Involvement of hypothalamic AMP-activated protein kinase in leptin-induced sympathetic nerve activation.

Tanida M, Yamamoto N, Shibamoto T, Rahmouni K

PloS one13 Feb 2013Cited by 74 (Europe PMC)

PMID23418591PMCIDPMC3572050DOI10.1371/journal.pone.0056660PepBankPUB-23418591

Summary

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.

CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study2

No result from this study comes from a test of the peptide.

Studies that did not test the peptide alone2

In this study, Melanotan II was a lab tool or a carrier, part of a mix, or the subject of a lab method. These results are not evidence about taking Melanotan II.

01AnimalNot a test of Melanotan II aloneAnimal study (in vivo)Mechanism
In rats, hypothalamic AMPKα2 knockdown did not change the sympatho-excitation in the kidney that MT-II induced.
In plain wordsIn rats, lowering AMPKα2 in the brain did not change how MT-II raised nerve activity to the kidney.
Peptide
Melanotan II
Outcome
No significant changeMT-II-induced renal sympatho-excitation after AMPKa2 knockdown
Study
ratn: not reported in source
Rats with hypothalamic AMPKα2 knockdown by siRNA
Outcome group
Receptor activity and mechanism · Cardiovascular
Source sentences
Summary
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.
2 context sentences(design, population, supporting numbers)
Summary · context
MT-II-induced sympatho-excitation in the kidney was unchanged in AMPKα2 siRNA-treated rats.
Summary · context
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.
In this study, Melanotan II was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Melanotan II.
Show in the study text Report a problemFND-2341859101
02AnimalNot a test of Melanotan II aloneAnimal study (in vivo)Mechanism
In rats, hypothalamic AMPKα2 knockdown attenuated the responses of nerve activity involving adipose tissue to MT-II.
In plain wordsIn rats, lowering AMPKα2 in the brain weakened the nerve-activity response of fat tissue to MT-II.
Peptide
Melanotan II
Outcome
DecreaseMT-II-induced adipose tissue sympathetic nerve responses after AMPKa2 knockdown
Study
ratn: not reported in source
Rats with hypothalamic AMPKα2 knockdown by siRNA
Outcome group
Receptor activity and mechanism · Metabolic and weight
Source sentences
Summary
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.
2 context sentences(design, population, supporting numbers)
Summary · context
However, responses of neural activities involving adipose tissue to MT-II were attenuated in AMPKα2 siRNA-treated rats.
Summary · context
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.
In this study, Melanotan II was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Melanotan II.
Show in the study text Report a problemFND-2341859102

AI wrote and checked these results. AI can make mistakes, so check important results against the source.

Version history

PepBank keeps every version of the data on this study. Status changes from Retraction Watch, Europe PMC and Crossref are listed with their source.

Version 2Current
10 Oct 2026, 09:43 UTC
Study results updated
Version 1
9 Oct 2026, 03:04 UTC
First added · source update from Europe PMC

Subjects

Terms as the source lists them.

PepBank is a research reference. Talk to a doctor before you use any peptide.