Evidence map›Paper›PMID 26466345›Full record

ArticlePloS one2015

Obesity Resistance and Enhanced Insulin Sensitivity in Ahnak-/- Mice Fed a High Fat Diet Are Related to Impaired Adipogenesis and Increased Energy Expenditure.

Jae Hoon Shin, Il Yong Kim, Yo Na Kim, Sun Mee Shin, Kyung Jin Roh, Seo Hyun Lee, Mira Sohn, Soo Young Cho, Sang Hyuk Lee, Chang-Yong Ko and 4 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.1field-weighted citation impact, top 22% 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

19 citing papers in PubMed, 31 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 4 institutions in 1 country.

Jae Hoon ShinLaboratory of Developmental Biology and Genomics, College of Veterinary Medicine, and BK21 Program for Veterinary Science, Seoul National University, Seoul, South Korea; Korea Mouse Phenotyping Center (KMPC), Seoul National University, Seoul, South Korea.
Il Yong KimLaboratory of Developmental Biology and Genomics, College of Veterinary Medicine, and BK21 Program for Veterinary Science, Seoul National University, Seoul, South Korea; Korea Mouse Phenotyping Center (KMPC), Seoul National University, Seoul, South Korea.
Yo Na KimLaboratory of Developmental Biology and Genomics, College of Veterinary Medicine, and BK21 Program for Veterinary Science, Seoul National University, Seoul, South Korea; Korea Mouse Phenotyping Center (KMPC), Seoul National University, Seoul, South Korea.
Sun Mee ShinDivision of Life Sciences, Ewha Womans University, Seoul, South Korea.
Kyung Jin RohLee Gil Ya Cancer and Diabetes Institute and Division of Endocrinology Gil Medical Center, Gachon University of Medicine and Science, Incheon, South Korea.
Seo Hyun LeeLaboratory of Developmental Biology and Genomics, College of Veterinary Medicine, and BK21 Program for Veterinary Science, Seoul National University, Seoul, South Korea; Korea Mouse Phenotyping Center (KMPC), Seoul National University, Seoul, South Korea.
Mira SohnDivision of Life Sciences, Ewha Womans University, Seoul, South Korea.
Soo Young ChoLaboratory of Developmental Biology and Genomics, College of Veterinary Medicine, and BK21 Program for Veterinary Science, Seoul National University, Seoul, South Korea; Korea Mouse Phenotyping Center (KMPC), Seoul National University, Seoul, South Korea.
Sang Hyuk LeeEwha Research Center for Systems Biology, Ewha Womans University, Seoul, South Korea.
Chang-Yong KoDepartment of Biomedical Engineering, College of Health Science, Institute of Medical Engineering, Yonsei University, Wonju, South Korea.
Han-Sung KimLaboratory of Developmental Biology and Genomics, College of Veterinary Medicine, and BK21 Program for Veterinary Science, Seoul National University, Seoul, South Korea; Korea Mouse Phenotyping Center (KMPC), Seoul National University, Seoul, South Korea.
Cheol Soo ChoiLee Gil Ya Cancer and Diabetes Institute and Division of Endocrinology Gil Medical Center, Gachon University of Medicine and Science, Incheon, South Korea.
Yun Soo BaeDivision of Life Sciences, Ewha Womans University, Seoul, South Korea.
Je Kyung SeongLaboratory of Developmental Biology and Genomics, College of Veterinary Medicine, and BK21 Program for Veterinary Science, Seoul National University, Seoul, South Korea; Korea Mouse Phenotyping Center (KMPC), Seoul National University, Seoul, South Korea; Interdisciplinary Program for Bioinformatics, Program for Cancer Biology and BIO-MAX Institute, Seoul National University, Seoul, South Korea.
Seoul National University · KREwha Womans University · KRGachon University Gil Medical Center · KRYonsei University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveRecent evidence has suggested that AHNAK expression is altered in obesity, although its role in adipose tissue development remains unclear. The objective of this study was to determine the molecular mechanism by which Ahnak influences adipogenesis and glucose homeostasis.

designWe investigated the in vitro role of AHNAK in adipogenesis using adipose-derived mesenchymal stem cells (ADSCs) and C3H10T1/2 cells. AHNAK-KO male mice were fed a high-fat diet (HFD; 60% calories from fat) and examined for glucose and insulin tolerances, for body fat compositions, and by hyperinsulinemic-euglycemic clamping. Energy expenditures were assessed using metabolic cages and by measuring the expression levels of genes involved in thermogenesis in white or brown adipose tissues.

resultsAdipogenesis in ADSCs was impaired in AHNAK-KO mice. The loss of AHNAK led to decreased BMP4/SMAD1 signaling, resulting in the downregulation of key regulators of adipocyte differentiation (P<0.05). AHNAK directly interacted with SMAD1 on the Pparγ2 promoter. Concomitantly, HFD-fed AHNAK-KO mice displayed reduced hepatosteatosis and improved metabolic profiles, including improved glucose tolerance (P<0.001), enhanced insulin sensitivity (P<0.001), and increased energy expenditure (P<0.05), without undergoing alterations in food intake and physical activity.

conclusionAHNAK plays a crucial role in body fat accumulation by regulating adipose tissue development via interaction with the SMAD1 protein and can be involved in metabolic homeostasis.

Indexed as

AdipogenesisEnergy MetabolismInsulin Resistance3T3 CellsAdipocytesAdipose Tissue, BrownAdipose Tissue, WhiteAnimalsBody CompositionCell DifferentiationDiet, High-FatGene Expression RegulationGlucoseGlucose Tolerance TestHomeostasisInsulinAhnak protein, mouseGlucoseInsulinMembrane ProteinsNeoplasm ProteinsSmad1 ProteinSmad1 protein, mouse

Identifiers

PMID26466345
PMCPMC4605776
OpenAlexW2149222021

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.