Evidence map›Paper›PMID 31882562›Full record

ArticleDiabetes2020

A Novel Model of Diabetic Complications: Adipocyte Mitochondrial Dysfunction Triggers Massive β-Cell Hyperplasia.

Christine M Kusminski, Alexandra L Ghaben, Thomas S Morley, Ricardo J Samms, Andrew C Adams, Yu An, Joshua A Johnson, Nolwenn Joffin, Toshiharu Onodera, Clair Crewe and 3 more

Open access · greenAbstract read
In one paragraph

Article in Diabetes, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
4.2field-weighted citation impact, top 5% 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

39 citing papers in PubMed, 45 citations in OpenAlex.

  1. Review
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  11. White adipose tissue mitochondrial bioenergetics in metabolic diseases.Reviews in endocrine & metabolic disorders · 2023
    Review
  12. Article
  13. Article
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  15. Overview of growth differentiation factor 15 in metabolic syndrome.Journal of cellular and molecular medicine · 2023
    Review
  16. Article
  17. Review
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  19. Iron and the Pathophysiology of Diabetes.Annual review of physiology · 2023
    Review
  20. Review
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 1 country.

Christine M KusminskiTouchstone Diabetes Center, Department of Internal Medicine, The University of Texas Southwestern Medical Center, Dallas, TX.
Alexandra L GhabenTouchstone Diabetes Center, Department of Internal Medicine, The University of Texas Southwestern Medical Center, Dallas, TX.
Thomas S MorleyTouchstone Diabetes Center, Department of Internal Medicine, The University of Texas Southwestern Medical Center, Dallas, TX.
Ricardo J SammsEli Lilly Research Laboratories, Division of Eli Lilly and Company, Indianapolis, IN.
Andrew C AdamsEli Lilly Research Laboratories, Division of Eli Lilly and Company, Indianapolis, IN.
Yu AnTouchstone Diabetes Center, Department of Internal Medicine, The University of Texas Southwestern Medical Center, Dallas, TX.
Joshua A JohnsonTouchstone Diabetes Center, Department of Internal Medicine, The University of Texas Southwestern Medical Center, Dallas, TX.
Nolwenn JoffinTouchstone Diabetes Center, Department of Internal Medicine, The University of Texas Southwestern Medical Center, Dallas, TX.
Toshiharu OnoderaTouchstone Diabetes Center, Department of Internal Medicine, The University of Texas Southwestern Medical Center, Dallas, TX.
Clair CreweTouchstone Diabetes Center, Department of Internal Medicine, The University of Texas Southwestern Medical Center, Dallas, TX.
William L HollandTouchstone Diabetes Center, Department of Internal Medicine, The University of Texas Southwestern Medical Center, Dallas, TX.ORCID 0000-0001-9950-1435
Ruth GordilloTouchstone Diabetes Center, Department of Internal Medicine, The University of Texas Southwestern Medical Center, Dallas, TX.
Philipp E SchererTouchstone Diabetes Center, Department of Internal Medicine, The University of Texas Southwestern Medical Center, Dallas, TX philipp.scherer@utsouthwestern.edu.ORCID 0000-0003-0680-3392
The University of Texas Southwestern Medical Center · USEli Lilly (United States) · US

Funding

Novel Mechanisms Regulating the Adipocyte-Brain-Hepatocyte AxisP01DK088761 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI SCHERER, PHILIPP E · 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
Liver-islet and intra-islet cross talk in alpha cell hyperplasia and beta cell regenerationR01DK112826 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI HOLLAND, WILLIAM L · 2017 to 2025
$3.4M
Sphingolipid-Mediated Dysregulation of Glucose and Energy Homeostasis in the CNSR01DK108833 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI HOLLAND, WILLIAM L · 2016 to 2020
$1.8M
NIDDK NIH HHS P01 DK088761NIDDK NIH HHS R01 DK055758NIDDK NIH HHS R01 DK099110NIDDK NIH HHS R01 DK108833NIDDK NIH HHS R01 DK112826
6 · The paper itself

Abstract

Obesity-associated type 2 diabetes mellitus (T2DM) entails insulin resistance and loss of β-cell mass. Adipose tissue mitochondrial dysfunction is emerging as a key component in the etiology of T2DM. Identifying approaches to preserve mitochondrial function, adipose tissue integrity, and β-cell mass during obesity is a major challenge. Mitochondrial ferritin (FtMT) is a mitochondrial matrix protein that chelates iron. We sought to determine whether perturbation of adipocyte mitochondria influences energy metabolism during obesity. We used an adipocyte-specific doxycycline-inducible mouse model of FtMT overexpression (FtMT-Adip mice). During a dietary challenge, FtMT-Adip mice are leaner but exhibit glucose intolerance, low adiponectin levels, increased reactive oxygen species damage, and elevated GDF15 and FGF21 levels, indicating metabolically dysfunctional fat. Paradoxically, despite harboring highly dysfunctional fat, transgenic mice display massive β-cell hyperplasia, reflecting a beneficial mitochondria-induced fat-to-pancreas interorgan signaling axis. This identifies the unique and critical impact that adipocyte mitochondrial dysfunction has on increasing β-cell mass during obesity-related insulin resistance.

Indexed as

AdipocytesAdiponectinAdipose Tissue, WhiteAnimalsEnergy MetabolismFerritinsFibroblast Growth FactorsGlucose Clamp TechniqueGlucose IntoleranceGrowth Differentiation Factor 15HyperplasiaInsulin ResistanceInsulin-Secreting CellsMiceMice, TransgenicMitochondriaAdiponectinAdipoq protein, mouseFerritinsfibroblast growth factor 21Fibroblast Growth FactorsGdf15 protein, mouseGrowth Differentiation Factor 15Mitochondrial ProteinsReactive Oxygen Species

Identifiers

PMID31882562
PMCPMC7034182
OpenAlexW2998406906

What OpenQuestion holds

Textmetadata
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.