scholarly journals Cephalic phase responses, craving and food intake in normal subjects

Appetite ◽  
2000 ◽  
Vol 35 (1) ◽  
pp. 45-55 ◽  
Author(s):  
C. Nederkoorn ◽  
F.T.Y. Smulders ◽  
A. Jansen
Keyword(s):  
Food Intake ◽  
Normal Subjects ◽  
Cephalic Phase

scholarly journals Characterization of obestatin in rat and human stomach and plasma, and its lack of acute effect on feeding behavior in rodents

2008 ◽  
Vol 198 (2) ◽  
pp. 339-346 ◽  
Author(s):  
Muhtashan S Mondal ◽  
Koji Toshinai ◽  
Hiroaki Ueno ◽  
Keiichi Koshinaka ◽  
Masamitsu Nakazato
Keyword(s):  
Amino Acid ◽  
Food Intake ◽  
Feeding Behavior ◽  
High Performance ◽  
Normal Subjects ◽  
Acute Effect ◽  
Rat Plasma ◽  
Reversed Phase ◽  
Human Stomach ◽  
Ghrelin Concentration

Obestatin is a 23-amino acid peptide, initially isolated from rat stomach as an endogenous ligand for the orphan G-protein-coupled receptor. Obestatin is derived from proteolytic cleavage of a 117-amino acid precursor, preproghrelin. Ghrelin increases food intake, body weight, and gastric emptying, whereas obestatin has the opposite effects. In this study, we characterized obestatin in both rat and human stomach, and investigated the peptide's effect on feeding behavior. Using reversed-phase high-performance liquid chromatography coupled with RIAs specific for rat and human obestatin, we detected a very small amount of obestatin, compared with ghrelin, in the gastric fundi. The ratios of obestatin to ghrelin are 0.0039 and 1.94% respectively in the rat and human gastric fundi. In humans, plasma obestatin accounted for 5.21% of the ghrelin concentration, whereas it was undetectable in rat plasma. Plasma ghrelin concentration decreased after a meal in normal subjects, whereas obestatin concentration did not change. When administered centrally or peripherally, obestatin did not suppress food intake in either free-feeding or fasted rodents. Administration of obestatin did not antagonize ghrelin-induced feeding. These findings indicate that obestatin is present at very low levels compared with ghrelin in both rat and human, and has no acute effect on feeding behavior.

scholarly journals Leptin inhibits gastric emptying in rats: role of CCK receptors and vagal afferent fibers

2007 ◽  
pp. 315-322 ◽  
Author(s):  
B Çakır ◽  
Ö Kasımay ◽  
E Devseren ◽  
BÇ Yeğen
Keyword(s):  
Gastric Emptying ◽  
Food Intake ◽  
Receptor Blocker ◽  
Adrenergic Blockade ◽  
Phenol Red ◽  
Gastric Emptying Rate ◽  
Cck Receptors ◽  
Afferent Fibers ◽  
Cephalic Phase ◽  
Vagal Afferent

Leptin regulates energy homeostasis and body weight by balancing energy intake and expenditure. It was recently reported that leptin, released into the gut lumen during the cephalic phase of gastric secretion, is capable of initiating intestinal nutrient absorption. Vagal afferent neurons also express receptors for both CCK and leptin, which are believed to interact in controlling food intake. The present study was undertaken to investigate the central and peripheral effects of leptin on gastric emptying rate. Under anesthesia, male Sprague-Dawley rats (250-300 g) were fitted with gastric Gregory cannulas (n=12) and some had additional cerebroventricular cannulas inserted into their right lateral ventricles. Following recovery, the rate of gastric emptying of saline (300 mOsm/kg H(2)O) was determined after instillation into the gastric fistula (3 ml, 37 degrees C, containing phenol red, 60 mg/l as a non-absorbable dilution marker). Gastric emptying rate was determined from the volume and phenol red concentrations recovered after 5 min. Leptin, injected intraperitoneally (i.p.; 10, 30, 60, 100 microg/kg) or intracerebroventricularly (i.c.v.; 5, 15 microg/rat) 15 min before the emptying, delayed gastric emptying rate of saline at the dose of 30 microg/kg or 15 microg/rat (p<0.001). When CCK(1) receptor blocker L-364,718 (1 mg/kg, i.p.), CCK(2) receptor blocker L-365,260 (1 mg/kg, ip) or adrenergic ganglion blocker bretylium tosylate (15 mg/kg, i.p.) was administered 15 min before ip leptin (30 microg/kg) injections, leptin-induced delay in gastric emptying was abolished only by the CCK(1) receptor blocker (p<0.001). However, the inhibitory effect of central leptin on gastric emptying was reversed by adrenergic blockade, but not by either CCK antagonists. Our results demonstrated that leptin delays gastric emptying. The peripheral effect of leptin on gastric motility appears to be mediated by CCK(1) receptors, suggesting the release of CCK and the involvement of vagal afferent fibers. On the other hand, the central effect of leptin on gastric emptying is likely to be mediated by adrenergic neurons. These results indicate the existence of a functional interaction between leptin and CCK receptors leading to inhibition of gastric emptying and short-term suppression of food intake, providing an additional feedback control in producing satiety.

Central cholinergic regulation of pancreatic polypeptide secretion in conscious dogs

1997 ◽  
Vol 154 (2) ◽  
pp. 311-317 ◽  
Author(s):  
M Okita ◽  
A Inui ◽  
S Baba ◽  
M Kasuga
Keyword(s):  
Food Intake ◽  
Pancreatic Polypeptide ◽  
Atropine Sulfate ◽  
Basal Secretion ◽  
Cholinergic Mechanisms ◽  
Glucose Levels ◽  
Plasma Pretreatment ◽  
Cephalic Phase ◽  
Cholinergic Tone ◽  
Blood Glucose Concentrations

Abstract The secretion of pancreatic polypeptide (PP) is regulated by fluctuations in blood glucose concentrations and food intake, in which vagal-cholinergic mechanisms play an important role, especially for the cephalic phase of PP secretion. In this study, we examined whether central cholinergic mechanisms are also important for PP secretion by relaying information in the brain to the vagus nerve and the muscarinic cholinergic receptors in the pancreas. Atropine sulfate (20–200 μg) was administered into the lateral cerebral ventricle and its effects on the basal secretion of PP as well as the secretions stimulated by insulin-induced hypoglycemia (Actrapid MC, 0·25 U/kg) and a mixed meal (243 kcal) were studied in seven dogs. Intralateral cerebroventricular (ILV) atropine (100 and 200 μg) abolished the fluctuations in basal PP secretion without appearing in the plasma. Pretreatment with 20, 100, and 200 μg ILV atropine significantly decreased the PP response to insulin-induced hypoglycemia, with the integrated PP response to 58, 32, and 26% of that of controls respectively. Atropine (100 μg ILV) significantly reduced the postprandial PP secretion in both the cephalic and the gastrointestinal phases, whereas increased insulin and glucose levels were unaffected. Centrally administered atropine was able to suppress the basal secretion of PP as well as the secretions stimulated by hypoglycemia and food intake. These findings suggest that (1) the spontaneous release of PP is governed by an oscillating, central cholinergic tone, and (2) the stimulating PP secretion is, at least in part, regulated by the central cholinergic system. Journal of Endocrinology (1997) 154, 311–317

Cephalic-phase insulin and glucagon release in normal subjects and in patients receiving pancreas transplantation

Metabolism ◽  
1995 ◽  
Vol 44 (9) ◽  
pp. 1153-1158 ◽  
Author(s):  
Antonio Secchi ◽  
Rossana Caldara ◽  
Andrea Caumo ◽  
Lucilla D. Monti ◽  
Doretta Bonfatti ◽  
...  
Keyword(s):  
Pancreas Transplantation ◽  
Normal Subjects ◽  
Glucagon Release ◽  
Cephalic Phase

Is food-intake a confusing factor for liver stiffness evaluation by 2D-SWE in normal subjects?

2018 ◽  
Vol 68 ◽  
pp. S654
Author(s):  
D. Gherhardt ◽  
A. Popescu ◽  
C. Foncea ◽  
T.-V. Moga ◽  
B. Marius ◽  
...  
Keyword(s):  
Food Intake ◽  
Liver Stiffness ◽  
Normal Subjects ◽  
Stiffness Evaluation

scholarly journals Effect of acute Δ9-tetrahydrocannabinol administration on subjective and metabolic hormone responses to food stimuli and food intake in healthy humans: a randomized, placebo-controlled study

2019 ◽  
Vol 109 (4) ◽  
pp. 1051-1063
Author(s):  
Nathalie Weltens ◽  
Inge Depoortere ◽  
Jan Tack ◽  
Lukas Van Oudenhove
Keyword(s):  
Food Intake ◽  
Endocannabinoid System ◽  
Oral Intake ◽  
Controlled Study ◽  
Low Calorie ◽  
Metabolic Hormones ◽  
Healthy Humans ◽  
Cephalic Phase ◽  
Hormone Responses ◽  
Metabolic Hormone

ABSTRACT Background The endocannabinoid system (ECS) is considered a key player in the neurophysiology of food reward. Animal studies suggest that the ECS stimulates the sensory perception of food, thereby increasing its incentive-motivational and/or hedonic properties and driving consumption, possibly via interactions with metabolic hormones. However, it remains unclear to what extent this can be extrapolated to humans. Objective We aimed to investigate the effect of oral Δ9-tetrahydrocannabinol (THC) on subjective and metabolic hormone responses to visual food stimuli and food intake. Methods Seventeen healthy subjects participated in a single-blinded, placebo-controlled, 2 × 2 crossover trial. In each of the 4 visits, subjective “liking” and “wanting” ratings of high- and low-calorie food images were acquired after oral THC or placebo administration. The effect on food intake was quantified in 2 ways: via ad libitum oral intake (half of the visits) and intragastric infusion (other half) of chocolate milkshake. Appetite-related sensations and metabolic hormones were measured at set time points throughout each visit. Results THC increased “liking” (P = 0.031) and “wanting” ratings (P = 0.0096) of the high-calorie, but not the low-calorie images, compared with placebo. Participants consumed significantly more milkshake after THC than after placebo during oral intake (P = 0.0005), but not intragastric infusion, of milkshake. Prospective food consumption ratings during the food image paradigm were higher after THC than after placebo (P = 0.0039). THC also increased plasma motilin (P = 0.0021) and decreased octanoylated ghrelin (P = 0.023) concentrations before milkshake consumption (i.e., in both oral intake and intragastric infusion test sessions), whereas glucagon-like peptide 1 responses to milkshake intake were attenuated by THC during both oral (P = 0.0002) and intragastric (P = 0.0055) administration. Conclusions These findings suggest that the ECS drives food intake by interfering with anticipatory, cephalic phase, and metabolic hormone responses. This trial was registered at clinicaltrials.gov as NCT02310347.

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