Evidence map›Paper›PMID 26987950›Full record

ArticleScientific reports2016

AHNAK deficiency promotes browning and lipolysis in mice via increased responsiveness to β-adrenergic signalling.

Jae Hoon Shin, Seo Hyun Lee, Yo Na Kim, Il Yong Kim, Youn Ju Kim, Dong Soo Kyeong, Hee Jung Lim, Soo Young Cho, Junhee Choi, Young Jin Wi and 4 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 2 pooled it
2.1field-weighted citation impact, top 13% 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

18 citing papers in PubMed, 2 syntheses or guidelines pooled it, 24 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

14 authors at 3 institutions in 2 countries.

Jae Hoon ShinLaboratory of Developmental Biology and Genomics, Institute for Veterinary Science, and BK21 Program for Veterinary Science, College of Veterinary Medicine, Seoul National University, Seoul, Republic of Korea.
Seo Hyun LeeLaboratory of Developmental Biology and Genomics, Institute for Veterinary Science, and BK21 Program for Veterinary Science, College of Veterinary Medicine, Seoul National University, Seoul, Republic of Korea.
Yo Na KimLaboratory of Developmental Biology and Genomics, Institute for Veterinary Science, and BK21 Program for Veterinary Science, College of Veterinary Medicine, Seoul National University, Seoul, Republic of Korea.
Il Yong KimKorea Mouse Phenotyping Center (KMPC), Seoul National University, Seoul, Republic of Korea.
Youn Ju KimLaboratory of Developmental Biology and Genomics, Institute for Veterinary Science, and BK21 Program for Veterinary Science, College of Veterinary Medicine, Seoul National University, Seoul, Republic of Korea.
Dong Soo KyeongLaboratory of Developmental Biology and Genomics, Institute for Veterinary Science, and BK21 Program for Veterinary Science, College of Veterinary Medicine, Seoul National University, Seoul, Republic of Korea.
Hee Jung LimKorea Mouse Phenotyping Center (KMPC), Seoul National University, Seoul, Republic of Korea.
Soo Young ChoKorea Mouse Phenotyping Center (KMPC), Seoul National University, Seoul, Republic of Korea.
Junhee ChoiDepartment of Life Science, College of Natural Sciences, Research Institute for Natural Sciences, Hanyang University, Seoul, Republic of Korea.
Young Jin WiDepartment of Life Science, College of Natural Sciences, Research Institute for Natural Sciences, Hanyang University, Seoul, Republic of Korea.
Jae-Hoon ChoiDepartment of Life Science, College of Natural Sciences, Research Institute for Natural Sciences, Hanyang University, Seoul, Republic of Korea.
Yeo Sung YoonDepartment of Anatomy and Cell Biology, College of Veterinary Medicine, Research Institute for Veterinary Science, Seoul National University, Seoul, South Korea.
Yun Soo BaeDivision of Life Sciences, Ewha Womans University, Seoul, Republic of Korea.
Je Kyung SeongLaboratory of Developmental Biology and Genomics, Institute for Veterinary Science, and BK21 Program for Veterinary Science, College of Veterinary Medicine, Seoul National University, Seoul, Republic of Korea.
Seoul National University · KRHanyang University · KREwha Womans University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In adipose tissue, agonists of the β3-adrenergic receptor (ADRB3) regulate lipolysis, lipid oxidation, and thermogenesis. The deficiency in the thermogenesis induced by neuroblast differentiation-associated protein AHNAK in white adipose tissue (WAT) of mice fed a high-fat diet suggests that AHNAK may stimulate energy expenditure via development of beige fat. Here, we report that AHNAK deficiency promoted browning and thermogenic gene expression in WAT but not in brown adipose tissue of mice stimulated with the ADRB3 agonist CL-316243. Consistent with the increased thermogenesis, Ahnak(-/-) mice exhibited an increase in energy expenditure, accompanied by elevated mitochondrial biogenesis in WAT depots in response to CL-316243. Additionally, AHNAK-deficient WAT contained more eosinophils and higher levels of type 2 cytokines (IL-4/IL-13) to promote browning of WAT in response to CL-316243. This was associated with enhanced sympathetic tone in the WAT via upregulation of adrb3 and tyrosine hydroxylase (TH) in response to β-adrenergic activation. CL-316243 activated PKA signalling and enhanced lipolysis, as evidenced by increased phosphorylation of hormone-sensitive lipase and release of free glycerol in Ahnak(-/-) mice compared to wild-type mice. Overall, these findings suggest an important role of AHNAK in the regulation of thermogenesis and lipolysis in WAT via β-adrenergic signalling.

Indexed as

LipolysisAdipose Tissue, BrownAdipose Tissue, WhiteAnimalsDiet, High-FatDioxolesEnergy MetabolismGene Expression RegulationMembrane ProteinsMiceNeoplasm ProteinsReceptors, Adrenergic, betaSignal TransductionThermogenesisAhnak protein, mouseDioxolesdisodium (R,R)-5-(2-((2-(3-chlorophenyl)-2-hydroxyethyl)-amino)propyl)-1,3-benzodioxole-2,3-dicarboxylateMembrane ProteinsNeoplasm ProteinsReceptors, Adrenergic, beta

Identifiers

PMID26987950
PMCPMC4796812
OpenAlexW2321336459

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.