by these findings.

Animals↗

PubMed1978

Constituents of chyme responsible for postprandial intestinal hyperemia.

While local venous outflow was measured in anesthetized dogs, various constituents of intestinal chyme were placed in the jejunal lumen to identify those responsible for postprandial intestinal hyperemia. Digested food and its supernatant increased local blood flow, whereas its precipitate, undigested food, and pancreatic enzymes did not. In the jejunum bile alone had no effect, but it markedly enhanced the hyperemic effect of digested food. Bile in the ileal lumen, however, increased local blood flow. At physiological postprandial concentrations in the jejunum, glucose, and micellar solutions of oleic acid and monoolein increased flow, but taurocholate and 16 common dietary amino acids did not. The hyperemic effect of lipids required the presence of taurocholate. Of the 16 amino acids, only Glu and Asp increased flow at 10 times the physiological concentrations (28 and 20 mM, respectively). The study indicates that the constituents of chyme responsible for postprandial intestinal hyperemia are the hydrolytic products of food, especially those of carbohydrates and fats and that bile plays an important role in the hyperemia.

Amino Acids↗

PubMed1978

[Bile lipid composition of cholecystectomized patients during fasting and in postprandial periods].

Fasting state, 1 and 3 hours postprandial biliary lipid periods are studied in 19 cholecystectomized gallstone patients. Methodological items togeher with the characteristics of the kind of diet: normocaloric; lipids, 15% (50% of which are obtained from animals); proteins, 25%; and carbohydrates, 60% are established. It is concluded that biliary lipids are not quantitatively modified in the subjects on established diet respect fasting, 1 and 3 hours postprandial periods, particularly pointing out that the biliary cholesterol saturation rate remains unchanged--supersaturated--for fasting state, as well as for postprandial periods. We believe that the lack of observable changes may be in relation with the characteristics of the employed diet, which is usually suggested to people suffering from cholecystopathies in Argentina.

Bile↗

PubMed2026

Premeal insulin administration lowers postprandial blood glucose and increases myocardial microvascular blood flow in people with type 1 diabetes: a randomised, crossover clinical trial.

AIMS/HYPOTHESIS: We aimed to evaluate whether prandial insulin timing affects vascular function in people with type 1 diabetes. Our hypothesis was that premeal insulin administration would lead to greater myocardial microvascular blood flow (MBF) via blunting postprandial hyperglycaemia. METHODS: People with type 1 diabetes between 18 and 35 years of age with BMI <30 kg/m2 underwent two protocols with a 1:1 randomised crossover design wherein prandial insulin was injected either 15 min before or 15 min after meal intake began. To provide a physiological comparison, age-, sex- and BMI-matched control participants completed one study where they consumed the same meal but received no exogenous insulin. Glucose, insulin, vascular function (including ultrasound measures of myocardial and skeletal muscle microvascular perfusion, aortic stiffness, brachial artery endothelial function) and biomarkers of systemic inflammation and endothelial dysfunction were assessed at baseline and then 2 h after meal ingestion within each protocol. The primary outcome was change in myocardial MBF within each protocol. Study personnel assessing outcomes were masked to group assignment. RESULTS: Eighteen people with type 1 diabetes and 18 matched control participants were analysed within each protocol. Glucose area under the curve was significantly greater (p=0.015) in the postmeal insulin study compared with the premeal insulin study in participants with type 1 diabetes. Myocardial microvascular flow velocity significantly increased (p=0.031) with premeal insulin administration in people with type 1 diabetes and this consequently led to greater myocardial MBF (p=0.044). There were no changes in myocardial MBF within the other protocols. Changes in vital signs were similar between all protocols. CONCLUSIONS/INTERPRETATION: Appropriately timed premeal insulin led to lower postprandial blood glucose along with increased myocardial MBF in people with type 1 diabetes. Further work is needed to determine the underlying aetiology of these changes. TRIAL REGISTRATION: ClinicalTrials.gov NCT04730882.

Humans↗

PubMed1977

Greater bioavailability of digoxin solution in capsules. Studies in the postprandial state.

A liquid concentrate of digoxin administered as a capsule has recently been found to be better absorbed by normal subjects in the fasting state than a standard tablet or even a solution as such. It was not known whether the enchanced bioavailability of the encapsulated digoxin solution could also be demonstrated when given postprandially. In a crossover study single 0.4 mg doses of digoxin solution in a capsule, a solution in 10% ethanol as such, and a standard tablet were given to 12 normal volunteers immediately following a high-fat breakfast. The mean area under the serum concentration-time curve (AUC) and 6-day cumulative urinary glycoside excretion (CUE) were greater after the capsule than that of either the solution or the tablet. The latter two preparations appeared to be bioequivalent. Intersubject variability in the CUE was less than with the AUC, but did not differ when the three drug formulations were compared. The bioavailability of an encapsulated liquid digoxin concentrate was thus also found to be enhanced when administered postprandially.

Adult↗

PubMed1978

Determinants of fasting and postprandial serum bile acid levels in healthy man.

The relationship between serum levels of conjugates of cholic acid measured by radioimmunoassay, bile acid absorption, and hepatic clearance was studied in order to define the determinants of fasting and postprandial serum bile acids in healthy man. Acute or chronic interruption of the enterohepatic circulation caused a significant decrease in basal serum levels of cholyl conjugates, while liquid or solid meals caused a marked and reproducible increase in serum cholyl conjugates. A temporal correlation was demonstrated postprandially or after intravenous cholecystokinin between intestinal transit of bile acids and simultaneous changes in levels of serum cholyl conjugates. Finally, the plasma disappearance of intravenously injected cholylglycine was shown to be unaffected by serum levels of endogenous cholyl conjugates. These data are consistent with the interpretation that, in the presence of normal hepatic function, the major determinant of serum bile acids is their rate of intestinal absorption.

Adult↗

PubMed1979

Control of human postprandial pancreatic exocrine secretion: a function of the gastroduodenal region.

Regulation of the exocrine pancreatic secretion elicited by a meal in man is incompletely understood. In this study, we attempted to localize in the gastrointestinal tract areas that control postprandial trypsin secretion and to determine the effects of individual components of jejunal chyme on the meal-stimulated trypsin secretion. Trypsin outputs elicited by ingesting a mixed-nutrient meal and diverting it at the ligament of Treitz proximal to an occlusive balloon were compared with those occurring when the same meal was ingested, diverted at the ligament of Treitz, and immediately reinfused distal to the balloon, a procedure that exposed the entire gastrointestinal tract to chyme. Two different meals, one of semielemental and one of complex nutrients, were used with similar results. Trypsin outputs were similar whether or not jejunal chyme was diverted. In addition, no component--exogenous nutrients or endogenous secretions--of chyme reaching the jejunum after a meal further modified the trypsin secretion elicited by the gastroduodenal segment. This finding suggests that the gastroduodenal segment is sufficient to elicit the entire postprandial trypsin output and is the physiologic determinant of meal-stimulated trypsin secretion.

Adult↗

PubMed1979

The effects of the alpha-glucosidase inhibitor BAY g 5421 (Acarbose) on postprandial blood glucose, serum insulin, and triglyceride levels: dose-time-response relationships in man.

In a double-blind quadruple cross-over study the effect of a new alpha-glucosidase inhibitor (BAY g 5421) on postprandial blood glucose, serum insulin, and serum triglyceride increases was tested in 24 male healthy volunteers. They received before a standardized breakfast 50, 100, or 200 mg of BAY g 5421 or a placebo per os. The dose-time-response relationships were calculated and the drug tolerance was assessed. There was a statistically significant inhibition of the postprandial increases of the blood glucose, serum insulin, and triglyceride values. Further analysis showed no dose-dependent effect of the drug on the blood glucose values, whereas the serum insulin and triglyceride values were affected in a dose-dependent fashion. The maximal inhibitory effect on the serum insulin levels occurred 69 min after breakfast and on the serum triglyceride levels 104 min after breakfast. One hundred and 200 mg of BAY g 5421 were equally inhibitory-effective on the serum insulin levels, whereas the highest dose used was markedly more effective on serum triglyceride values than lower doses. Based on these results, a dosage of 100--200 mg of BAY g 5421/meal is recommended for clinical trials in metabolic diseases.

Administration, Oral↗