Evidence map›Paper›PMID 31914415›Full record

ReviewThe Journal of biological chemistry2020

Opportunities and challenges in the therapeutic activation of human energy expenditure and thermogenesis to manage obesity.

Kong Y Chen, Robert J Brychta, Zahraa Abdul Sater, Thomas M Cassimatis, Cheryl Cero, Laura A Fletcher, Nikita S Israni, James W Johnson, Hannah J Lea, Joyce D Linderman and 3 more

Open access · hybridAbstract readReview
In one paragraph

Review in The Journal of biological chemistry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed
8.6field-weighted citation impact, top 2% 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

68 citing papers in PubMed, 106 citations in OpenAlex.

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8 more citing papers are in PubMed but not listed here.

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 1 institution in 1 country.

Kong Y ChenDiabetes, Endocrinology, and Obesity Branch, Intramural Research Program, NIDDK, National Institutes of Health, Bethesda, Maryland 20892. Electronic address: kong.chen@nih.gov.
Robert J BrychtaDiabetes, Endocrinology, and Obesity Branch, Intramural Research Program, NIDDK, National Institutes of Health, Bethesda, Maryland 20892.
Zahraa Abdul SaterDiabetes, Endocrinology, and Obesity Branch, Intramural Research Program, NIDDK, National Institutes of Health, Bethesda, Maryland 20892.
Thomas M CassimatisDiabetes, Endocrinology, and Obesity Branch, Intramural Research Program, NIDDK, National Institutes of Health, Bethesda, Maryland 20892.
Cheryl CeroDiabetes, Endocrinology, and Obesity Branch, Intramural Research Program, NIDDK, National Institutes of Health, Bethesda, Maryland 20892.
Laura A FletcherDiabetes, Endocrinology, and Obesity Branch, Intramural Research Program, NIDDK, National Institutes of Health, Bethesda, Maryland 20892.
Nikita S IsraniDiabetes, Endocrinology, and Obesity Branch, Intramural Research Program, NIDDK, National Institutes of Health, Bethesda, Maryland 20892.
James W JohnsonDiabetes, Endocrinology, and Obesity Branch, Intramural Research Program, NIDDK, National Institutes of Health, Bethesda, Maryland 20892.
Hannah J LeaDiabetes, Endocrinology, and Obesity Branch, Intramural Research Program, NIDDK, National Institutes of Health, Bethesda, Maryland 20892.
Joyce D LindermanDiabetes, Endocrinology, and Obesity Branch, Intramural Research Program, NIDDK, National Institutes of Health, Bethesda, Maryland 20892.
Alana E O'MaraDiabetes, Endocrinology, and Obesity Branch, Intramural Research Program, NIDDK, National Institutes of Health, Bethesda, Maryland 20892.
Kenneth Y ZhuDiabetes, Endocrinology, and Obesity Branch, Intramural Research Program, NIDDK, National Institutes of Health, Bethesda, Maryland 20892.
Aaron M CypessDiabetes, Endocrinology, and Obesity Branch, Intramural Research Program, NIDDK, National Institutes of Health, Bethesda, Maryland 20892. Electronic address: aaron.cypess@nih.gov.
National Institutes of Health · US

Funding

The NIH Inter-Institute Training Program in Endocrinology, Diabetes & MetabolismZIEDK075100 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI MUNIYAPPA, RANGANATH · 2009 to 2025
$18.0M
Development of obesity and metabolic clinical research programsZIADK071014 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI CHEN, KONG · 2009 to 2025
$12.3M
Physiological Responses to Activation of Human Brown Adipose TissueZIADK075116 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI CYPESS, AARON · 2015 to 2025
$6.1M
The Molecular, Cellular, and Genetic characterization of Human Adipose Tissue and its Role in MetabolismZIADK075112 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI CYPESS, AARON · 2015 to 2025
$2.8M
Role of BK-Beta 1 in flow-dependent K+ secretion in the CNTR01DK071014 · NIDDK · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI SANSOM, STEVEN · 2007 to 2015
$2.7M
Mechanisms Underlying Adipose Tissue ThermogenesisZIADK075115 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI CYPESS, AARON · 2015 to 2025
$1.8M
Genetic Environmental Relationship Between Bone, Obesity and Leptin in MiceR01DK075112 · NIDDK · WASHINGTON UNIVERSITY · PI CHEVERUD, JAMES M · 2006 to 2010
$1.5M
HTS for Detection of deltaF508 CFTR at the Cell SurfaceR01DK071013 · NIDDK · UNIV OF NORTH CAROLINA CHAPEL HILL · PI RIORDAN, JOHN R · 2005 to 2007
$747k
NIDDK NIH HHS R01 DK071013NIDDK NIH HHS R01 DK071014NIDDK NIH HHS R01 DK075112
6 · The paper itself

Abstract

The current obesity pandemic results from a physiological imbalance in which energy intake chronically exceeds energy expenditure (EE), and prevention and treatment strategies remain generally ineffective. Approaches designed to increase EE have been informed by decades of experiments in rodent models designed to stimulate adaptive thermogenesis, a long-term increase in metabolism, primarily induced by chronic cold exposure. At the cellular level, thermogenesis is achieved through increased rates of futile cycling, which are observed in several systems, most notably the regulated uncoupling of oxidative phosphorylation from ATP generation by uncoupling protein 1, a tissue-specific protein present in mitochondria of brown adipose tissue (BAT). Physiological activation of BAT and other organ thermogenesis occurs through β-adrenergic receptors (AR), and considerable effort over the past 5 decades has been directed toward developing AR agonists capable of safely achieving a net negative energy balance while avoiding unwanted cardiovascular side effects. Recent discoveries of other BAT futile cycles based on creatine and succinate have provided additional targets. Complicating the current and developing pharmacological-, cold-, and exercise-based methods to increase EE is the emerging evidence for strong physiological drives toward restoring lost weight over the long term. Future studies will need to address technical challenges such as how to accurately measure individual tissue thermogenesis in humans; how to safely activate BAT and other organ thermogenesis; and how to sustain a negative energy balance over many years of treatment.

Indexed as

Energy MetabolismThermogenesisAdipose Tissue, BrownBody WeightDisease ManagementEnergy IntakeHumansMitochondriaObesityOxidative PhosphorylationReceptors, Adrenergic, betaReceptors, Adrenergic, betaadipocyteadrenergic receptorenergy expenditureenergy metabolismimagingmetabolic disorderobesitypharmacologysympathomimeticthermogenesis

Identifiers

PMID31914415
PMCPMC7029124
OpenAlexW2996797552

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.