scholarly journals Gastric Sensory and Motor Functions and Energy Intake in Health and Obesity—Therapeutic Implications

Nutrients ◽  
2021 ◽  
Vol 13 (4) ◽  
pp. 1158
Author(s):  
Lizeth Cifuentes ◽  
Michael Camilleri ◽  
Andres Acosta
Keyword(s):  
Energy Consumption ◽  
Gastric Emptying ◽  
Food Intake ◽  
Gastric Volume ◽  
Obesity Management ◽  
Bariatric Endoscopy ◽  
Motor Functions ◽  
Therapeutic Implications ◽  
Intestinal Functions

Sensory and motor functions of the stomach, including gastric emptying and accommodation, have significant effects on energy consumption and appetite. Obesity is characterized by energy imbalance; altered gastric functions, such as rapid gastric emptying and large fasting gastric volume in obesity, may result in increased food intake prior to reaching usual fullness and increased appetite. Thus, many different interventions for obesity, including different diets, anti-obesity medications, bariatric endoscopy, and surgery, alter gastric functions and gastrointestinal motility. In this review, we focus on the role of the gastric and intestinal functions in food intake, pathophysiology of obesity, and obesity management.

LPS inhibits fasted plasma ghrelin levels in rats: role of IL-1 and PGs and functional implications

2006 ◽  
Vol 291 (4) ◽  
pp. G611-G620 ◽  
Author(s):  
Lixin Wang ◽  
Nicole R. Basa ◽  
Almaas Shaikh ◽  
Andrew Luckey ◽  
David Heber ◽  
...  
Keyword(s):  
Blood Glucose ◽  
Gastric Emptying ◽  
Food Intake ◽  
Intravenous Injection ◽  
Plasma Levels ◽  
Inhibitory Action ◽  
Functional Implications ◽  
Urocortin 1 ◽  
Fasted Rats

LPS injected intraperitoneally decreases fasted plasma levels of ghrelin at 3 h postinjection in rats. We characterized the inhibitory action of LPS on plasma ghrelin and whether exogenous ghrelin restores LPS-induced suppression of food intake and gastric emptying in fasted rats. Plasma ghrelin and insulin and blood glucose were measured after intraperitoneal injection of LPS, intravenous injection of IL-1β and urocortin 1, and in response to LPS under conditions of blockade of IL-1 or CRF receptors by subcutaneous injection of IL-1 receptor antagonist (IL-1Ra) or astressin B, respectively, and prostaglandin (PG) synthesis by intraperitoneal indomethacin. Food intake and gastric emptying were measured after intravenous injection of ghrelin at 5 h postintraperitoneal LPS injection. LPS inhibited the elevated fasted plasma ghrelin levels by 47.6 ± 4.9%, 58.9 ± 3.3%, 74.4 ± 2.7%, and 48.9 ± 8.7% at 2, 3, 5, and 7 h postinjection, respectively, and values returned to preinjection levels at 24 h. Insulin levels were negatively correlated to those of ghrelin, whereas there was no significant correlation between glucose and ghrelin. IL-1Ra and indomethacin prevented the first 3-h decline in ghrelin levels induced by LPS, whereas astressin B did not. IL-1β inhibited plasma ghrelin levels, whereas urocortin 1 had no influence. Ghrelin injected intravenously prevented an LPS-induced 87% reduction of gastric emptying and 61% reduction of food intake. These data showed that IL-1 and PG pathways are part of the early mechanisms by which LPS suppresses fasted plasma ghrelin and that exogenous ghrelin can normalize LPS-induced-altered digestive functions.

scholarly journals Postgraduate Symposium The role of fat in gastric emptying and satiety: acute and chronic effects

2009 ◽  
Vol 68 (1) ◽  
pp. 89-97 ◽  
Author(s):  
Miriam Clegg ◽  
Amir Shafat
Keyword(s):  
Gastric Emptying ◽  
Food Intake ◽  
Gastrointestinal Transit ◽  
Positive Energy ◽  
Low Fat ◽  
Low Fat Diet ◽  
The Metabolic Syndrome ◽  
Increase Food Intake ◽  
Positive Energy Balance

Dietary fat is an important factor in the aetiology of obesity and the metabolic syndrome. It has been widely debated whether gastric emptying (GE) is altered in obesity. GE times have been reported as both longer and shorter in obese individuals compared with matched lean individuals. However, the general consensus is that GE is accelerated and satiety is lower in obesity. Research has implicated a high-fat (HF) diet in these findings. A single HF meal has a longer GE time than a low-fat meal and can even delay GE of the subsequent meal. However, an HF diet has shown different effects. Feeding a HF diet adapts gastrointestinal function to reduce GE times in comparison with a low-fat diet. Increased GE may lead to decreased satiety and faster onset of subsequent eating episodes. Further results have suggested that consuming an HF diet for 14 d increases the GE rate of HF food but not low-fat food. Consuming HF diets for 2 weeks has also been shown to increase food intake. Decreased satiation following an HF diet may cause increased food intake and a positive energy balance, potentially resulting in a gradual increase in adiposity. Recent results have suggested that gastrointestinal transit is accelerated following only 3 d on a HF diet. The variable GE times reported in obesity may be associated with interactions between the HF diet and obesity and not simply the obese state.

scholarly journals Bile acid composition regulates GPR119-dependent intestinal lipid sensing and food intake regulation in mice

Gut ◽  
2020 ◽  
Vol 69 (9) ◽  
pp. 1620-1628 ◽  
Author(s):  
Sei Higuchi ◽  
Tiara R Ahmad ◽  
Donovan A Argueta ◽  
Pedro A Perez ◽  
Chen Zhao ◽  
...  
Keyword(s):  
Gastric Emptying ◽  
Food Intake ◽  
Dietary Lipid ◽  
Chow Diet ◽  
Distal Intestine ◽  
Gut Hormone ◽  
Lipid Sensing ◽  
Food Intake Regulation ◽  
Intake Regulation

ObjectivesLipid mediators in the GI tract regulate satiation and satiety. Bile acids (BAs) regulate the absorption and metabolism of dietary lipid in the intestine, but their effects on lipid-regulated satiation and satiety are completely unknown. Investigating this is challenging because introducing excessive BAs or eliminating BAs strongly impacts GI functions. We used a mouse model (Cyp8b1–/– mice) with normal total BA levels, but alterations in the composition of the BA pool that impact multiple aspects of intestinal lipid metabolism. We tested two hypotheses: BAs affect food intake by (1) regulating production of the bioactive lipid oleoylethanolamide (OEA), which enhances satiety; or (2) regulating the quantity and localisation of hydrolysed fat in small intestine, which controls gastric emptying and satiation.DesignWe evaluated OEA levels, gastric emptying and food intake in wild-type and Cyp8b1–/– mice. We assessed the role of the fat receptor GPR119 in these effects using Gpr119–/– mice.ResultsCyp8b1–/– mice on a chow diet showed mild hypophagia. Jejunal OEA production was blunted in Cyp8b1–/– mice, thus these data do not support a role for this pathway in the hypophagia of Cyp8b1–/– mice. On the other hand, Cyp8b1 deficiency decreased gastric emptying, and this was dependent on dietary fat. GPR119 deficiency normalised the gastric emptying, gut hormone levels, food intake and body weight of Cyp8b1–/– mice.ConclusionBAs regulate gastric emptying and satiation by determining fat-dependent GPR119 activity in distal intestine.

scholarly journals Central Nesfatin-1 Reduces Dark-Phase Food Intake and Gastric Emptying in Rats: Differential Role of Corticotropin-Releasing Factor2 Receptor

Endocrinology ◽  
2009 ◽  
Vol 150 (11) ◽  
pp. 4911-4919 ◽  
Author(s):  
Andreas Stengel ◽  
Miriam Goebel ◽  
Lixin Wang ◽  
Jean Rivier ◽  
Peter Kobelt ◽  
...  
Keyword(s):  
Gastric Emptying ◽  
Food Intake ◽  
Nucleus Tractus Solitarius ◽  
Hypothalamic Nucleus ◽  
Reduce Food Intake ◽  
Dark Phase ◽  
Crf2 Receptor ◽  
Brain Ventricle ◽  
Dose Dependent

Nesfatin-1, derived from nucleobindin2, is expressed in the hypothalamus and reported in one study to reduce food intake (FI) in rats. To characterize the central anorexigenic action of nesfatin-1 and whether gastric emptying (GE) is altered, we injected nesfatin-1 into the lateral brain ventricle (intracerebroventricular, icv) or fourth ventricle (4v) in chronically cannulated rats or into the cisterna magna (intracisternal, ic) under short anesthesia and compared with ip injection. Nesfatin-1 (0.05 μg/rat, icv) decreased 2–3 h and 3–6 h dark-phase FI by 87 and 45%, respectively, whereas ip administration (2 μg/rat) had no effect. The corticotropin-releasing factor (CRF)1/CRF2 antagonist astressin-B or the CRF2 antagonist astressin2-B abolished icv nesfatin-1’s anorexigenic action, whereas an astressin2-B analog, devoid of CRF-receptor binding affinity, did not. Nesfatin-1 icv induced a dose-dependent reduction of GE by 26 and 43% that was not modified by icv astressin2-B. Nesfatin-1 into the 4v (0.05 μg/rat) or ic (0.5 μg/rat) decreased cumulative dark-phase FI by 29 and 60% at 1 h and by 41 and 37% between 3 and 5 h, respectively. This effect was neither altered by ic astressin2-B nor associated with changes in GE. Cholecystokinin (ip) induced Fos expression in 43% of nesfatin-1 neurons in the paraventricular hypothalamic nucleus and 24% of those in the nucleus tractus solitarius. These data indicate that nesfatin-1 acts centrally to reduce dark phase FI through CRF2-receptor-dependent pathways after forebrain injection and CRF2-receptor-independent pathways after hindbrain injection. Activation of nesfatin-1 neurons by cholecystokinin at sites regulating food intake may suggest a role in gut peptide satiation effect.

scholarly journals The role of a pre-load beverage on gastric volume and food intake: comparison between non-caloric carbonated and non-carbonated beverage

2011 ◽  
Vol 10 (1) ◽  
Author(s):  
Rosario Cuomo ◽  
Maria Flavia Savarese ◽  
Giovanni Sarnelli ◽  
Emanuele Nicolai ◽  
Adriana Aragri ◽  
...  
Keyword(s):  
Food Intake ◽  
Gastric Volume ◽  
Carbonated Beverage

Rates of Gastric Emptying in Young Cod

1970 ◽  
Vol 27 (7) ◽  
pp. 1177-1189 ◽  
Author(s):  
A. V. Tyler
Keyword(s):  
Gastric Emptying ◽  
Food Intake ◽  
Intestinal Absorption ◽  
Gastric Volume ◽  
Acclimation Temperature ◽  
Rate Data ◽  
Time Intervals ◽  
Digestion Rate ◽  
Straight Line ◽  
Depletion Rate

Stomachs of young cod were opened at various time intervals after they had voluntarily eaten measured meals. More digested food left the stomach in the first few hours after the meal was given than towards the end of digestion. Instantaneous depletion rate increased rapidly with increase in acclimation temperature from 2 to 15 C. The rate was not increased at 19 C and was possibly depressed. Fish would not feed at 21 C. When meal size was varied, a straight-line relation was found between rate of gastric emptying and quantity of food in the stomach. This implies that in young cod intestinal absorption is coupled to food intake by regulation of the gastric volume. It is likely that digestion rate data could be used to estimate daily rations for fish in their own environment by measuring quantity of food in the stomach.

Proglumide, a cholecystokinin antagonist, increases gastric emptying in rats

1987 ◽  
Vol 252 (2) ◽  
pp. R353-R360 ◽  
Author(s):  
G. Shillabeer ◽  
J. S. Davison
Keyword(s):  
Gastric Emptying ◽  
Food Intake ◽  
Physiological Role ◽  
Liquid Food ◽  
Dilution Technique ◽  
Cholecystokinin Antagonist ◽  
Gastric Intubation ◽  
Specific Antagonist ◽  
Cck Antagonist

Injection of cholecystokinin (CCK) reduces food intake and delays gastric emptying. We have previously shown that endogenous CCK also reduces food intake. This may be achieved by a delay in gastric emptying. We investigated the role of CCK in gastric emptying by inhibiting the actions of CCK released by a meal, using a CCK antagonist, proglumide. We postulated that inhibition of CCK should induce an increase in gastric emptying. Gastric emptying was determined in rats by a marker dilution technique using direct gastric intubation. Proglumide (150 mg/kg) significantly accelerated emptying of liquid food by 12.8% (P less than 0.005, n = 12) when injected intraperitoneally following a food preload. Proglumide injected before feeding was ineffective. Oral proglumide, which inhibited gastrin-stimulated acid secretion, was also ineffective. We concluded that proglumide increased gastric emptying by acting on a factor released by the preload, and since proglumide is a specific antagonist, this factor was probably CCK. Therefore CCK may play a physiological role in the regulation of gastric emptying.

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.

Peripheral urocortin inhibits gastric emptying and food intake in mice: differential role of CRF receptor 2

2001 ◽  
Vol 281 (5) ◽  
pp. R1401-R1410 ◽  
Author(s):  
Lixin Wang ◽  
Vicente Martínez ◽  
Jean E. Rivier ◽  
Yvette Taché
Keyword(s):  
Gastric Emptying ◽  
Food Intake ◽  
Corticotropin Releasing Factor ◽  
Delay Gastric Emptying ◽  
Urocortin 1 ◽  
Urocortin 3 ◽  
Cumulative Food Intake

Intraperitoneal urocortin inhibits gastric emptying and food intake in mice. We investigated corticotropin-releasing factor receptor (CRF-R) subtypes involved in intraperitoneal urocortin actions using selective CRF-R antagonists. Gastric emptying was measured 2 h after a chow meal, and food intake was measured hourly after an 18-h fast in mice. Urocortin (3 μg/kg ip) inhibited gastric emptying by 88%. The CRF-R1/CRF-R2 antagonist astressin B (30 μg/kg ip) and the selective CRF-R2 antagonist antisauvagine-30 (100 μg/kg ip) completely antagonized urocortin action, whereas the selective CRF-R1 antagonist CP-154,526 (10 mg/kg ip) had no effect. Urocortin (1–10 μg/kg ip) dose dependently decreased the 2-h cumulative food intake by 30–62%. Urocortin (3 μg/kg)-induced hypophagia was completely antagonized by astressin B (30 μg/kg ip) and partially (35 and 31%) by antisauvagine-30 (100 or 200 μg/kg ip). The CRF-R1 antagonists CP-154,526 or DMP904 (10 mg/kg ip) had no effect. Capsaicin did not alter urocortin-inhibitory actions while blocking the satiety effect of intraperitoneal CCK. These data indicate that intraperitoneal urocortin-induced decrease in feeding is only partly mediated by CRF-R2, whereas urocortin action to delay gastric emptying of a meal involves primarily CRF-R2.

Gastric and duodenal features of meals mediate controls of liquid gastric emptying during fill in rhesus monkeys

1999 ◽  
Vol 277 (5) ◽  
pp. R1282-R1290 ◽  
Author(s):  
Timothy H. Moran ◽  
Susan Knipp ◽  
Gary J. Schwartz
Keyword(s):  
Gastric Emptying ◽  
Negative Feedback ◽  
Glucose Concentration ◽  
Rhesus Monkeys ◽  
Physiological Saline ◽  
Gastric Volume ◽  
Feedback Controls ◽  
Lower Glucose ◽  
Concentration Dependency

To study the dynamics of liquid gastric emptying in rhesus monkeys under conditions that simulated gastric fill during a meal, we measured the gastric emptying of liquid glucose at various concentrations and volumes when administered intragastrically at rates ranging from 12.5 to 37.5 ml/min. Glucose gastric emptying was faster during than following the period of gastric fill. At a single glucose concentration, volume infused rather than the rate of filling determined the volume emptied. Lower glucose concentrations emptied more slowly than physiological saline. As glucose concentration increased, emptying during fill slowed. Duodenal glucose infusions greatly slowed the rate of saline emptying during fill, demonstrating duodenal feedback control. Although casein hydrolosate emptied more rapidly than glucose, the dynamics of volume and concentration dependency and the role of duodenal feedback were similar. These data reveal that both gastric volume and duodenal negative feedback controls important in gastric emptying following stomach filling also contribute to its control during fill.

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