The Rheumatologist
COVID-19 News
  • Connect with us:
  • Facebook
  • Twitter
  • LinkedIn
  • YouTube
  • Feed
  • Home
  • Conditions
    • Rheumatoid Arthritis
    • SLE (Lupus)
    • Crystal Arthritis
      • Gout Resource Center
    • Spondyloarthritis
    • Osteoarthritis
    • Soft Tissue Pain
    • Scleroderma
    • Vasculitis
    • Systemic Inflammatory Syndromes
    • Guidelines
  • Resource Centers
    • Ankylosing Spondylitis Resource Center
    • Gout Resource Center
    • Rheumatoid Arthritis Resource Center
    • Systemic Lupus Erythematosus Resource Center
  • Drug Updates
    • Biologics & Biosimilars
    • DMARDs & Immunosuppressives
    • Topical Drugs
    • Analgesics
    • Safety
    • Pharma Co. News
  • Professional Topics
    • Ethics
    • Legal
    • Legislation & Advocacy
    • Career Development
      • Certification
      • Education & Training
    • Awards
    • Profiles
    • President’s Perspective
    • Rheuminations
  • Practice Management
    • Billing/Coding
    • Quality Assurance/Improvement
    • Workforce
    • Facility
    • Patient Perspective
    • Electronic Health Records
    • Apps
    • Information Technology
    • From the College
    • Multimedia
      • Audio
      • Video
  • Resources
    • Issue Archives
    • ACR Convergence
      • Systemic Lupus Erythematosus Resource Center
      • Rheumatoid Arthritis Resource Center
      • Gout Resource Center
      • Abstracts
      • Meeting Reports
      • ACR Convergence Home
    • American College of Rheumatology
    • ACR ExamRheum
    • Research Reviews
    • ACR Journals
      • Arthritis & Rheumatology
      • Arthritis Care & Research
      • ACR Open Rheumatology
    • Rheumatology Image Library
    • Treatment Guidelines
    • Rheumatology Research Foundation
    • Events
  • About Us
    • Mission/Vision
    • Meet the Authors
    • Meet the Editors
    • Contribute to The Rheumatologist
    • Subscription
    • Contact
  • Advertise
  • Search
You are here: Home / Articles / Decode the Crosstalk Between Bones, Brain, and Fat

Decode the Crosstalk Between Bones, Brain, and Fat

April 1, 2010 • By Kathy Holliman

  • Tweet
  • Email
Print-Friendly Version / Save PDF

Use of another mouse model indicated that bone mass accrual through brain-derived serotonin occurs by a decrease in sympathetic tone. The brain-derived serotonin apparently uses the Htr2c receptor—the most abundant serotonergic receptor in the hypothalamus—that mediates brain serotonin regulation of bone mass, a function that is independent of its influence through the same receptor on energy metabolism, the researchers reported in Cell.

You Might Also Like
  • Sensory Nerves May Be Key for Osteoporosis
  • Orexin’s Yin/Yang Functions Regulate Bone Remodeling
  • Insight into Crosstalk Between Bone & Immune Systems
Explore This Issue
April 2010
Also By This Author
  • ACR, EULAR Approve New Classification Criteria for Primary Sjögren’s Syndrome

Studies using a different mouse model indicated that brain-derived serotonin acts on ventromedial hypothalamic neurons through Htr2c “to decrease sympathetic activity and to favor bone mass accrual,” Dr. Karsenty said.

ad goes here:advert-1
ADVERTISEMENT
SCROLL TO CONTINUE

Unexpected Results

Dr. Karsenty and colleagues reported that their understanding of regulation of bone mass by serotonin led to unexpected observations. First, “depending on its site of synthesis, serotonin regulates bone mass accrual in opposite directions: it inhibits it when synthesized in the duodenum and favors it when acting as a neurotransmitter.”1 They noted that this seems to be the first example of a molecule that has different influences on bone remodeling that is dependent on the site of synthesis.

The second unexpected observation was that, even though brain-derived serotonin represents only about 5% of the total pool of serotonin in the body, its influence on bone remodeling “is dominant over that exerted by gut-derived serotonin. Since [brain-derived serotonin] is regulated by leptin, these results infer that leptin regulation of bone mass is more important than the one exerted by gut-derived serotonin.”

ad goes here:advert-2
ADVERTISEMENT
SCROLL TO CONTINUE

Based on that observation, the researchers predict that “using leptin as a treatment for obesity would favor the appearance of osteoporosis.”1

Kathy Holliman is a medical journalist based in New Jersey.

References

  1. Yadav VK, Oury F, Suda N, et al. A serotonin-dependent mechanism explains the leptin regulation of bone mass, appetite, and energy expenditure. Cell. 2009;138:976-989.
  2. Le NK, Sowa H, Hinoi E, et al. Endocrine regulation of energy metabolism by the skeleton. Cell. 2007;130:456-469.

Pages: 1 2 3 | Single Page

Filed Under: Conditions Tagged With: bone remodeling, Genes, leptin, leptin–serotonin pathway, Osteoporosis, ResearchIssue: April 2010

You Might Also Like:
  • Sensory Nerves May Be Key for Osteoporosis
  • Orexin’s Yin/Yang Functions Regulate Bone Remodeling
  • Insight into Crosstalk Between Bone & Immune Systems
  • Researchers Probe the Role of Fat Cells in Inflammation

Rheumatology Research Foundation

The Foundation is the largest private funding source for rheumatology research and training in the U.S.

Learn more »

Simple Tasks

Learn more about the ACR’s public awareness campaign and how you can get involved. Help increase visibility of rheumatic diseases and decrease the number of people left untreated.

Visit the Simple Tasks site »

American College of Rheumatology

Visit the official website for the American College of Rheumatology.

Visit the ACR »

The Rheumatologist newsmagazine reports on issues and trends in the management and treatment of rheumatic diseases. The Rheumatologist reaches 11,500 rheumatologists, internists, orthopedic surgeons, nurse practitioners, physician assistants, nurses, and other healthcare professionals who practice, research, or teach in the field of rheumatology.

About Us / Contact Us / Advertise / Privacy Policy / Terms of Use

  • Connect with us:
  • Facebook
  • Twitter
  • LinkedIn
  • YouTube
  • Feed

Copyright © 2006–2021 American College of Rheumatology. All rights reserved.

ISSN 1931-3268 (print)
ISSN 1931-3209 (online)

loading Cancel
Post was not sent - check your email addresses!
Email check failed, please try again
Sorry, your blog cannot share posts by email.
This site uses cookies: Find out more.