Evidence map›Paper›PMID 35802723›Full record

ArticlePloS one2022

The gene knockout of angiotensin II type 1a receptor improves high-fat diet-induced obesity in rat via promoting adipose lipolysis.

Aiyun Li, Wenjuan Shi, Jin Wang, Xuejiao Wang, Yan Zhang, Zhandong Lei, Xiang-Ying Jiao

Open access · goldAbstract read
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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 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

7 citing papers in PubMed, 10 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

7 authors at 1 institution in 1 country.

Aiyun LiKey Laboratory of Cellular Physiology (Shanxi Medical University), Ministry of Education, and The Department of Physiology, Shanxi Medical University, Taiyuan, China.
Wenjuan ShiKey Laboratory of Cellular Physiology (Shanxi Medical University), Ministry of Education, and The Department of Physiology, Shanxi Medical University, Taiyuan, China.
Jin WangKey Laboratory of Cellular Physiology (Shanxi Medical University), Ministry of Education, and The Department of Physiology, Shanxi Medical University, Taiyuan, China.
Xuejiao WangKey Laboratory of Cellular Physiology (Shanxi Medical University), Ministry of Education, and The Department of Physiology, Shanxi Medical University, Taiyuan, China.
Yan ZhangKey Laboratory of Cellular Physiology (Shanxi Medical University), Ministry of Education, and The Department of Physiology, Shanxi Medical University, Taiyuan, China.
Zhandong LeiKey Laboratory of Cellular Physiology (Shanxi Medical University), Ministry of Education, and The Department of Physiology, Shanxi Medical University, Taiyuan, China.
Xiang-Ying JiaoKey Laboratory of Cellular Physiology (Shanxi Medical University), Ministry of Education, and The Department of Physiology, Shanxi Medical University, Taiyuan, China.ORCID 0000-0003-1182-9052
Shanxi Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsThe renin-angiotensin system (RAS) is over-activated and the serum angiotensin II (Ang II) level increased in obese patients, while their correlations were incompletely understood. This study aims to explore the role of Ang II in diet-induced obesity by focusing on adipose lipid anabolism and catabolism.

methodsRat model of AT1aR gene knockout were established to investigate the special role of Ang II on adipose lipid metabolism. Wild-type (WT) and AT1aR gene knockout (AT1aR-/-) SD rats were fed with normal diet or high-fat diet for 12 weeks. Adipose morphology and adipose lipid synthesis and lipolysis were examined.

resultsAT1aR deficiency activated lipolysis-related enzymes and increased the levels of NEFAs and glycerol released from adipose tissue in high-fat diet rats, while did not affect triglycerides synthesis. Besides, AT1aR knockout promoted energy expenditure and fatty acids oxidation in adipose tissue. cAMP levels and PKA phosphorylation in the adipose tissue were significantly increased in AT1aR-/- rats fed with high-fat. Activated PKA could promote adipose lipolysis and thus improved adipose histomorphology and insulin sensitivity in high-fat diet rats.

conclusionsAT1aR deficiency alleviated adipocyte hypertrophy in high-fat diet rats by promoting adipose lipolysis probably via cAMP/PKA pathway, and thereby delayed the onset of obesity and related metabolic diseases.

Indexed as

Diet, High-FatLipolysisObesityReceptor, Angiotensin, Type 1Adipose TissueAngiotensin IIAnimalsFatty Acids, NonesterifiedGene Knockout TechniquesRatsRats, Sprague-DawleyAgtr1a protein, ratAngiotensin IIFatty Acids, NonesterifiedReceptor, Angiotensin, Type 1

Identifiers

PMID35802723
PMCPMC9269876
OpenAlexW4284968976

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.