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

Adipose tissue dysfunction in obesity and lipodystrophy.

Abhimanyu Garg1

  • 1Department of Internal Medicine, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390, USA. Abhimanyu.garg@utsouthwestern.edu

Clinical Cornerstone
|January 9, 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

Familial Generalized and Partial Lipodystrophies Due to Rare Biallelic Variants in <i>LMNA</i>.

International journal of molecular sciences·2026
Same author

Genotype-Phenotype Heterogeneity Among Patients with Lipodystrophy Harboring Rare POLD1 Variants.

The Journal of clinical endocrinology and metabolism·2026
Same author

Novel Homozygous Variants in CIDEC and WRN in a Young Female with Lipodystrophy and Thyroid Cancer.

International journal of molecular sciences·2026
Same author

Response to letter to the editor by Matsubara and colleagues.

Journal of clinical lipidology·2026
Same author

A recurrent ACAA2 variant causes a dominant syndrome of lipodystrophy, lipomatosis, infantile steatohepatitis, and hypoglycemia.

The Journal of clinical investigation·2025
Same author

Erratum. Gain of Function NOTCH3 Variants Cause Familial Partial Lipodystrophy Due to Activation of Senescence Pathways. Diabetes 2025;74:427-438.

Diabetes·2025
Same journal

Treatment of overweight and obesity: lifestyle, pharmacologic, and surgical options.

Clinical cornerstone·2009
Same journal

Guiding clinical decisions on abdominal obesity and cardiometabolic risk.

Clinical cornerstone·2009
Same journal

Overweight and obesity: the pathogenesis of cardiometabolic risk.

Clinical cornerstone·2009
Same journal

Obesity as a disease state: a new paradigm for diagnosis and treatment.

Clinical cornerstone·2009
Same journal

Pathogenesis of cardiometabolic risk as it relates to overweight and obesity. Introduction.

Clinical cornerstone·2009
Same journal

Should clinicians routinely determine rhinitis subtype on initial diagnosis and evaluation? A debate among experts.

Clinical cornerstone·2009
See all related articles

Adipose tissue stores energy and releases fatty acids, but its dysfunction, marked by altered adipocytokine release, can lead to insulin resistance and metabolic issues like obesity or lipodystrophy.

Area of Science:

  • Metabolic biology
  • Endocrinology

Background:

  • Adipose tissue primarily stores energy as triglycerides and releases free fatty acids and glycerol.
  • It secretes adipocytokines (e.g., leptin, adiponectin) with systemic effects on metabolism and energy homeostasis.
  • Adipose tissue also plays roles in hormone aromatization and mechanical protection.

Purpose of the Study:

  • To elucidate the multifaceted roles of adipose tissue in energy storage and metabolic regulation.
  • To highlight the significance of adipocytokines in systemic metabolic control.
  • To examine the consequences of adipose tissue dysfunction, including insulin resistance.

Main Methods:

  • Review of existing literature on adipose tissue physiology and function.
  • Analysis of the endocrine, autocrine, and paracrine actions of adipocytokines.

Related Experiment Videos

  • Examination of metabolic complications associated with adipose tissue dysfunction.

    • Main Results:

    • Adipose tissue regulates energy balance through triglyceride storage and fatty acid release.
    • Adipocytokines secreted by adipose tissue influence brain, liver, and muscle function.
    • Dysfunctional adipose tissue, seen in obesity and lipodystrophy, is linked to insulin resistance.

    Conclusions:

    • Adipose tissue is a critical endocrine organ regulating energy homeostasis and metabolism.
    • Altered adipocytokine and free fatty acid release from adipose tissue are implicated in metabolic disorders.
    • Maintaining adipose tissue function is vital for preventing metabolic complications.