Journal article
Involvement of hypothalamic AMP-activated protein kinase in leptin-induced sympathetic nerve activation
PloS one, Vol.8(2), pp.e56660-e56660
2013
DOI: 10.1371/journal.pone.0056660
PMCID: PMC3572050
PMID: 23418591
Abstract
In mammals, leptin released from the white adipose tissue acts on the central nervous system to control feeding behavior, cardiovascular function, and energy metabolism. Central leptin activates sympathetic nerves that innervate the kidney, adipose tissue, and some abdominal organs in rats. AMP-activated protein kinase (AMPK) is essential in the intracellular signaling pathway involving the activation of leptin receptors (ObRb). We investigated the potential of AMPKα2 in the sympathetic effects of leptin using in vivo siRNA injection to knockdown AMPKα2 in rats, to produce reduced hypothalamic AMPKα2 expression. Leptin effects on body weight, food intake, and blood FFA levels were eliminated in AMPKα2 siRNA-treated rats. Leptin-evoked enhancements of the sympathetic nerve outflows to the kidney, brown and white adipose tissues were attenuated in AMPKα2 siRNA-treated rats. To check whether AMPKα2 was specific to sympathetic changes induced by leptin, we examined the effects of injecting MT-II, a melanocortin-3 and -4 receptor agonist, on the sympathetic nerve outflows to the kidney and adipose tissue. MT-II-induced sympatho-excitation in the kidney was unchanged in AMPKα2 siRNA-treated rats. However, responses of neural activities involving adipose tissue to MT-II were attenuated in AMPKα2 siRNA-treated rats. These results suggest that hypothalamic AMPKα2 is involved not only in appetite and body weight regulation but also in the regulation of sympathetic nerve discharges to the kidney and adipose tissue. Thus, AMPK might function not only as an energy sensor, but as a key molecule in the cardiovascular, thermogenic, and lipolytic effects of leptin through the sympathetic nervous system.
Details
- Title: Subtitle
- Involvement of hypothalamic AMP-activated protein kinase in leptin-induced sympathetic nerve activation
- Creators
- Mamoru Tanida - Department of Physiology II, Kanazawa Medical University, Uchinada, Ishikawa, Japan. mtanida@kanazawa-med.ac.jpNaoki YamamotoToshishige ShibamotoKamal Rahmouni
- Resource Type
- Journal article
- Publication Details
- PloS one, Vol.8(2), pp.e56660-e56660
- DOI
- 10.1371/journal.pone.0056660
- PMID
- 23418591
- PMCID
- PMC3572050
- NLM abbreviation
- PLoS One
- ISSN
- 1932-6203
- eISSN
- 1932-6203
- Publisher
- Public Library of Science; United States
- Grant note
- P01 HL084207 / NHLBI NIH HHS
- Language
- English
- Date published
- 2013
- Academic Unit
- Iowa Neuroscience Institute; Neuroscience and Pharmacology; Internal Medicine
- Record Identifier
- 9984040574102771
Metrics
21 Record Views