Evidence map›Paper›PMID 33791724›Full record

ArticlemedRxiv : the preprint server for health sciences2021

Hyperglycemia in Acute COVID-19 is Characterized by Adipose Tissue Dysfunction and Insulin Resistance.

Moritz Reiterer, Mangala Rajan, Nicolás Gómez-Banoy, Jennifer D Lau, Luis G Gomez-Escobar, Ankit Gilani, Sergio Alvarez-Mulett, Evan T Sholle, Vasuretha Chandar, Yaron Bram and 11 more

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

Article in medRxiv : the preprint server for health sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed, 19 citations in OpenAlex.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

21 authors at 2 institutions in 1 country.

Moritz ReitererWeill Center for Metabolic Health, Cardiovascular Research Institute, Division of Cardiology, Department of Medicine, Weill Cornell Medicine, New York, NY, USA.
Mangala RajanDepartment of Medicine, Weill Cornell Medicine, New York, NY, USA.
Nicolás Gómez-BanoyWeill Center for Metabolic Health, Cardiovascular Research Institute, Division of Cardiology, Department of Medicine, Weill Cornell Medicine, New York, NY, USA.
Jennifer D LauDepartment of Medicine, Weill Cornell Medicine, New York, NY, USA.
Luis G Gomez-EscobarDivision of Pulmonary and Critical Care Medicine, Department of Medicine, Weill Cornell Medicine, New York, NY, USA.
Ankit GilaniWeill Center for Metabolic Health, Cardiovascular Research Institute, Division of Cardiology, Department of Medicine, Weill Cornell Medicine, New York, NY, USA.
Sergio Alvarez-MulettDivision of Pulmonary and Critical Care Medicine, Department of Medicine, Weill Cornell Medicine, New York, NY, USA.
Evan T SholleInformation Technologies & Services Department, Weill Cornell Medicine, New York, NY, USA.
Vasuretha ChandarDivision of Gastroenterology and Hepatology, Department of Medicine, Weill Cornell Medicine, New York, NY, USA.
Yaron BramDivision of Gastroenterology and Hepatology, Department of Medicine, Weill Cornell Medicine, New York, NY, USA.
Katherine HoffmanDivision of Pulmonary and Critical Care Medicine, Department of Medicine, Weill Cornell Medicine, New York, NY, USA.
Alfonso Rubio-NavarroWeill Center for Metabolic Health, Cardiovascular Research Institute, Division of Cardiology, Department of Medicine, Weill Cornell Medicine, New York, NY, USA.
Skyler UhlDepartment of Microbiology, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Alpana P ShuklaWeill Center for Metabolic Health, Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, Weill Cornell Medicine, New York, NY, USA.
Parag GoyalDepartment of Medicine, Weill Cornell Medicine, New York, NY, USA.
Benjamin R tenOeverDepartment of Microbiology, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Laura C AlonsoWeill Center for Metabolic Health, Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, Weill Cornell Medicine, New York, NY, USA.
Robert E SchwartzDivision of Gastroenterology and Hepatology, Departments of Medicine and Physiology, Biophysics and Systems Biology, Weill Cornell Medicine, New York, NY, USA.
Edward J SchenckDivision of Pulmonary and Critical Care Medicine, Department of Medicine, Weill Cornell Medicine, New York, NY, USA.
Monika M SaffordDepartment of Medicine, Weill Cornell Medicine, New York, NY, USA.
James C LoWeill Center for Metabolic Health, Cardiovascular Research Institute, Division of Cardiology, Department of Medicine, Weill Cornell Medicine, New York, NY, USA.
Cornell University · USIcahn School of Medicine at Mount Sinai · US

Funding

Disparities in COVID Disease Severity and Outcomes in New York CityUL1TR002384 · NCATS · WEILL MEDICAL COLL OF CORNELL UNIV · PI JULIANNE L IMPERATO-MCGINLEY · 2017 to 2026
$86.2M
Genetic Viral and Host Adaptations to Breach Species Barriers of HCVR01AI107301 · NIAID · PRINCETON UNIVERSITY · PI Thomas Pietschmann, Alexander Ploss · 2013 to 2026
$6.0M
Dusp26 regulation of beta cell homeostasisR01DK121140 · NIDDK · WEILL MEDICAL COLL OF CORNELL UNIV · PI James C Lo · 2020 to 2026
$2.7M
Optimization of the engineered 3D hepatic microenvironment enhances pluripotent stem cell derived hepatocyteR01DK121072 · NIDDK · WEILL MEDICAL COLL OF CORNELL UNIV · PI SCHWARTZ, ROBERT E · 2020 to 2024
$2.6M
An Obesity-Induced Kinase that Regulates Adipose Homeostasis and Metabolic DiseasesR01DK121844 · NIDDK · WEILL MEDICAL COLL OF CORNELL UNIV · PI LO, JAMES C · 2019 to 2023
$2.1M
Modeling Hepatoblastoma using pluripotent stem cell derived hepatocyte-like cellsR01CA234614 · NCI · WEILL MEDICAL COLL OF CORNELL UNIV · PI SCHWARTZ, ROBERT E · 2019 to 2023
$1.9M
NCATS NIH HHS UL1 TR002384NCI NIH HHS R01 CA234614NIAID NIH HHS R01 AI107301NIDDK NIH HHS R01 DK121072NIDDK NIH HHS R01 DK121140NIDDK NIH HHS R01 DK121844
6 · The paper itself

Abstract

COVID-19 has proven to be a metabolic disease resulting in adverse outcomes in individuals with diabetes or obesity. Patients infected with SARS-CoV-2 and hyperglycemia suffer from longer hospital stays, higher risk of developing acute respiratory distress syndrome (ARDS), and increased mortality compared to those who do not develop hyperglycemia. Nevertheless, the pathophysiological mechanism(s) of hyperglycemia in COVID-19 remains poorly characterized. Here we show that insulin resistance rather than pancreatic beta cell failure is the prevalent cause of hyperglycemia in COVID-19 patients with ARDS, independent of glucocorticoid treatment. A screen of protein hormones that regulate glucose homeostasis reveals that the insulin sensitizing adipokine adiponectin is reduced in hyperglycemic COVID-19 patients. Hamsters infected with SARS-CoV-2 also have diminished expression of adiponectin. Together these data suggest that adipose tissue dysfunction may be a driver of insulin resistance and adverse outcomes in acute COVID-19.

Identifiers

PMID33791724
PMCPMC8010756
OpenAlexW3137415266

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.