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...
Glucose Homeostasis: Regulation of Blood Glucose01:02

Glucose Homeostasis: Regulation of Blood Glucose

Carbohydrates consumed through foods are converted into glucose, a crucial energy source for the body. In the prandial state, high blood glucose levels stimulate the secretion of insulin from the pancreas. Insulin inhibits hepatic glucose production and stimulates glucose uptake and metabolism by muscle and adipose tissue. The excess glucose is converted into glycogen and stored in the liver and muscles.
During fasting, when blood glucose levels are low, the pancreas secretes glucagon. it...
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...
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...
Metabolic States of the Body: Fasting and Starvation01:24

Metabolic States of the Body: Fasting and Starvation

During the initial hours of fasting, the body uses up its glycogen stores as an energy source. Once these glycogen reserves are depleted, the body begins breaking down stored triglycerides and structural proteins. During this stage, glycerol becomes a key substrate for gluconeogenesis, while free fatty acids undergo beta-oxidation to provide energy for tissues, such as skeletal muscle. In the fasting state, the body spares protein breakdown as much as possible to conserve muscle and structural...
Cell Specific Gene Expression01:58

Cell Specific Gene Expression

Multicellular organisms contain a variety of structurally and functionally distinct cell types, but the DNA in all the cells originated from the same parent cells. The differences in the cells can be attributed to the differential gene expression. Liver cells, whose functions include detoxification of blood, production of bile to metabolize fats, and synthesis of proteins essential for metabolism, must express a specific set of genes to perform their functions. Gene expression also varies with...

You might also read

Related Articles

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

Sort by
Same author

Andes Virus Exposure and Nosocomial Transmission Events to Healthcare Personnel: A Systematic Review.

Clinical infectious diseases : an official publication of the Infectious Diseases Society of America·2026
Same author

Disseminated herpes zoster with hepatic necrosis in a patient with newly diagnosed HIV.

The Lancet. Infectious diseases·2026
Same author

Diagnostic Utility of Endoscopic Features and Endoscopic Ultrasonography for Ulcerative Colitis-Associated Neoplasia: A Retrospective Study on the Role of Endoscopic Submucosal Dissection as a Total Biopsy.

Cancers·2026
Same author

Whole-brain connectome analysis for elucidating specific structural neural networks in idiopathic normal-pressure hydrocephalus.

Magma (New York, N.Y.)·2026
Same author

Effectiveness and safety of combination immunotherapy with or without ipilimumab according to PD-L1 expression in patients with non-small cell lung cancer: a multi-center retrospective cohort study.

Translational lung cancer research·2026
Same author

MRI-based cerebrospinal fluid volumetric indices for predicting tap test response in idiopathic normal pressure hydrocephalus.

Radiological physics and technology·2026

Related Experiment Video

Updated: Jun 5, 2026

Isolation of Targeted Hypothalamic Neurons for Studies of Hormonal, Metabolic, and Electrical Regulation
09:29

Isolation of Targeted Hypothalamic Neurons for Studies of Hormonal, Metabolic, and Electrical Regulation

Published on: August 4, 2023

Leptin controls ketone body utilization in hypothalamic neuron.

Ryota Narishima1, Masahiro Yamasaki, Shinya Hasegawa

  • 1Department of Health Chemistry, Hoshi University, 2-4-41, Ebara, Shinagawa-ku, Tokyo 142-8501, Japan.

Neuroscience Letters
|January 4, 2011
PubMed
Summary

Leptin signaling regulates ketone body utilization in the brain. Leptin treatment increases acetoacetyl-CoA synthetase (AACS) expression in neural cells by suppressing AMPK activity, suggesting a role in appetite control.

More Related Videos

Experimental Approach to Examine Leptin Signaling in the Carotid Bodies and its Effects on Control of Breathing
05:45

Experimental Approach to Examine Leptin Signaling in the Carotid Bodies and its Effects on Control of Breathing

Published on: October 25, 2019

Live Images of GLUT4 Protein Trafficking in Mouse Primary Hypothalamic Neurons Using Deconvolution Microscopy
08:47

Live Images of GLUT4 Protein Trafficking in Mouse Primary Hypothalamic Neurons Using Deconvolution Microscopy

Published on: December 7, 2017

Related Experiment Videos

Last Updated: Jun 5, 2026

Isolation of Targeted Hypothalamic Neurons for Studies of Hormonal, Metabolic, and Electrical Regulation
09:29

Isolation of Targeted Hypothalamic Neurons for Studies of Hormonal, Metabolic, and Electrical Regulation

Published on: August 4, 2023

Experimental Approach to Examine Leptin Signaling in the Carotid Bodies and its Effects on Control of Breathing
05:45

Experimental Approach to Examine Leptin Signaling in the Carotid Bodies and its Effects on Control of Breathing

Published on: October 25, 2019

Live Images of GLUT4 Protein Trafficking in Mouse Primary Hypothalamic Neurons Using Deconvolution Microscopy
08:47

Live Images of GLUT4 Protein Trafficking in Mouse Primary Hypothalamic Neurons Using Deconvolution Microscopy

Published on: December 7, 2017

Area of Science:

  • Neuroendocrinology
  • Metabolic Neuroscience
  • Molecular Biology

Background:

  • Leptin, an appetite-controlling peptide from adipose tissue, influences metabolism.
  • Leptin deficiency-induced obesity previously showed suppressed acetoacetyl-CoA synthetase (AACS) gene expression in white adipose tissue.
  • AACS is a key enzyme for ketone body utilization in lipid synthesis.

Purpose of the Study:

  • To clarify the effects of leptin on ketone body utilization within the central nervous system.
  • To investigate the impact of leptin signaling on AACS expression in the brain.

Main Methods:

  • In situ hybridization analysis was performed on ob/ob and db/db mice.
  • AACS mRNA levels were examined in specific hypothalamic nuclei (Arcuate Nucleus and Ventromedial Hypothalamic Nucleus).
  • Experiments involved primary cultured neural cells and N41 neural-like cells, including treatment with leptin, AMPK inducers, and inhibitors.

Main Results:

  • Leptin deficiency reduced AACS mRNA levels in the Arcuate Nucleus and Ventromedial Hypothalamic Nucleus of the hypothalamus.
  • Leptin treatment increased AACS mRNA levels in both primary cultured neural cells and N41 neural-like cells.
  • In N41 cells, leptin's effect on AACS expression was mediated by the suppression of AMP-activated protein kinase (AMPK) activity.

Conclusions:

  • Leptin up-regulates AACS expression in neural cells by suppressing AMPK activity through neural leptin signaling.
  • Deficiency in this leptin-mediated regulation of AACS may contribute to neurological disorders related to central appetite control.
  • This study highlights a novel role for leptin in regulating brain metabolism and appetite.