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

Specific decrease of mitochondrial thermogenic capacity in brown adipose tissue of obese SHR/N-cp rats

C Atgié1, A Marette, M Desautels

  • 1Department of Physiology, Laval University Medical School, Quebec, Canada.

The American Journal of Physiology
|December 1, 1993
PubMed
Summary

Obese diabetic rats show a significant thermogenic defect in brown adipose tissue (BAT), with reduced mitochondrial function. The liver, however, exhibits hypertrophy and increased metabolic activity, suggesting a key role in energy balance for these animals.

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

Host-Microbe Interplay in the Cardiometabolic Benefits of Dietary Polyphenols.

Trends in endocrinology and metabolism: TEM·2019
Same author

Paneth cell α-defensins HD-5 and HD-6 display differential degradation into active antimicrobial fragments.

Proceedings of the National Academy of Sciences of the United States of America·2019
Same author

Yogurt, diet quality and lifestyle factors.

European journal of clinical nutrition·2016
Same author

Distinct patterns of tissue-specific lipid accumulation during the induction of insulin resistance in mice by high-fat feeding.

Diabetologia·2013
Same author

RARgamma and TRbeta expressions are decreased in PBMC and SWAT of obese subjects in weight gain.

Journal of physiology and biochemistry·2010
Same author

Possible mechanisms of weight loss of Siberian hamsters (Phodopus sungorus sungorus) exposed to short photoperiod.

Journal of physiology and biochemistry·2010

Area of Science:

  • Metabolic research
  • Endocrinology
  • Obesity research

Background:

  • Type II diabetes is characterized by severe insulin resistance.
  • Brown adipose tissue (BAT) plays a crucial role in thermogenesis and energy expenditure.
  • Understanding metabolic defects in obesity is key to developing therapeutic strategies.

Purpose of the Study:

  • To investigate the metabolic properties of BAT, liver, and skeletal muscles in obese diabetic rats.
  • To determine if insulin resistance in obese animals is linked to a thermogenic defect in BAT.
  • To explore the role of the liver in energy balance in obese diabetic models.

Main Methods:

  • Comparison of metabolic parameters in lean and obese diabetic SHR/N-cp rats.
  • Assessment of brown adipocyte respiratory response to various stimuli.

Related Experiment Videos

  • Measurement of BAT cytochrome oxidase activity, uncoupling protein content, and mitochondrial GDP binding.
  • Analysis of liver and skeletal muscle tissue for changes in protein and DNA content.

    • Main Results:

    • Obese rats displayed a two-thirds decrease in brown adipocyte respiratory response, indicating a postreceptor defect.
    • Key indicators of BAT thermogenic capacity (cytochrome oxidase activity, uncoupling protein, GDP binding) were reduced by two-thirds.
    • Liver tissue in obese rats showed a two- to threefold increase in cytochrome oxidase activity, protein, and DNA content, suggesting hypertrophy.
    • Skeletal muscle parameters remained unchanged in obese rats.

    Conclusions:

    • Severe insulin resistance in obese diabetic rats is associated with a significant thermogenic defect in brown adipose tissue.
    • The liver plays a major role in energy balance in obese rats, potentially compensating for BAT dysfunction.
    • Hyperphagia and hyperinsulinemia in obese rats may drive liver hypertrophy and increased metabolic activity.