Evidence map›Paper›PMID 25695886›Full record

ArticleThe Journal of clinical endocrinology and metabolism2015

Elevated serum advanced glycation endproducts in obese indicate risk for the metabolic syndrome: a link between healthy and unhealthy obesity?

Jaime Uribarri, Weijing Cai, Mark Woodward, Elizabeth Tripp, Laurie Goldberg, Renata Pyzik, Kalle Yee, Laurie Tansman, Xue Chen, Venkatesh Mani and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical endocrinology and metabolism, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
83citing papers in PubMed, 5 pooled it
9.7field-weighted citation impact, top 1% 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

83 citing papers in PubMed, 5 syntheses or guidelines pooled it, 141 citations in OpenAlex.

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  13. Role of ChREBP-PPARα-FGF21 Axis in Metabolic Dysfunction of MASLD.International journal of molecular sciences · 2025
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23 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

12 authors at 2 institutions in 3 countries.

Jaime UribarriDepartment of Geriatrics, Division of Experimental Diabetes (W.C., E.T., L.G., R.P., K.Y., L.T., X.C., H.V.), Department of Medicine, Division of Nephrology (J.U., H.V.), and Translational and Molecular Imaging Institute (V.M., Z.A.F.), The Icahn School of Medicine at Mt Sinai, New York, New York 10029; and George Institute for Global Health (M.W.), University of Oxford, Oxford OX1 3QX, United Kingdom, and University of Sydney, Sydney 2006, Australia.
Weijing Cai
Mark Woodward
Elizabeth Tripp
Laurie Goldberg
Renata Pyzik
Kalle Yee
Laurie Tansman
Xue Chen
Venkatesh Mani
Zahi A Fayad
Helen Vlassara
Imaging Center · USGeorge Institute for Global Health · GB

Funding

ZIPRASIDONE (GEODON) AUGMENTATION IN SEROTONIN REUPTAKE INHIBITOR-RESISTANT OBM01RR000071 · NCRR · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI NEWCORN, JEFFREY H · 1985 to 2009
$41.5M
Effects of Glycoxidative Stress on Human AgingR01DK091231 · NIDDK · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI HE, JOHN CIJIANG · 2010 to 2014
$3.1M
NCRR NIH HHS M01 RR000071NCRR NIH HHS MO1-RR-00071NIDDK NIH HHS DK091231NIDDK NIH HHS R01 DK091231
6 · The paper itself

Abstract

contextAlthough obesity can predispose to the metabolic syndrome (MS), diabetes, and cardiovascular disease, not all obese subjects develop MS, hence the need for new indicators of risk for this syndrome. Advanced glycation end products (AGEs) correlate with factors involved in the MS, including inflammation and insulin resistance (IR). Because AGEs can be derived from food and are modifiable, it is important to determine whether they are a risk factor for MS.

objectiveThe objective of this study was to assess the association of endogenous and exogenous AGEs with MS criteria.

designThe following data were collected in a cross-sectional study of subjects with and without the MS: serum AGEs (sAGEs) and mononuclear cell AGEs, metabolites, pro- and antiinflammatory markers, body fat mass measures, including abdominal magnetic resonance imaging, and caloric and dietary AGE (dAGE) consumption.

settingThe study was conducted in the general community.

participantsParticipants included 130 MS and 139 non-MS subjects of both sexes, older than 50 years.

resultssAGEs ((ϵ)N-carboxymethyllysine, methylglyoxal) were markedly elevated in obese persons with more than one other MS criteria but not in obese without MS criteria. sAGEs directly correlated with markers of IR (HOMA) and inflammation (leptin, TNFα, RAGE) and inversely with innate defenses (SIRT1, AGE receptor 1 [AGER1], glyoxalase-I, adiponectin). sAGEs correlated with dAGEs but not with calories, nutrient consumption, or fat mass measures. Consumption of dAGE, but not of calories, was markedly higher in MS than in non-MS.

conclusionHigh sAGEs, a modifiable risk factor for IR, may indicate risk for the MS, type 2 diabetes, and cardiovascular disease. High dietary AGE consumption and serum AGE levels may link healthy obesity to at-risk obesity.

Indexed as

AgedCross-Sectional StudiesFemaleGlycation End Products, AdvancedHumansInsulin ResistanceMaleMetabolic SyndromeMiddle AgedObesityRisk FactorsGlycation End Products, Advanced

Identifiers

PMID25695886
PMCPMC4422896
OpenAlexW2098765624

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.