Does ingested fat produce satiety?

1996 ◽  
Vol 270 (4) ◽  
pp. R761-R765 ◽  
Author(s):  
C. C. Horn ◽  
M. G. Tordoff ◽  
M. I. Friedman
Keyword(s):  
Gastrointestinal Tract ◽  
Food Intake ◽  
Feeding Behavior ◽  
Corn Oil ◽  
Substantial Reduction ◽  
Liquid Diet ◽  
Short Term ◽  
Diet Intake ◽  
Marked Suppression ◽  
Fat Meal

Administration of fat directly into the gastrointestinal tract of rats produces a rapid and often substantial reduction of feeding behavior. This contrasts with the normal consumption of a fat meal, which produces little change in subsequent food intake. To determine whether procedural differences account for this discrepancy, we examined the satiating effect of ingested fat on food intake of rats maintained under feeding conditions similar to those employed in studies involving gastrointestinal delivery of fat (i.e., food deprivation, liquid diet). Ingestion of approximately 1.5 ml corn oil had no effect on subsequent liquid diet intake until 90 min after oil ingestion. When rats ingested oil 4 h before access to the liquid diet, to allow time for additional gastrointestinal clearance, liquid diet intake was reduced by 13% in the first 30 min of access. These findings indicate that ingested fat decreases short-term intake slightly, but only if time is allowed for postabsorptive delivery. The results question the physiological significance of the marked suppression of food intake observed in response to administration of fat directly into the gastrointestinal tract.

scholarly journals Hindbrain glucagon-like peptide-1 neurons track intake volume and contribute to injection stress-induced hypophagia in meal-entrained rats

2016 ◽  
Vol 310 (10) ◽  
pp. R906-R916 ◽  
Author(s):  
Alison D. Kreisler ◽  
Linda Rinaman
Keyword(s):  
Food Intake ◽  
Potential Role ◽  
Liquid Diet ◽  
Neural Activation ◽  
Intracerebroventricular Injection ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
Diet Intake ◽  
Published Research ◽  
Diet Type

Published research supports a role for central glucagon-like peptide 1 (GLP-1) signaling in suppressing food intake in rodent species. However, it is unclear whether GLP-1 neurons track food intake and contribute to satiety, and/or whether GLP-1 signaling contributes to stress-induced hypophagia. To examine whether GLP-1 neurons track intake volume, rats were trained to consume liquid diet (LD) for 1 h daily until baseline intake stabilized. On test day, schedule-fed rats consumed unrestricted or limited volumes of LD or unrestricted volumes of diluted (calorically matched to LD) or undiluted Ensure. Rats were perfused after the test meal, and brains processed for immunolocalization of cFos and GLP-1. The large majority of GLP-1 neurons expressed cFos in rats that consumed satiating volumes, regardless of diet type, with GLP-1 activation proportional to intake volume. Since GLP-1 signaling may limit intake only when such large proportions of GLP-1 neurons are activated, a second experiment examined the effect of central GLP-1 receptor (R) antagonism on 2 h intake in schedule-fed rats. Compared with baseline, intracerebroventricular vehicle (saline) suppressed Ensure intake by ∼11%. Conversely, intracerebroventricular injection of vehicle containing GLP-1R antagonist increased intake by ∼14% compared with baseline, partly due to larger second meals. We conclude that GLP-1 neural activation effectively tracks liquid diet intake, that intracerebroventricular injection suppresses intake, and that central GLP-1 signaling contributes to this hypophagic effect. GLP-1 signaling also may contribute to satiety after large volumes have been consumed, but this potential role is difficult to separate from a role in the hypophagic response to intracerebroventricular injection.

Satiating effect of fat in diabetic rats: gastrointestinal and postabsorptive factors

1988 ◽  
Vol 255 (1) ◽  
pp. R123-R127
Author(s):  
N. K. Edens ◽  
M. I. Friedman
Keyword(s):  
Gastric Emptying ◽  
Food Intake ◽  
Corn Oil ◽  
Ketone Bodies ◽  
Stomach Contents ◽  
Diabetic Rats ◽  
Physiological Basis ◽  
Streptozotocin Diabetic Rats ◽  
Fat Feeding ◽  
Fat Meal

Streptozotocin-diabetic rats decrease food intake more than normal animals in response to a fat test meal. To determine the physiological basis of this differential response, we examined the effects of an ingested corn oil meal on food intake, gastrointestinal fill, and plasma triglycerides, glycerol, and ketone bodies. Hyperphagic diabetic rats decreased intake of a high-carbohydrate, low-fat stock diet starting 2-4 h after the fat meal, whereas normal rats did not. Gastric emptying was accelerated and intestinal mass and contents were increased in diabetic rats. The fat meal reduced gastric emptying and increased stomach contents in diabetic and normal rats starting within 2 h of ingestion. Intestinal fill decreased in diabetic animals after the oil meal. Triglycerides and glycerol increased transiently after fat ingestion in normal and diabetic rats, whereas ketone body concentrations rose only in diabetic rats starting 1-3 h after fat ingestion. The results indicate that the differential effect of a fat meal on food intake in normal and diabetic rats is related to differences in the postabsorptive metabolism of the ingested fat rather than to effects of fat feeding on gastrointestinal fill or clearance.

scholarly journals Potential modulation of plasma ghrelin and glucagon-like peptide-1 by anorexigenic cannabinoid compounds, SR141716A (rimonabant) and oleoylethanolamide

2004 ◽  
Vol 92 (5) ◽  
pp. 757-761 ◽  
Author(s):  
Patrice D. Cani ◽  
Maite Lasa Montoya ◽  
Audrey M. Neyrinck ◽  
Nathalie M. Delzenne ◽  
Didier M. Lambert
Keyword(s):  
Gastrointestinal Tract ◽  
Food Intake ◽  
Receptor Antagonist ◽  
Food Consumption ◽  
Cannabinoid Receptor ◽  
Short Term ◽  
Cannabinoid Compounds ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
Fasted Rats

The CB1 cannabinoid receptor antagonist, N-piperidino-5-(4-chlorophenyl)-1-(2,4-dichlorophenyl)-4-methylpyrazole-3-carboxamide (rimonabant; SR141716A), and oleoylethanolamide (OEA) are known to reduce food consumption, by, at least partially, a peripheral regulation of feeding. The effects of systemic SR141716A or OEA (5 mg/kg) administrations on food consumption in 24 h food-deprived and fed rats were investigated. In fasted rats, SR141716A and OEA produced an inhibition in food intake measurable the first 20 min following injection. The increase in ghrelin levels observed in the vehicle-injected rats was abolished in animals receiving OEA and significantly reduced with SR141716A. Neither OEA nor SR141716A modified glucagon-like peptide-1 (7–36) amide portal levels 20 min after the administration. In fed rats, plasma ghrelin levels of SR141716A- and OEA-treated rats were 35% lower as compared with those of the vehicle-injected rats. These results show an influence of cannabinoid agents on circulating ghrelin levels and suggest that their short-term action on appetite seems to be in accordance with the control of secretion of gastrointestinal orexigenic peptides, mainly expressed in the upper part of the gastrointestinal tract.

Leptin response to carbohydrate or fat meal and association with subsequent satiety and energy intake

1999 ◽  
Vol 277 (5) ◽  
pp. E855-E861 ◽  
Author(s):  
M. Romon ◽  
P. Lebel ◽  
C. Velly ◽  
N. Marecaux ◽  
J. C. Fruchart ◽  
...  
Keyword(s):  
Food Intake ◽  
Energy Intake ◽  
Healthy Subjects ◽  
Insulin Response ◽  
Blood Sampling ◽  
Fat Intake ◽  
Short Term ◽  
The Impact ◽  
Fat Meal ◽  
Carbohydrate Meal

To assess the impact of the macronutrient content of a meal on the postprandial leptin response and its relationship with postprandial satiety, 22 young healthy subjects (11 men and 11 women) were given, in a randomized order, an isoenergetic meal [carbohydrate (81%) or fat (79%)] or remained fasting. Blood sampling and hunger and satiety scores were collected hourly during 9 h after the meal. Spontaneous intake was measured at a buffet meal at 9 h postprandially. In both genders, leptin response was higher after the carbohydrate meal than after the fat meal and while fasting. In women, leptin levels were higher after the fat meal than while fasting. Leptin response was significantly correlated to insulin response ( r = 0.51, P < 0.0001). Hunger and satiety ratings and subsequent energy intake were not different after carbohydrate or fat intake. In conclusion, a carbohydrate meal induces higher postprandial leptin levels than an isoenergetic fat meal. Short-term regulation of postprandial satiety and food intake is not influenced by circulating leptin.

scholarly journals Intermittent fasting improves metabolic flexibility in short-term high-fat diet-fed mice

2019 ◽  
Vol 317 (5) ◽  
pp. E773-E782 ◽  
Author(s):  
Mara A. Dedual ◽  
Stephan Wueest ◽  
Marcela Borsigova ◽  
Daniel Konrad
Keyword(s):  
Food Intake ◽  
Feeding Behavior ◽  
Hepatic Steatosis ◽  
Glucose Intolerance ◽  
High Fat Diet ◽  
Metabolic Flexibility ◽  
High Fat ◽  
Short Term ◽  
Inactive Phase ◽  
Ad Libitum

Four days of high-fat diet (HFD) feeding are sufficient to induce glucose intolerance and hepatic steatosis in mice. While prolonged HFD-induced metabolic complications are partly mediated by increased food intake during the light (inactive) phase, such a link has not yet been established in short-term HFD-fed mice. Herein, we hypothesized that a short bout of HFD desynchronizes feeding behavior, thereby contributing to glucose intolerance and hepatic steatosis. To this end, 12-wk-old C57BL/6J littermates were fed a HFD for 4 days either ad libitum or intermittently. Intermittent-fed mice were fasted for 8 h during their inactive phase. Initiation of HFD led to an immediate increase in food intake already during the first light phase. Moreover, glucose tolerance was significantly impaired in ad libitum- but not in intermittent HFD-fed mice, indicating that desynchronized feeding behavior contributes to short-term HFD-induced glucose intolerance. Of note, overall food intake was similar between the groups, as was body weight. However, intermittent HFD-fed mice revealed higher fat depot weights. Phosphorylation of hormone sensitivity lipase and free fatty acid release from isolated adipocytes were significantly elevated, suggesting increased lipolysis in intermittent HFD-fed mice. Moreover, hepatic mRNA expression of lipogenetic enzymes and liver triglyceride levels were significantly increased in intermittent HFD-fed mice. Importantly, food deprivation decreased respiratory exchange ratio promptly in intermittent- but not in ad libitum HFD-fed mice. In conclusion, retaining a normal feeding pattern prevented HFD-induced impairment of metabolic flexibility in short-term HFD-fed mice.

Dietary Fat Level and Short-Term Effects of a High-Fat Meal on Food Intake and Metabolism

1998 ◽  
Vol 42 (2) ◽  
pp. 75-89 ◽  
Author(s):  
Christa J. Silberbauer ◽  
Bettina Jacober ◽  
Wolfgang Langhans
Keyword(s):  
Food Intake ◽  
Dietary Fat ◽  
High Fat ◽  
Short Term ◽  
Fat Level ◽  
Fat Meal ◽  
Short Term Effects

scholarly journals Cholecystokinin suppresses food intake by inhibiting gastric emptying

1982 ◽  
Vol 242 (5) ◽  
pp. R491-R497 ◽  
Author(s):  
T. H. Moran ◽  
P. R. McHugh
Keyword(s):  
Gastric Emptying ◽  
Food Intake ◽  
Feeding Behavior ◽  
Macaca Mulatta ◽  
Short Term ◽  
Physiological Mechanisms ◽  
Gastric Distention ◽  
Intravenous Infusions ◽  
A Chain ◽  
Saline Test

In a search for the physiological mechanisms that could mediate and characterize a satiety function for the hormone cholecystokinin (CCK), we examined in Macaca mulatta the effect of intraperitoneal injections (0.1-0.8 microgram/kg) and intravenous infusions (60-240 ng.kg-1.h-1) of the C-terminal octapeptide of CCK on gastric emptying of saline test meals. Within these dose ranges, gastric emptying was inhibited by this hormone to a degree comparable with that produced by intraintestinal nutrient. The onset of the inhibition is rapid and its effect brief. At the doses of CCK that produce gastric inhibition, CCK would not affect feeding in a fasted monkey unless the stomach was filled with saline. This result suggests that a satiety influence of circulating CCK is an indirect one. The satiety effect depends upon inhibition of gastric emptying, which then leads to gastric distention with further food injection. CCK thus can be considered a link in a chain of physiological elements producing the short-term satiety that leads to the appropriate interruption of a meal or bout of feeding behavior.

Polychlorinated biphenyl induced hepatocyte alterations

1987 ◽  
Vol 45 ◽  
pp. 716-717
Author(s):  
D.N. Collins ◽  
J.N. Turner ◽  
K.O. Brosch ◽  
R.F. Seegal
Keyword(s):  
Lipid Droplets ◽  
Wistar Rats ◽  
Homovanillic Acid ◽  
Polychlorinated Biphenyl ◽  
Corn Oil ◽  
Environmental Pollutants ◽  
Short Term ◽  
Pcb Congeners ◽  
Urinary Levels ◽  
The Brain

Polychlorinated biphenyls (PCBs) are a ubiquitous class of environmental pollutants with toxic and hepatocellular effects, including accumulation of fat, proliferated smooth endoplasmic recticulum (SER), and concentric membrane arrays (CMAs) (1-3). The CMAs appear to be a membrane storage and degeneration organelle composed of a large number of concentric membrane layers usually surrounding one or more lipid droplets often with internalized membrane fragments (3). The present study documents liver alteration after a short term single dose exposure to PCBs with high chlorine content, and correlates them with reported animal weights and central nervous system (CNS) measures. In the brain PCB congeners were concentrated in particular regions (4) while catecholamine concentrations were decreased (4-6). Urinary levels of homovanillic acid a dopamine metabolite were evaluated (7).Wistar rats were gavaged with corn oil (6 controls), or with a 1:1 mixture of Aroclor 1254 and 1260 in corn oil at 500 or 1000 mg total PCB/kg (6 at each level).

Obesity and adiposity: the culprit of dietary protein efficacy

2020 ◽  
Vol 134 (4) ◽  
pp. 389-401
Author(s):  
Carla El-Mallah ◽  
Omar Obeid
Keyword(s):  
Food Intake ◽  
Behavioural Change ◽  
Physiological Mechanism ◽  
Short Term ◽  
The Past ◽  
Body Adiposity ◽  
Reduce Sugar ◽  
Eye Opening ◽  
Potential Strategy ◽  
Limitations And Exceptions

Abstract Obesity and increased body adiposity have been alarmingly increasing over the past decades and have been linked to a rise in food intake. Many dietary restrictive approaches aiming at reducing weight have resulted in contradictory results. Additionally, some policies to reduce sugar or fat intake were not able to decrease the surge of obesity. This suggests that food intake is controlled by a physiological mechanism and that any behavioural change only leads to a short-term success. Several hypotheses have been postulated, and many of them have been rejected due to some limitations and exceptions. The present review aims at presenting a new theory behind the regulation of energy intake, therefore providing an eye-opening field for energy balance and a potential strategy for obesity management.

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