Evidence map›Paper›PMID 34303021›Full record

ArticleMolecular metabolism2021

Adipocyte CAMK2 deficiency improves obesity-associated glucose intolerance.

Wen Dai, Mayank Choubey, Sonal Patel, Harold A Singer, Lale Ozcan

Open access · goldAbstract read
In one paragraph

Article in Molecular metabolism, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
4.3field-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

31 citing papers in PubMed, 51 citations in OpenAlex.

  1. Review
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  6. CAMKIIδ Reinforces Lipid Metabolism and Promotes the Development of B Cell Lymphoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  7. Ethyl acetate extract ofFrontiers in pharmacology · 2025
    Article
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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

5 authors at 3 institutions in 2 countries.

Wen DaiDepartment of Medicine, Columbia University Irving Medical Center, New York, NY, USA; Department of Cardiology, The Second Xiangya Hospital, Central South University, Changsha, China.
Mayank ChoubeyDepartment of Medicine, Columbia University Irving Medical Center, New York, NY, USA.
Sonal PatelDepartment of Medicine, Columbia University Irving Medical Center, New York, NY, USA.
Harold A SingerDepartment of Molecular and Cellular Physiology, Albany Medical College, Albany, NY, USA.
Lale OzcanDepartment of Medicine, Columbia University Irving Medical Center, New York, NY, USA. Electronic address: lo2192@cumc.columbia.edu.
Columbia University Irving Medical Center · USAlbany Medical Center Hospital · USCentral South University · CN

Funding

CALCIUM/CALMODULIN ACTIVATED KINIASES IN SMOOTH MUSCLER01HL049426 · NHLBI · WEIS CENTER FOR RESEARCH-GEISINGER CLINC · PI SINGER, HAROLD A · 1994 to 2019
$6.2M
Role of Dach1 in Obesity-Induced Hepatic Insulin ResistanceR01DK106045 · NIDDK · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI OZCAN, LALE · 2016 to 2020
$1.8M
Hepatic Rap1 in glucose homeostasisR01DK124457 · NIDDK · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI OZCAN, LALE · 2020 to 2022
$1.4M
Calcium/Calmodulin Activated Kinases in Smooth MuscleR56HL049426 · NHLBI · ALBANY MEDICAL COLLEGE · PI SINGER, HAROLD A · 2008 to 2022
$975k
NHLBI NIH HHS R01 HL049426NHLBI NIH HHS R56 HL049426NIDDK NIH HHS R01 DK106045NIDDK NIH HHS R01 DK124457
6 · The paper itself

Abstract

objectiveObesity-related adipose tissue dysfunction has been linked to the development of insulin resistance, type 2 diabetes, and cardiovascular disease. Impaired calcium homeostasis is associated with altered adipose tissue metabolism; however, the molecular mechanisms that link disrupted calcium signaling to metabolic regulation are largely unknown. Here, we investigated the contribution of a calcium-sensing enzyme, calcium/calmodulin-dependent protein kinase II (CAMK2), to adipocyte function, obesity-associated insulin resistance, and glucose intolerance.

methodsTo determine the impact of adipocyte CAMK2 deficiency on metabolic regulation, we generated a conditional knockout mouse model and acutely deleted CAMK2 in mature adipocytes. We further used in vitro differentiated adipocytes to dissect the mechanisms by which CAMK2 regulates adipocyte function.

resultsCAMK2 activity was increased in obese adipose tissue, and depletion of adipocyte CAMK2 in adult mice improved glucose intolerance and insulin resistance without an effect on body weight. Mechanistically, we found that activation of CAMK2 disrupted adipocyte insulin signaling and lowered the amount of insulin receptor. Further, our results revealed that CAMK2 contributed to adipocyte lipolysis, tumor necrosis factor alpha (TNFα)-induced inflammation, and insulin resistance.

conclusionsThese results identify a new link between adipocyte CAMK2 activity, metabolic regulation, and whole-body glucose homeostasis.

Indexed as

AdipocytesAnimalsCalcium-Calmodulin-Dependent Protein Kinase Type 2Glucose IntoleranceMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicObesityCalcium-Calmodulin-Dependent Protein Kinase Type 2Camk2d protein, mouseCamk2g protein, mouseAdipocyte inflammationAdipose tissueCAMK2Glucose intoleranceInsulin resistanceInsulin signalingLipolysisObesity

Identifiers

PMID34303021
PMCPMC8365526
OpenAlexW3186830358

What Socratic 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 Socratic graph.