Evidence map›Paper›PMID 27689001›Full record

ArticleMolecular metabolism2016

Adiponectin potentiates the acute effects of leptin in arcuate Pomc neurons.

Jia Sun, Yong Gao, Ting Yao, Yiru Huang, Zhenyan He, Xingxing Kong, Kai-Jiang Yu, Rui-Tao Wang, Hongbo Guo, Jianqun Yan and 5 more

Open access · goldAbstract read
In one paragraph

Article in Molecular metabolism, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
4.8field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

37 citing papers in PubMed, 63 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

15 authors at 7 institutions in 2 countries.

Jia SunDepartment of Endocrinology, Zhujiang Hospital, Southern Medical University, Guangzhou, China; Division of Hypothalamic Research, The University of Texas Southwestern Medical Center at Dallas, Dallas, TX, USA.
Yong GaoNational Laboratory of Medical Molecular Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China; Division of Hypothalamic Research, The University of Texas Southwestern Medical Center at Dallas, Dallas, TX, USA.
Ting YaoDepartment of Physiology and Pathophysiology, Xi'an Jiaotong University School of Medicine, Xi'an, Shaanxi, China; Division of Hypothalamic Research, The University of Texas Southwestern Medical Center at Dallas, Dallas, TX, USA.
Yiru HuangDepartment of Neurosurgery, Zhujiang Hospital, Southern Medical University, Guangzhou, China; Division of Hypothalamic Research, The University of Texas Southwestern Medical Center at Dallas, Dallas, TX, USA.
Zhenyan HeDepartment of Neurosurgery, Zhujiang Hospital, Southern Medical University, Guangzhou, China; Division of Hypothalamic Research, The University of Texas Southwestern Medical Center at Dallas, Dallas, TX, USA.
Xingxing KongDivision of Endocrinology, Beth Israel Deaconess Medical Center and Harvard Medical School, Harvard University, Boston, MA, 02115, USA.
Kai-Jiang YuDepartment of Intensive Care Unit, The Third Affiliated Hospital, Harbin Medical University, No. 150 Haping St, Nangang District, Harbin, 150081, China.
Rui-Tao WangDepartment of Intensive Care Unit, The Third Affiliated Hospital, Harbin Medical University, No. 150 Haping St, Nangang District, Harbin, 150081, China.
Hongbo GuoDepartment of Neurosurgery, Zhujiang Hospital, Southern Medical University, Guangzhou, China.
Jianqun YanDepartment of Physiology and Pathophysiology, Xi'an Jiaotong University School of Medicine, Xi'an, Shaanxi, China.
Yongsheng ChangNational Laboratory of Medical Molecular Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
Hong ChenDepartment of Endocrinology, Zhujiang Hospital, Southern Medical University, Guangzhou, China.
Philipp E SchererTouchstone Diabetes Center, Department of Internal Medicine, The University of Texas Southwestern Medical Center at Dallas, Dallas, TX, 75390, USA.
Tiemin LiuDepartment of Intensive Care Unit, The Third Affiliated Hospital, Harbin Medical University, No. 150 Haping St, Nangang District, Harbin, 150081, China; Division of Hypothalamic Research, The University of Texas Southwestern Medical Center at Dallas, Dallas, TX, USA.
Kevin W WilliamsDivision of Hypothalamic Research, The University of Texas Southwestern Medical Center at Dallas, Dallas, TX, USA. Electronic address: Kevin.Williams@UTSouthwestern.edu.
The University of Texas Southwestern Medical Center · USZhujiang Hospital · CNChinese Academy of Medical Sciences & Peking Union Medical College · CNHarbin Medical University · CNSouthern Medical University · CNXi'an Jiaotong University · CNHarvard University · US

Funding

Novel Mechanisms Regulating the Adipocyte-Brain-Hepatocyte AxisP01DK088761 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI ELMQUIST, JOEL K. · 2010 to 2019
$17.4M
Adiponectin, A Protein Secreted From Adipose TissueR01DK055758 · NIDDK · YESHIVA UNIVERSITY · PI SCHERER, PHILIPP E · 2000 to 2024
$10.9M
White Adipose Tissue Physiology, Mitochondrial Function and AdiponectinR01DK099110 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI PHILIPP E SCHERER · 2013 to 2026
$6.7M
Central Mechanisms Regulating Acute Leptin and Insulin SignalingR01DK100699 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI WILLIAMS, KEVIN W · 2014 to 2018
$1.8M
The Role of IRF4 in Exercise Induced ThermogenesisK99DK106550 · NIDDK · BETH ISRAEL DEACONESS MEDICAL CENTER · PI KONG, XINGXING · 2015 to 2016
$180k
NIDDK NIH HHS K99 DK106550NIDDK NIH HHS P01 DK088761NIDDK NIH HHS R01 DK055758NIDDK NIH HHS R01 DK099110NIDDK NIH HHS R01 DK100699
6 · The paper itself

Abstract

objectiveAdiponectin receptors (AdipoRs) are located on neurons of the hypothalamus involved in metabolic regulation - including arcuate proopiomelanocortin (Pomc) and Neuropeptide Y/Agouti-related peptide (NPY/AgRP) neurons. AdipoRs play a critical role in regulating glucose and fatty acid metabolism by initiating several signaling cascades overlapping with Leptin receptors (LepRs). However, the mechanism by which adiponectin regulates cellular activity in the brain remains undefined.

methodsIn order to resolve this issue, we utilized neuron-specific transgenic mouse models to identify Pomc and NPY/AgRP neurons which express LepRs for patch-clamp electrophysiology experiments.

resultsWe found that leptin and adiponectin synergistically activated melanocortin neurons in the arcuate nucleus. Conversely, NPY/AgRP neurons were inhibited in response to adiponectin. The adiponectin-induced depolarization of arcuate Pomc neurons occurred via activation of Phosphoinositide-3-kinase (PI3K) signaling, independent of 5' AMP-activated protein kinase (AMPK) activity. Adiponectin also activated melanocortin neurons at various physiological glucose levels.

conclusionsOur results demonstrate a requirement for PI3K signaling in the acute adiponectin-induced effects on the cellular activity of arcuate melanocortin neurons. Moreover, these data provide evidence for PI3K as a substrate for both leptin and adiponectin to regulate energy balance and glucose metabolism via melanocortin activity.

Indexed as

DiabetesElectrophysiologyEnergy balanceMelanocortinObesityPatch-clamp

Identifiers

PMID27689001
PMCPMC5034606
OpenAlexW2512823779

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.