Evidence map›Paper›PMID 35436297›Full record

ArticlePloS one2022

Serum Amyloid A is not obligatory for high-fat, high-sucrose, cholesterol-fed diet-induced obesity and its metabolic and inflammatory complications.

Ailing Ji, Andrea C Trumbauer, Victoria P Noffsinger, Hayce Jeon, Avery C Patrick, Frederick C De Beer, Nancy R Webb, Lisa R Tannock, Preetha Shridas

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
3.1field-weighted citation impact, top 8% 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

12 citing papers in PubMed, 1 synthesis or guideline pooled it, 14 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Serum amyloid A in HFpEF and cardiometabolic diseases.Basic research in cardiology · 2026
    Review
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  5. 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

9 authors at 1 institution in 1 country.

Ailing JiDepartment of Internal Medicine, University of Kentucky, Lexington, Kentucky, United States of America.
Andrea C TrumbauerSaha Cardiovascular Research Center, University of Kentucky, Lexington, Kentucky, United States of America.
Victoria P NoffsingerDepartment of Internal Medicine, University of Kentucky, Lexington, Kentucky, United States of America.
Hayce JeonPharmacology and Nutritional Sciences, University of Kentucky, Lexington, Kentucky, United States of America.
Avery C PatrickPharmacology and Nutritional Sciences, University of Kentucky, Lexington, Kentucky, United States of America.ORCID 0000-0002-1094-1432
Frederick C De BeerDepartment of Internal Medicine, University of Kentucky, Lexington, Kentucky, United States of America.
Nancy R WebbPharmacology and Nutritional Sciences, University of Kentucky, Lexington, Kentucky, United States of America.
Lisa R TannockDepartment of Internal Medicine, University of Kentucky, Lexington, Kentucky, United States of America.
Preetha ShridasDepartment of Internal Medicine, University of Kentucky, Lexington, Kentucky, United States of America.ORCID 0000-0002-2532-4007
University of Kentucky · US

Funding

WU P&FP30DK020579 · NIDDK · WASHINGTON UNIVERSITY · PI FUMIHIKO URANO · 2013 to 2026
$27.1M
Pilot Projects ProgramP30GM127211 · NIGMS · UNIVERSITY OF KENTUCKY · PI CASSIS, LISA A · 2018 to 2022
$5.7M
Serum Amyloid A, Inflammasome Activation, and Abdominal Aortic AneurysmsR01HL134731 · NHLBI · UNIVERSITY OF KENTUCKY · PI DE BEER, FREDERICK C., WEBB, NANCY R · 2017 to 2020
$2.1M
Mechanisms regulating the atherogenic activities of serum amyloid AR01HL147381 · NHLBI · UNIVERSITY OF KENTUCKY · PI SHRIDAS, PREETHA · 2020 to 2023
$2.0M
Mechanisms linking obesity and abdominal aortic aneurysmI01BX004275 · VA · VA MEDICAL CENTER - LEXINGTON, KY · PI KAROUNOS, DENNIS G · 2019 to 2022
–
BLRD VA I01 BX004275NHLBI NIH HHS R01 HL134731NHLBI NIH HHS R01 HL147381NIDDK NIH HHS P30 DK020579NIGMS NIH HHS P30 GM127211
6 · The paper itself

Abstract

Several studies in the past have reported positive correlations between circulating Serum amyloid A (SAA) levels and obesity. However, based on limited number of studies involving appropriate mouse models, the role of SAA in the development of obesity and obesity-related metabolic consequences has not been established. Accordingly, herein, we have examined the role of SAA in the development of obesity and its associated metabolic complications in vivo using mice deficient for all three inducible forms of SAA: SAA1.1, SAA2.1 and SAA3 (TKO). Male and female mice were rendered obese by feeding a high fat, high sucrose diet with added cholesterol (HFHSC) and control mice were fed rodent chow diet. Here, we show that the deletion of SAA does not affect diet-induced obesity, hepatic lipid metabolism or adipose tissue inflammation. However, there was a modest effect on glucose metabolism. The results of this study confirm previous findings that SAA levels are elevated in adipose tissues as well as in the circulation in diet-induced obese mice. However, the three acute phase SAAs do not play a causative role in the development of obesity or obesity-associated adipose tissue inflammation and dyslipidemia.

Indexed as

Serum Amyloid A ProteinSucroseAnimalsCholesterolDiet, High-FatFemaleInflammationMaleMiceMice, Inbred C57BLObesityCholesterolSerum Amyloid A ProteinSucrose

Identifiers

PMID35436297
PMCPMC9015120
OpenAlexW4224253757

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.