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 Experiment Videos

Adiponectin: starving for attention.

Gregory R Steinberg1, Bruce E Kemp

  • 1St. Vincent's Institute, Department of Medicine, University of Melbourne, 41 Victoria Parade, Fitzroy, Victoria 3065, Australia. gsteinberg@svi.edu.au

Cell Metabolism
|July 10, 2007
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

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

Sort by
Same author

Feasibility, reproducibility, and cold-induced energy expenditure using whole-room calorimetry in adults and children.

Journal of the Endocrine Society·2026
Same author

HER2-driven mammary tumorigenesis enhances bioenergetics despite reductions in mitochondrial content.

eLife·2026
Same author

Canagliflozin is a novel androgen receptor pathway inhibitor for castrate-sensitive and castrate-resistant prostate cancer.

Cancer letters·2026
Same author

Remodeling of the Mouse Liver and Skeletal Muscle Metabolome in Response to Continuous Acute Exercise and Disruption of AMPK-Glycogen Interactions.

Metabolites·2026
Same author

ASCC3 promotes chemosensitivity in colorectal cancer cells.

Scientific reports·2026
Same author

Incretin and Glucagon Signalling in MASLD and MASH: Integrating Metabolic Pathways With Disease Progression.

Diabetes, obesity & metabolism·2026
Same journal

AARS1 promotes tumor progression and immune evasion via ATF6 lactylation-mediated tryptophan metabolism in hepatocellular carcinoma.

Cell metabolism·2026
Same journal

Reactive species as regulators of immune cell metabolism, tolerance, and autoimmunity.

Cell metabolism·2026
Same journal

The interplay between the microbiome and immune cells in metabolic homeostasis and disease.

Cell metabolism·2026
Same journal

The metabolic basis of regulated cell death.

Cell metabolism·2026
Same journal

Gut microbiota-derived lysine phenylacetylation impairs mitochondrial function and is alleviated by SIRT3.

Cell metabolism·2026
Same journal

Methionine-supplemented longevity diet increases growth hormone, GLP-1, and FGF21; reduces frailty; and promotes healthspan.

Cell metabolism·2026
See all related articles

Adiponectin, a hormone from fat cells, boosts appetite and lowers energy use by activating AMPK in the brain. This finding sheds light on how the body manages energy balance.

Area of Science:

  • Endocrinology
  • Neuroscience
  • Metabolism

Background:

  • Energy balance is crucial for health, regulated by appetite and energy expenditure.
  • Adiponectin is a hormone secreted by adipocytes, with known roles in glucose and lipid metabolism.

Purpose of the Study:

  • To investigate the role of adiponectin in regulating appetite and energy expenditure.
  • To determine the hypothalamic mechanisms through which adiponectin exerts its effects.

Main Methods:

  • The study involved experiments investigating the effects of adiponectin on feeding behavior and energy expenditure.
  • Specific focus was placed on the role of AMP-activated protein kinase (AMPK) in the hypothalamus.

Main Results:

  • Adiponectin administration was found to increase appetite.

Related Experiment Videos

  • Adiponectin was shown to reduce energy expenditure.
  • These effects were mediated by the stimulation of AMPK in the hypothalamus.
  • Conclusions:

    • Adiponectin acts centrally within the hypothalamus to influence energy homeostasis.
    • Adiponectin's stimulation of hypothalamic AMPK plays a key role in increasing appetite and decreasing energy expenditure.