Evidence map›Paper›PMID 29341865›Full record

ArticlePhysiological genomics2018

Evidence of genetic predisposition for metabolically healthy obesity and metabolically obese normal weight.

Lam O Huang, Ruth J F Loos, Tuomas O Kilpeläinen

Open access · bronzeAbstract read
In one paragraph

Article in Physiological genomics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

24 citing papers in PubMed, 34 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

3 authors at 2 institutions in 2 countries.

Lam O HuangNovo Nordisk Foundation Center for Basic Metabolic Research, Section for Metabolic Genetics, Faculty of Health and Medical Sciences, University of Copenhagen , Copenhagen , Denmark.
Ruth J F LoosThe Charles Bronfman Institute for Personalized Medicine, Icahn School of Medicine at Mount Sinai , New York, New York.
Tuomas O KilpeläinenNovo Nordisk Foundation Center for Basic Metabolic Research, Section for Metabolic Genetics, Faculty of Health and Medical Sciences, University of Copenhagen , Copenhagen , Denmark.ORCID 0000-0002-8349-3028
University of Copenhagen · DKChild Health and Development Institute · US

Funding

Search for obesity-associated genes with protective effects on metabolic healthR01DK107786 · NIDDK · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI LOOS, RUTH JF · 2017 to 2020
$2.3M
NIDDK NIH HHS R01 DK107786
6 · The paper itself

Abstract

Obesity has evolved into a global pandemic that constitutes a major threat to public health. The majority of obesity-related health care costs are due to cardiometabolic complications, such as insulin resistance, dyslipidemia, and hypertension, which are risk factors for Type 2 diabetes and cardiovascular disease. However, many obese individuals, often called metabolically healthy obese (MHO), seem to be protected from these cardiometabolic complications. Conversely, there is a group of individuals who suffer from cardiometabolic complications despite being of normal weight; a condition termed metabolically obese normal weight (MONW). Recent large-scale genomic studies have provided evidence that a number of genetic variants show an association with increased adiposity but a favorable cardiometabolic profile, an indicator for the genetic basis of the MHO and MONW phenotypes. Many of these loci are located in or near genes that implicate pathways involved in adipogenesis, fat distribution, insulin signaling, and insulin resistance. It has been suggested that a threshold for subcutaneous adipose tissue expandability may be at play in the manifestation of MHO and MONW, where expiry of adipose tissue storage capacity could lead to ectopic lipid accumulation in non-adipose tissues such as liver, muscle, heart, and pancreatic beta cells. Understanding the genetic aspects of the mechanisms that underpin MHO and MONW is crucial to define appropriate public health action points and to develop effective intervention measures.

Indexed as

Genetic Predisposition to DiseaseAdipose TissueAdiposityBody WeightGenetic LociGenome-Wide Association StudyHumansInsulin ResistanceObesity, Metabolically Benignadipositycardiometabolic diseasegenomicsmetabolically healthy obesitymetabolically obese normal weight

Identifiers

PMID29341865
PMCPMC6048453
OpenAlexW2777264221

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.