scholarly journals A limbic circuit selectively links active escape to food suppression

eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Estefania P Azevedo ◽  
Bowen Tan ◽  
Lisa E Pomeranz ◽  
Violet Ivan ◽  
Robert Fetcho ◽  
...  
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Food Consumption ◽  
Lateral Hypothalamus ◽  
Neural Circuits ◽  
Lateral Septum ◽  
Behavioral Effects ◽  
Viable Option ◽  
Glucagon Like Peptide ◽  
Active Escape

Stress has pleiotropic physiologic effects, but the neural circuits linking stress to these responses are not well understood. Here, we describe a novel population of lateral septum neurons expressing neurotensin (LSNts) in mice that are selectively tuned to specific types of stress. LSNts neurons increase their activity during active escape, responding to stress when flight is a viable option, but not when associated with freezing or immobility. Chemogenetic activation of LSNts neurons decreases food intake and body weight, without altering locomotion and anxiety. LSNts neurons co-express several molecules including Glp1r (glucagon-like peptide one receptor) and manipulations of Glp1r signaling in the LS recapitulates the behavioral effects of LSNts activation. Activation of LSNts terminals in the lateral hypothalamus (LH) also decreases food intake. These results show that LSNts neurons are selectively tuned to active escape stress and can reduce food consumption via effects on hypothalamic pathways.

BODY WEIGHT AND FOOD CONSUMPTION OF LACTATING RATS NURSING VARIOUS SIZES OF LITTERS

1967 ◽  
Vol 38 (3) ◽  
pp. 263-268 ◽  
Author(s):  
K. ÔTA ◽  
A. YOKOYAMA
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Food Consumption ◽  
Ovarian Function ◽  
Experimental Period ◽  
Close Correlation ◽  
Female Rats ◽  
Linear Relationships ◽  
Rate Of Increase ◽  
Daily Gain

SUMMARY Changes in body weight and food consumption during lactation in rats nursing various sizes of litters were studied. The rate of increase in body weight of the mother rats during the experimental period (day 3–14 of lactation) was very similar in mothers with different numbers (2, 4, 8 and 12) of suckling pups/litter. It is suggested that the weight increase of adult female rats during lactation is related more closely to the alteration of ovarian function caused by the suckling stimulus than to the enhanced food intake during this period. Both the food intake of mother rats and the daily gain in weight of litters increased as the number of suckling pups/litter increased and as lactation advanced. Linear relationships were observed between the logarithm of the litter size and both the food intake of the mother rats and the weight gain of the litters. The presence of a close correlation between the food intake of mother rats and the quantity of milk produced by them is suggested.

scholarly journals Effect of Chronic Central Administration of Glucagon-Like Peptide-1 (7-36) Amide on Food Consumption and Body Weight in Normal and Obese Rats

1998 ◽  
Vol 6 (2) ◽  
pp. 147-156 ◽  
Author(s):  
Harry R. Davis ◽  
Deborra E. Mullins ◽  
Jesse M. Pines ◽  
Lizbeth M. Hoos ◽  
Constance F. France ◽  
...  
Keyword(s):  
Body Weight ◽  
Food Consumption ◽  
Central Administration ◽  
Obese Rats ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

Appetite hormones and addiction

2018 ◽  
Author(s):  
David J. Nutt ◽  
Liam J. Nestor
Keyword(s):  
Eating Disorder ◽  
Food Intake ◽  
Food Consumption ◽  
Neural Substrates ◽  
Reward Sensitivity ◽  
Substance Addiction ◽  
Alcohol And Drugs ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
The Brain

Many of the same behavioural and brain disturbances observed in addiction are also seen in obesity and binge-eating disorder. This suggests that there are shared neural substrates between substance addiction and compulsive food consumption. Food intake and appetite are regulated by numerous appetite hormones that exert their effects through brain systems involved in reward sensitivity, stress, impulsivity, and compulsivity. There is now emerging evidence that appetite hormones (e.g. ghrelin, glucagon-like peptide-1, orexin) can modulate addictive behaviours (e.g. craving) and the intake of alcohol and drugs. Therefore, there is an emerging shift into a new field of testing drugs that affect appetite hormones and their receptors in the brain, and their use in regulating the brain mechanisms that lead to relapse in addiction disorders.

Capsaicin-sensitive fibers are required for the anorexic action of systemic but not central bombesin

1999 ◽  
Vol 276 (6) ◽  
pp. R1617-R1622 ◽  
Author(s):  
David Michaud ◽  
Hymie Anisman ◽  
Zul Merali
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Food Intake ◽  
Neural Circuits ◽  
Body Weight Gain ◽  
Systemic Effects ◽  
Neuronal System ◽  
Afferent Neurons ◽  
The Brain

Bombesin (BN) suppresses food intake in rats whether given centrally or systemically. Although the brain BN-sensitive receptors are known to be essential for the anorexic effect of systemic BN, the mode of communication between the gut and the brain remains unclear. This study assessed whether the anorexic effect of systemic BN is mediated humorally or via neural circuits. Afferent neurons were lesioned using capsaicin (50 mg/kg sc) on postnatal day 2, and responses to BN were assessed during adulthood. Capsaicin treatment decreased body weight gain significantly from postnatal age 4–7 wk. Peripheral BN (4–16 μg/kg ip) dose dependently suppressed food intake in control animals. However, this effect was completely blocked in capsaicin-treated rats. In contrast to systemic effects, feeding-suppressant effects of centrally administered BN (0.01–0.5 μg icv) were not affected by capsaicin treatment. This research suggests that peripheral BN communicates with the brain via a neuronal system(s) whose afferent arm is constituted of capsaicin-sensitive C and/or Aδ-fibers, whereas the efferent arm of this satiety- and/or anorexia-mediating circuitry is capsaicin resistant.

scholarly journals An evaluation of the relation between food consumption rate and equilibrium body-weight in male rats

1988 ◽  
Vol 60 (1) ◽  
pp. 151-160 ◽  
Author(s):  
Tom W. Gettys ◽  
Susan Mills ◽  
Donald M. Henrickst
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Food Consumption ◽  
Consumption Rate ◽  
Growth Efficiency ◽  
Intake Rate ◽  
Total Intake ◽  
Food Consumption Rate ◽  
Maintenance Requirements ◽  
Food Intake Rate

1. Two experimental approaches were employed to assess the relation between food consumption rate and maintenance requirements in male weanling rats. The first approach involved restricting food intake in rats previously given free access to food from weaning to 59 d of age. The second approach involved restriction of food intake to various levels after weaning. Maintenance requirements (g foodid per g body-weight (W)) were estimated by dividing the rate of food consumption by the resulting equilibrium W (EBW) for each animal. In addition, food consumption was partitioned into growth-independent (maintenance) and growth-dependent (gain) components by alternately setting W and specific growth rate (W') to zero in an equation relating food intake rate to W and W. Coupling coefficients representing maintenance consumption (g food/d per g W) and gain consumption (g food/g gain) were estimated for each animal by least squares.2. Both techniques for estimating maintenance consumption provided similar estimates within and across experiments, and regardless of when food restriction was imposed or its severity, consumption for maintenance was about 5% W/d.3. The EBW to which animals in each treatment group aspired was directly proportional to that group's food intake rate.4. Coventional measures of growth efficiency were also related to food intake; efficiency decreased with decreasing food intake. Partitioning food consumption into maintenance and gain components revealed that as the rate of food intake decreased, the proportion of total intake consumed for maintenance increased. The results suggest that growth efficiency declines during food intake restriction because proportionately more of total intake is used for maintenance, leaving less available for gain.

Glucagon-like peptide 1 as a regulator of food intake and body weight: therapeutic perspectives

2002 ◽  
Vol 440 (2-3) ◽  
pp. 269-279 ◽  
Author(s):  
Juris J. Meier ◽  
Baptist Gallwitz ◽  
Wolfgang E. Schmidt ◽  
Michael A. Nauck
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

A laboratory environment previously associated with a palatablediet can result in overfeeding in rats

2016 ◽  
Author(s):  
Alma Gabriela Martínez ◽  
Antonio López-Espinoza ◽  
Patricia Josefina López-Uriarte ◽  
Claudia Patricia Beltrán-Miranda ◽  
Hugo Daniel Miguel-Gómez ◽  
...  
Keyword(s):  
Food Intake ◽  
Food Consumption ◽  
Eating Behavior ◽  
Behavioral Effects ◽  
Laboratory Animals ◽  
Palatable Food ◽  
Laboratory Environment ◽  
Enriched Environments

Enriched and non-enriched laboratory environments produce various biological and behavioral effects on laboratory animals. One of the most impacted aspects in this regard is eating behavior. We examined associations between enriched vs. non-enriched environments and palatable vs. non-palatable diets on food intake in rats. Experiment 1 demonstrated that there are no significant differences in palatable food consumption irrespective of whether rats were exposed to enriched or non-enriched environments (P>0.05). In contrast, experiment 2 demonstrated that a combination of exposure to either of these environments and palatable food is enough to produce overfeeding in rats (P less than 0.05). These outcomes in rats may offer significant inferences in regards to the regulation of eating behavior in humans.

scholarly journals Repeated Intracerebroventricular Administration of Glucagon-Like Peptide-1-(7–36) Amide or Exendin-(9–39) Alters Body Weight in the Rat**This work was supported by the United Kingdom Medical Research Council.

Endocrinology ◽  
1999 ◽  
Vol 140 (1) ◽  
pp. 244-250 ◽  
Author(s):  
Karim Meeran ◽  
Donal O’Shea ◽  
C. Mark B. Edwards ◽  
Mandy D. Turton ◽  
Melanie M. Heath ◽  
...  
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Neuropeptide Y ◽  
Research Council ◽  
Medical Research Council ◽  
Reduce Food Intake ◽  
The United Kingdom ◽  
Ad Libitum ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

Abstract Central nervous system glucagon-like peptide-1-(7–36) amide (GLP-1) administration has been reported to acutely reduce food intake in the rat. We here report that repeated intracerebroventricular (icv) injection of GLP-1 or the GLP-1 receptor antagonist, exendin-(9–39), affects food intake and body weight. Daily icv injection of 3 nmol GLP-1 to schedule-fed rats for 6 days caused a reduction in food intake and a decrease in body weight of 16 ± 5 g (P < 0.02 compared with saline-injected controls). Daily icv administration of 30 nmol exendin-(9–39) to schedule-fed rats for 3 days caused an increase in food intake and increased body weight by 7 ± 2 g (P < 0.02 compared with saline-injected controls). Twice daily icv injections of 30 nmol exendin-(9–39) with 2.4 nmol neuropeptide Y to ad libitum-fed rats for 8 days increased food intake and increased body weight by 28 ± 4 g compared with 14 ± 3 g in neuropeptide Y-injected controls (P < 0.02). There was no evidence of tachyphylaxis in response to icv GLP-1 or exendin-(9–39). GLP-1 may thus be involved in the regulation of body weight in the rat.

Effect of galanin on food intake in rats: involvement of lateral and ventromedial hypothalamic sites

1993 ◽  
Vol 264 (2) ◽  
pp. R355-R361 ◽  
Author(s):  
R. R. Schick ◽  
S. Samsami ◽  
J. P. Zimmermann ◽  
T. Eberl ◽  
C. Endres ◽  
...  
Keyword(s):  
Food Intake ◽  
Food Consumption ◽  
Paraventricular Nucleus ◽  
Lateral Hypothalamus ◽  
Ventromedial Hypothalamus ◽  
Initial Increase ◽  
Intracerebroventricular Injection ◽  
Fasted Rats ◽  
Stimulation Of ◽  
Cumulative Food Intake

Galanin has previously been reported to elicit feeding in satiated animals when injected into the hypothalamic paraventricular nucleus. It is not known, however, 1) whether this action is due to activation of feeding signals or suppression of satiety signals or both or 2) whether other hypothalamic regions such as the lateral hypothalamus (LH) or the ventromedial hypothalamus (VMH) are involved in this action. The effects of galanin on food intake were therefore examined in satiated and in fasted rats both after intracerebroventricular injection (0.1, 1, and 10 micrograms/10 microliters) and after microinjection (1 and 5 micrograms/0.5 microliters) into the LH and VMH. Twenty minutes after intracerebroventricular injection, galanin significantly and dose dependently augmented food intake by up to sevenfold in freely feeding rats and by up to 79% in fasted animals. The galanin-induced augmentation of cumulative food intake up to 2 h after injection was due to the initial increase in food consumption during the 0 to 20-min interval. This suggests that galanin acts by activation of feeding behavior and not by suppression of satiety signals in these fasted animals, in which satiety signals are presumably not initially operative. Twenty minutes after intrahypothalamic injections into both the LH and VMH, galanin (5 micrograms) significantly increased food consumption, fivefold in freely feeding rats and 30-35% in fasted rats. Thus stimulation of feeding by centrally injected galanin also involves loci within the LH and VMH.

scholarly journals Effects of glucagon-like peptide 1 on appetite and body weight: focus on the CNS

2013 ◽  
Vol 221 (1) ◽  
pp. T1-T16 ◽  
Author(s):  
L van Bloemendaal ◽  
J S ten Kulve ◽  
S E la Fleur ◽  
R G Ijzerman ◽  
M Diamant
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Physiological Role ◽  
Brain Regions ◽  
Gastric Distension ◽  
Cns Activity ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

The delivery of nutrients to the gastrointestinal tract after food ingestion activates the secretion of several gut-derived mediators, including the incretin hormone glucagon-like peptide 1 (GLP-1). GLP-1 receptor agonists (GLP-1RA), such as exenatide and liraglutide, are currently employed successfully in the treatment of patients with type 2 diabetes mellitus. GLP-1RA improve glycaemic control and stimulate satiety, leading to reductions in food intake and body weight. Besides gastric distension and peripheral vagal nerve activation, GLP-1RA induce satiety by influencing brain regions involved in the regulation of feeding, and several routes of action have been proposed. This review summarises the evidence for a physiological role of GLP-1 in the central regulation of feeding behaviour and the different routes of action involved. Also, we provide an overview of presently available data on pharmacological stimulation of GLP-1 pathways leading to alterations in CNS activity, reductions in food intake and weight loss.

Sign in / Sign up

Export Citation Format

Share Document