scholarly journals Oxytocin and Food Intake Control: Neural, Behavioral, and Signaling Mechanisms

2021 ◽  
Vol 22 (19) ◽  
pp. 10859
Author(s):  
Clarissa M. Liu ◽  
Mai O. Spaulding ◽  
Jessica J. Rea ◽  
Emily E. Noble ◽  
Scott E. Kanoski
Keyword(s):  
Food Intake ◽  
Size Control ◽  
Reproductive Function ◽  
Hypothalamic Nucleus ◽  
Signaling Mechanisms ◽  
Model Research ◽  
Control Food ◽  
Melanin Concentrating Hormone ◽  
Sites Of Action ◽  
Behavioral Mechanisms

The neuropeptide oxytocin is produced in the paraventricular hypothalamic nucleus and the supraoptic nucleus of the hypothalamus. In addition to its extensively studied influence on social behavior and reproductive function, central oxytocin signaling potently reduces food intake in both humans and animal models and has potential therapeutic use for obesity treatment. In this review, we highlight rodent model research that illuminates various neural, behavioral, and signaling mechanisms through which oxytocin’s anorexigenic effects occur. The research supports a framework through which oxytocin reduces food intake via amplification of within-meal physiological satiation signals rather than by altering between-meal interoceptive hunger and satiety states. We also emphasize the distributed neural sites of action for oxytocin’s effects on food intake and review evidence supporting the notion that central oxytocin is communicated throughout the brain, at least in part, through humoral-like volume transmission. Finally, we highlight mechanisms through which oxytocin interacts with various energy balance-associated neuropeptide and endocrine systems (e.g., agouti-related peptide, melanin-concentrating hormone, leptin), as well as the behavioral mechanisms through which oxytocin inhibits food intake, including effects on nutrient-specific ingestion, meal size control, food reward-motivated responses, and competing motivations.

scholarly journals Melanin-concentrating hormone and food intake control: Sites of action, peptide interactions, and appetition

Peptides ◽  
2021 ◽  
Vol 137 ◽  
pp. 170476
Author(s):  
Magen N. Lord ◽  
Keshav Subramanian ◽  
Scott E. Kanoski ◽  
Emily E. Noble
Keyword(s):  
Food Intake ◽  
Peptide Interactions ◽  
Melanin Concentrating Hormone ◽  
Sites Of Action ◽  
Intake Control

scholarly journals Glucokinase Regulates Reproductive Function, Glucocorticoid Secretion, Food Intake, and Hypothalamic Gene Expression

Endocrinology ◽  
2007 ◽  
Vol 148 (4) ◽  
pp. 1928-1932 ◽  
Author(s):  
Xue-jun Yang ◽  
Jason Mastaitis ◽  
Tooru Mizuno ◽  
Charles V. Mobbs
Keyword(s):  
Gene Expression ◽  
Food Intake ◽  
Reproductive Function

scholarly journals Adjustment of Whey:Casein Ratio from 20:80 to 60:40 in Milk Formulation Affects Food Intake and Brainstem and Hypothalamic Neuronal Activation and Gene Expression in Laboratory Mice

Foods ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 658
Author(s):  
Erin L. Wood ◽  
David G. Christian ◽  
Mohammed Arafat ◽  
Laura K. McColl ◽  
Colin G. Prosser ◽  
...  
Keyword(s):  
Food Intake ◽  
Area Postrema ◽  
Energy Levels ◽  
Early Gene ◽  
Hypothalamic Nucleus ◽  
Laboratory Mice ◽  
Neuronal Activation ◽  
Short Term ◽  
Animal Milk ◽  
The Impact

Adjustment of protein content in milk formulations modifies protein and energy levels, ensures amino acid intake and affects satiety. The shift from the natural whey:casein ratio of ~20:80 in animal milk is oftentimes done to reflect the 60:40 ratio of human milk. Studies show that 20:80 versus 60:40 whey:casein milks differently affect glucose metabolism and hormone release; these data parallel animal model findings. It is unknown whether the adjustment from the 20:80 to 60:40 ratio affects appetite and brain processes related to food intake. In this set of studies, we focused on the impact of the 20:80 vs. 60:40 whey:casein content in milk on food intake and feeding-related brain processes in the adult organism. By utilising laboratory mice, we found that the 20:80 whey:casein milk formulation was consumed less avidly and was less preferred than the 60:40 formulation in short-term choice and no-choice feeding paradigms. The relative PCR analyses in the hypothalamus and brain stem revealed that the 20:80 whey:casein milk intake upregulated genes involved in early termination of feeding and in an interplay between reward and satiety, such as melanocortin 3 receptor (MC3R), oxytocin (OXT), proopiomelanocortin (POMC) and glucagon-like peptide-1 receptor (GLP1R). The 20:80 versus 60:40 whey:casein formulation intake differently affected brain neuronal activation (assessed through c-Fos, an immediate-early gene product) in the nucleus of the solitary tract, area postrema, ventromedial hypothalamic nucleus and supraoptic nucleus. We conclude that the shift from the 20:80 to 60:40 whey:casein ratio in milk affects short-term feeding and relevant brain processes.

Parenteral nutrition, brain glycogen, and food intake

1993 ◽  
Vol 265 (6) ◽  
pp. R1387-R1391
Author(s):  
M. M. Meguid ◽  
J. L. Beverly ◽  
Z. J. Yang ◽  
J. R. Gleason ◽  
R. A. Meguid ◽  
...  
Keyword(s):  
Food Intake ◽  
Parenteral Nutrition ◽  
Plasma Glucose ◽  
Glycogen Content ◽  
Fischer 344 Rats ◽  
Brain Glycogen ◽  
Fischer 344 ◽  
Control Food ◽  
Control Food Intake ◽  
Infusion Period

To determine whether brain glycogen concentrations change during parenteral nutrition, Fischer 344 rats with jugular vein catheters received 0.9 N saline or parenteral nutrition providing 100% of daily calories (PN-100). Rats were killed after 4 days of PN-100 and serially after PN-100 was stopped. Food intake decreased during PN-100 to approximately 15% of control, but total kilocalories eaten and infused over the 4-day PN-100 period was approximately 130% of control. Food intake of PN-100 rats remained low for 3-4 days post-PN-100. At the end of the 4-day PN-100 period, plasma glucose and insulin (P = 0.01) and whole brain glycogen (P < 0.005) were higher than but similar to control within 24 h of PN-100 being stopped. When PN-100 rats were not allowed to eat during the infusion period, plasma glucose was lower, plasma insulin higher, and brain glycogen content the same as in control rats after 4 days of PN-100. The increased brain glycogen was the likely consequence of the hyperglycemia and hyperinsulinemia during PN-100 and was not causally associated with the reduced food intake either during or immediately after PN-100.

The short term feeding behaviour of pigs given access to foods differing in bulk content

2002 ◽  
Vol 2002 ◽  
pp. 27-27
Author(s):  
E. C. Whittemore ◽  
I. Kyriazakis ◽  
G.C. Emmans ◽  
B.J. Tolkamp ◽  
C. A. Morgan ◽  
...  
Keyword(s):  
Food Intake ◽  
Feeding Behaviour ◽  
Daily Intake ◽  
Growing Pigs ◽  
Feeding Time ◽  
Short Term ◽  
Control Food ◽  
Bulk Content ◽  
High Bulk ◽  
Different Levels

We need to improve our understanding of the factors that are important for the control of food intake on high bulk foods. The study of short term feeding behaviour (STFB) may help to do this. The objective of this experiment was to study the effects of giving foods differing in bulk content on the STFB of growing pigs. It was expected that the foods would result in different levels of daily intake and that this would be reflected as differences in STFB between the foods. Two hypotheses were developed based on ideas about the way in which a physical constraint to intake could arise. H1; there would be less diurnal variation in feeding on high bulk foods that limit intake. H2; feeding patterns on bulky foods would be less flexible than those on a control food when feeding time is limited by reducing time of access to the feeder.

Central Peptidergic Mechanisms in Autonomic Control

1992 ◽  
Vol 70 (5) ◽  
pp. 772-772
Author(s):  
Alastair V. Ferguson
Keyword(s):  
Current Knowledge ◽  
Reproductive Function ◽  
Autonomic Control ◽  
Physiological Effects ◽  
Highly Qualified ◽  
Binding Studies ◽  
Physiological Control ◽  
Queen's University ◽  
Sites Of Action ◽  
The Brain

Since the recognition in the 1970s that peptides may play more diverse physiological roles than suggested by their original recognition as circulating hormones, there has been an explosion of information regarding the potential central nervous system actions of these substances. Pharmacological binding studies have described an extensive distribution of many different groups of peptidergic receptors suggesting potential sites of action for specific peptides within the brain. Many of these receptor localizations were found within the blood brain barrier indicating that these substances were released locally and perhaps acted as neurotransmitters. Over the years, experiments demonstrating physiological effects of locally administered peptides in regions where receptors for that molecule are localized have added credibility to such a hypothesis. The explosion of interest in the peptides as potential chemical messengers within the brain has since led to the description of multiple peptidergic neuronal systems within the brain. In addition, there are now many different reports of postsynaptic effects of exogenous administration of peptides on single neurons. Similarly, many studies have reported more broad-based physiological effects resulting from actions of peptides within the central nervous system.The manuscripts that follow summarize presentations in a symposium to examine the "Central Peptidergic Mechanisms in Autonomic Control," which was part of the program at the Canadian Federation of Biological Sciences annual meeting held at Queen's University in Kingston in July of 1991. The express purpose of this symposium in its inception was to provide a forum for consideration of the CNS actions of peptides in the context of a systems physiology approach. We hoped to consider our current knowledge of the roles of peptides in the brain as they relate to the control of specific physiological systems. Therefore rather than presenting a consideration of individual peptides, and each one's multitude of potential roles, the manuscripts presented in the following section have addressed what is known of central peptidergic involvement in the physiological control of reproductive function (W. K. Samson), cardiovascular regulation (A. V. Ferguson), thermoregulatory control (Q. J. Pittman), and drinking (M. Evered).I should like to take this opportunity to thank all who contributed to this symposium, in particular the speakers without whose cooperation it would not have been possible. I am also indebted to the sponsors of the symposium: Merck Frosst, Warner Lambert, Sandoz, the Canadian Physiological Society, and the Faculty of Medicine at Queen's University, whose generous support permitted such a highly qualified group of invited speakers to attend.

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