Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Regulation of Food Intake01:30

Regulation of Food Intake

Short-term regulation of food intake primarily involves neural signals from the gastrointestinal (GI) tract, blood nutrient levels, and GI tract hormones. Communication between the gut and brain via vagal nerve fibers plays a significant role in evaluating the contents of the gut. Clinical studies have shown that protein ingestion produces a more prolonged response in these nerve fibers compared to an equivalent amount of glucose. Additionally, the activation of stretch receptors caused by GI...
Glucagon-like Receptor Agonists01:24

Glucagon-like Receptor Agonists

Incretins include glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), which stimulate insulin secretion post-meals. In type 2 diabetes, GIP's efficacy is reduced, making GLP-1 a viable drug target. GIP originates from preproGIP.
GLP-1, when administered in high doses intravenously, triggers insulin secretion, inhibits glucagon release, slows gastric emptying, reduces food intake, and restores normal insulin secretion. However, its rapid inactivation by the...
Insulin: The Receptor and Signaling Pathways01:28

Insulin: The Receptor and Signaling Pathways

Insulin action is mediated through a receptor tyrosine kinase, akin to the IGF-1 receptor. The number of receptors per cell varies significantly, from 40 on erythrocytes to 300,000 on adipocytes and hepatocytes. The insulin receptor consists of linked α/β subunit dimers, forming a heterotetramer glycoprotein with two extracellular α subunits and two β subunits spanning the membrane. The α subunits inhibit the inherent tyrosine kinase activity of the β subunits, but this inhibition is released...
Hormones Regulating Blood Glucose01:16

Hormones Regulating Blood Glucose

Insulin is released by beta cells of the pancreas when blood glucose levels are high. It facilitates glucose absorption and utilization in insulin-dependent cells with insulin receptors on their plasma membranes. Insulin promotes glucose uptake by increasing the number of glucose transport proteins in the cell membrane, allowing glucose to enter the cell. As a result, glucose utilization and ATP production are enhanced.
In addition to accelerating glucose uptake and utilization, insulin has...
Spare Receptors01:30

Spare Receptors

Some receptors remain unoccupied even when an agonist produces a maximal response. Such empty ones are called spare receptors. In presence of spare receptors the maximum effect of an agonist drug is achieved with fewer than 100% of the receptors being occupied. To determine the presence of spare receptors, scientists often compare the concentration of the drug needed to produce 50% of the maximum effect (EC50) with the concentration of the drug needed to occupy 50% of the receptors (Kd). If the...
Glucose Homeostasis: Pancreatic Islets and Insulin Secretion01:27

Glucose Homeostasis: Pancreatic Islets and Insulin Secretion

The pancreatic islets comprising only 1%-2% of the volume are highly vascularized and innervated mini-organs. They contain five endocrine cell types, including β cells that secrete insulin, which is synthesized as a single polypeptide chain, preproinsulin, processed to proinsulin, and finally to insulin and C-peptide. This process is complex and regulated, involving the Golgi complex, the endoplasmic reticulum, and the secretory granules of the β cell.
Insulin and C-peptide are co-secreted in...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Gluten affects behaviors related to activity and anxiety in mice fed high-fat diets.

Journal of neurophysiology·2025
Same author

Early changes in passively sensed homestay predict depression symptom improvement during digital behavioral activation.

Behaviour research and therapy·2025
Same author

Sleep and diurnal alternative polyadenylation sites associated with human APA-linked brain disorders.

Npj biological timing and sleep·2024
Same author

Engagement, Acceptability, and Effectiveness of the Self-Care and Coach-Supported Versions of the Vira Digital Behavior Change Platform Among Young Adults at Risk for Depression and Obesity: Pilot Randomized Controlled Trial.

JMIR mental health·2024
Same author

Sleep and diurnal alternative polyadenylation sites associated with human APA-linked brain disorders.

Research square·2024
Same author

Identification of sleep and circadian alternative polyadenylation sites associated with APA-linked human brain disorders.

Research square·2024
Same journal

Mitochondria produce lactate to vent redox pressure.

Trends in endocrinology and metabolism: TEM·2026
Same journal

Beyond fat storage: neuronal lipid droplets regulate whole-body metabolism.

Trends in endocrinology and metabolism: TEM·2026
Same journal

HDL resuscitates cells from ferroptosis.

Trends in endocrinology and metabolism: TEM·2026
Same journal

2-Methylbutyrylcarnitine (2MBC).

Trends in endocrinology and metabolism: TEM·2026
Same journal

Decoding growth hormone actions on human growth plate stem cells.

Trends in endocrinology and metabolism: TEM·2026
Same journal

Androgen loss backfires: Brain gate for tumor immunity.

Trends in endocrinology and metabolism: TEM·2026
See all related articles

Related Experiment Video

Updated: Jun 19, 2026

Progressive-ratio Responding for Palatable High-fat and High-sugar Food in Mice
11:16

Progressive-ratio Responding for Palatable High-fat and High-sugar Food in Mice

Published on: May 3, 2012

Insulin, leptin and reward.

Jon F Davis1, Derrick L Choi, Stephen C Benoit

  • 1Department of Psychiatry North, E, Lab 334, University of Cincinnati, 2170 East Galbraith Road, Cincinnati, OH 45237, USA. Jon.Davis@uc.edu

Trends in Endocrinology and Metabolism: TEM
|October 13, 2009
PubMed
Summary
This summary is machine-generated.

Feeding for pleasure contributes to obesity. This review explores how insulin and leptin hormones regulate reward-based feeding behaviors, offering insights into obesity management.

More Related Videos

Studying Food Reward and Motivation in Humans
12:09

Studying Food Reward and Motivation in Humans

Published on: March 19, 2014

A RAPID Method for Blood Processing to Increase the Yield of Plasma Peptide Levels in Human Blood
11:36

A RAPID Method for Blood Processing to Increase the Yield of Plasma Peptide Levels in Human Blood

Published on: April 28, 2016

Related Experiment Videos

Last Updated: Jun 19, 2026

Progressive-ratio Responding for Palatable High-fat and High-sugar Food in Mice
11:16

Progressive-ratio Responding for Palatable High-fat and High-sugar Food in Mice

Published on: May 3, 2012

Studying Food Reward and Motivation in Humans
12:09

Studying Food Reward and Motivation in Humans

Published on: March 19, 2014

A RAPID Method for Blood Processing to Increase the Yield of Plasma Peptide Levels in Human Blood
11:36

A RAPID Method for Blood Processing to Increase the Yield of Plasma Peptide Levels in Human Blood

Published on: April 28, 2016

Area of Science:

  • Neuroscience
  • Endocrinology
  • Obesity Research

Background:

  • Non-homeostatic feeding, or eating for pleasure, is a significant factor in global obesity.
  • Obesity disrupts hormonal balance, affecting energy regulation and body weight.
  • Insulin and leptin, adiposity hormones, are elevated in obesity and normally reduce feeding.

Purpose of the Study:

  • To review the role of insulin and leptin in regulating reward-related feeding behaviors.
  • To understand how these hormones influence appetite and metabolism via hypothalamic and midbrain circuits.

Main Methods:

  • Literature review of studies on insulin, leptin, and feeding behavior.
  • Analysis of research on hypothalamic and midbrain reward circuits.
  • Examination of hormonal signaling in appetite regulation.

Main Results:

  • Insulin and leptin can dampen feeding behavior by acting on hypothalamic appetite-regulating circuits.
  • Evidence suggests these hormones inhibit the rewarding aspects of feeding through midbrain pathways.
  • This action contributes to maintaining stable energy balance and body weight.

Conclusions:

  • Insulin and leptin play a crucial role in regulating the rewarding components of feeding.
  • Understanding these hormonal mechanisms is vital for developing strategies to combat obesity.
  • Targeting insulin and leptin signaling may offer therapeutic potential for obesity and related feeding disorders.