Searching the Resource Information Network

Our searching services are busy right now. Please try again later

  • Register
X
Forgot Password

If you have forgotten your password you can enter your email here and get a temporary password sent to your email.

X

Leaving Community

Are you sure you want to leave this community? Leaving the community will revoke any permissions you have been granted in this community.

No
Yes

Leptin-dependent control of glucose balance and locomotor activity by POMC neurons.

Lihong Huo | Kevin Gamber | Sarah Greeley | Jose Silva | Nicholas Huntoon | Xing-Hong Leng | Christian Bjørbaek
Cell metabolism | 2009

Leptin plays a pivotal role in regulation of energy balance. Via unknown central pathways, leptin also affects peripheral glucose homeostasis and locomotor activity. We hypothesized that, specifically, pro-opiomelanocortin (POMC) neurons mediate those actions. To examine this possibility, we applied Cre-Lox technology to express leptin receptors (ObRb) exclusively in POMC neurons of the morbidly obese, profoundly diabetic, and severely hypoactive leptin receptor-deficient Lepr(db/db) mice. Here, we show that expression of ObRb only in POMC neurons leads to a marked decrease in energy intake and a modest reduction in body weight in Lepr(db/db) mice. Remarkably, blood glucose levels are entirely normalized. This normalization occurs independently of changes in food intake and body weight. In addition, physical activity is greatly increased despite profound obesity. Our results suggest that leptin signaling exclusively in POMC neurons is sufficient to stimulate locomotion and prevent diabetes in the severely hypoactive and hyperglycemic obese Lepr(db/db) mice.

Pubmed ID: 19490908

Research resources used in this publication

None found

Additional research tools detected in this publication

Antibodies used in this publication

None found

Associated grants

  • Agency: NIDDK NIH HHS, United States
    Id: R01 DK065743-01A1
  • Agency: NIDDK NIH HHS, United States
    Id: R01 DK065743-02
  • Agency: NIDDK NIH HHS, United States
    Id: R01 DK065743-04
  • Agency: NIDDK NIH HHS, United States
    Id: R01 DK065743-03
  • Agency: NIDDK NIH HHS, United States
    Id: P30 DK046200
  • Agency: NIDDK NIH HHS, United States
    Id: R01 DK060673-04
  • Agency: NIDDK NIH HHS, United States
    Id: DK65743
  • Agency: NIDDK NIH HHS, United States
    Id: R01 DK060673-05
  • Agency: NIDDK NIH HHS, United States
    Id: R01 DK060673-01
  • Agency: NIDDK NIH HHS, United States
    Id: DK46200
  • Agency: NIDDK NIH HHS, United States
    Id: R01 DK060673
  • Agency: NIDDK NIH HHS, United States
    Id: R01 DK065743
  • Agency: NIDDK NIH HHS, United States
    Id: R01 DK060673-02
  • Agency: NIDDK NIH HHS, United States
    Id: DK60673
  • Agency: NIDDK NIH HHS, United States
    Id: R01 DK060673-03

Publication data is provided by the National Library of Medicine ® and PubMed ®. Data is retrieved from PubMed ® on a weekly schedule. For terms and conditions see the National Library of Medicine Terms and Conditions.

This is a list of tools and resources that we have found mentioned in this publication.


Applied Biosystems (tool)

RRID:SCR_005039

An Antibody supplier

View all literature mentions

Primer Express (tool)

RRID:SCR_014326

Software that allows users to manually or automatically design custom primers and probes for gene quantitation and allelic discrimination (SNP) real-time PCR applications. It supports assays based on TaqMan and SYBR Green I dye chemistries.

View all literature mentions