Evidence map›Paper›PMID 33034335›Full record

ArticleLab on a chip2020

Fattening chips: hypertrophy, feeding, and fasting of human white adipocytes

Benjamin D Pope, Curtis R Warren, Madeleine O Dahl, Christina V Pizza, Douglas E Henze, Nina R Sinatra, Grant M Gonzalez, Huibin Chang, Qihan Liu, Aaron L Glieberman and 3 more

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Lab on a chip, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

6 citing papers in PubMed, 16 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

13 authors at 2 institutions in 4 countries.

Benjamin D PopeDisease Biophysics Group, Wyss Institute for Biologically Inspired Engineering, Harvard John A. Paulson School of Engineering and Applied Sciences, Harvard University, Pierce Hall, Room 318, 29 Oxford Street, Cambridge, MA 02138, USA. kkparker@seas.harvard.edu and Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA.ORCID 0000-0003-1847-9163
Curtis R WarrenBeth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA.
Madeleine O DahlDisease Biophysics Group, Wyss Institute for Biologically Inspired Engineering, Harvard John A. Paulson School of Engineering and Applied Sciences, Harvard University, Pierce Hall, Room 318, 29 Oxford Street, Cambridge, MA 02138, USA. kkparker@seas.harvard.edu.
Christina V PizzaDisease Biophysics Group, Wyss Institute for Biologically Inspired Engineering, Harvard John A. Paulson School of Engineering and Applied Sciences, Harvard University, Pierce Hall, Room 318, 29 Oxford Street, Cambridge, MA 02138, USA. kkparker@seas.harvard.edu.
Douglas E HenzeDisease Biophysics Group, Wyss Institute for Biologically Inspired Engineering, Harvard John A. Paulson School of Engineering and Applied Sciences, Harvard University, Pierce Hall, Room 318, 29 Oxford Street, Cambridge, MA 02138, USA. kkparker@seas.harvard.edu.
Nina R SinatraDisease Biophysics Group, Wyss Institute for Biologically Inspired Engineering, Harvard John A. Paulson School of Engineering and Applied Sciences, Harvard University, Pierce Hall, Room 318, 29 Oxford Street, Cambridge, MA 02138, USA. kkparker@seas.harvard.edu.
Grant M GonzalezDisease Biophysics Group, Wyss Institute for Biologically Inspired Engineering, Harvard John A. Paulson School of Engineering and Applied Sciences, Harvard University, Pierce Hall, Room 318, 29 Oxford Street, Cambridge, MA 02138, USA. kkparker@seas.harvard.edu.
Huibin ChangDisease Biophysics Group, Wyss Institute for Biologically Inspired Engineering, Harvard John A. Paulson School of Engineering and Applied Sciences, Harvard University, Pierce Hall, Room 318, 29 Oxford Street, Cambridge, MA 02138, USA. kkparker@seas.harvard.edu.
Qihan LiuDisease Biophysics Group, Wyss Institute for Biologically Inspired Engineering, Harvard John A. Paulson School of Engineering and Applied Sciences, Harvard University, Pierce Hall, Room 318, 29 Oxford Street, Cambridge, MA 02138, USA. kkparker@seas.harvard.edu.
Aaron L GliebermanDisease Biophysics Group, Wyss Institute for Biologically Inspired Engineering, Harvard John A. Paulson School of Engineering and Applied Sciences, Harvard University, Pierce Hall, Room 318, 29 Oxford Street, Cambridge, MA 02138, USA. kkparker@seas.harvard.edu.
John P FerrierDisease Biophysics Group, Wyss Institute for Biologically Inspired Engineering, Harvard John A. Paulson School of Engineering and Applied Sciences, Harvard University, Pierce Hall, Room 318, 29 Oxford Street, Cambridge, MA 02138, USA. kkparker@seas.harvard.edu.
Chad A CowanBeth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA and Harvard Stem Cell Institute, Cambridge, MA 02138, USA.
Kevin Kit ParkerDisease Biophysics Group, Wyss Institute for Biologically Inspired Engineering, Harvard John A. Paulson School of Engineering and Applied Sciences, Harvard University, Pierce Hall, Room 318, 29 Oxford Street, Cambridge, MA 02138, USA. kkparker@seas.harvard.edu and Harvard Stem Cell Institute, Cambridge, MA 02138, USA.ORCID 0000-0002-5968-7535
Harvard University · USBeth Israel Deaconess Medical Center · US

Funding

Isogenic Human Pluripotent Stem Cell-Based Models of Human Disease MutationsR01DK097768 · NIDDK · BROAD INSTITUTE, INC. · PI COWAN, CHAD ALBERT, ZHANG, FENG · 2012 to 2016
$11.0M
Integrating lipid genotyes and phenotypes in iPS derived hepatocytes/adipocytesU01HL107440 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI COWAN, CHAD ALBERT, DEO, RAHUL CHANDRAKANT · 2011 to 2015
$9.0M
Human Pluripotent Stem Cell and Progenitor Models of Cardiac and Blood DiseasesU01HL100408 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI COWAN, CHAD ALBERT, MELTON, DOUGLAS A · 2009 to 2015
$8.9M
Production of clinical-grade diabetes patient-specific induced pluripotent stem cell lines intended for autologous beta cell replacement therapyUC4DK104165 · NIDDK · HARVARD UNIVERSITY · PI MELTON, DOUGLAS A · 2014 to 2017
$7.3M
Mouse Neurodevelopmental Behavior CoreU54HD090255 · NICHD · BOSTON CHILDREN'S HOSPITAL · PI POMEROY, SCOTT LOREN · 2016 to 2020
$5.2M
Human Cell-Based Models of Primary Adipocyte DisordersR01DK095384 · NIDDK · HARVARD UNIVERSITY · PI COWAN, CHAD ALBERT · 2012 to 2016
$1.8M
NHLBI NIH HHS U01 HL100408NHLBI NIH HHS U01 HL107440NICHD NIH HHS U54 HD090255NIDDK NIH HHS R01 DK095384NIDDK NIH HHS R01 DK097768NIDDK NIH HHS UC4 DK104165
6 · The paper itself

Abstract

Adipose is a distributed organ that performs vital endocrine and energy homeostatic functions. Hypertrophy of white adipocytes is a primary mode of both adaptive and maladaptive weight gain in animals and predicts metabolic syndrome independent of obesity. Due to the failure of conventional culture to recapitulate adipocyte hypertrophy, technology for production of adult-size adipocytes would enable applications such as in vitro testing of weight loss therapeutics. To model adaptive adipocyte hypertrophy in vitro, we designed and built fat-on-a-chip using fiber networks inspired by extracellular matrix in adipose tissue. Fiber networks extended the lifespan of differentiated adipocytes, enabling growth to adult sizes. By micropatterning preadipocytes in a native cytoarchitecture and by adjusting cell-to-cell spacing, rates of hypertrophy were controlled independent of culture time or differentiation efficiency. In vitro hypertrophy followed a nonlinear, nonexponential growth model similar to human development and elicited transcriptomic changes that increased overall similarity with primary tissue. Cells on the chip responded to simulated meals and starvation, which potentiated some adipocyte endocrine and metabolic functions. To test the utility of the platform for therapeutic development, transcriptional network analysis was performed, and retinoic acid receptors were identified as candidate drug targets. Regulation by retinoid signaling was suggested further by pharmacological modulation, where activation accelerated and inhibition slowed hypertrophy. Altogether, this work presents technology for mature adipocyte engineering, addresses the regulation of cell growth, and informs broader applications for synthetic adipose in pharmaceutical development, regenerative medicine, and cellular agriculture.

Indexed as

Adipocytes, WhiteFastingAdipose TissueAdultAnimalsHumansHypertrophyObesity

Identifiers

PMID33034335
PMCPMC7818847
OpenAlexW3087379327

What OpenQuestion holds

Textmetadata
LicenceTDM
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.