Evidence map›Paper›PMID 36219316›Full record

ArticleJournal of endocrinological investigation2023

Calorie restriction ameliorates hyperglycemia, modulates the disordered gut microbiota, and mitigates metabolic endotoxemia and inflammation in type 2 diabetic rats.

L Zhang, T Zhang, J Sun, Y Huang, T Liu, Z Ye, J Hu, G Zhang, H Chen, Z Ye and 2 more

Abstract read
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In one paragraph

Article in Journal of endocrinological investigation, 2023. 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
3.5field-weighted citation impact, top 6% 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, 43 citations in OpenAlex.

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  14. Frontiers in immunology · 2024
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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

12 authors at 2 institutions in 1 country.

L Zhang *The Seventh Affiliated Hospital, Sun Yat-Sen University, Shenzhen, 518107, China.
T Zhang *The Seventh Affiliated Hospital, Sun Yat-Sen University, Shenzhen, 518107, China.
J SunPeking University Shenzhen Hospital, Shenzhen, 518035, China.
Y HuangThe First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, 510080, China.
T LiuThe Seventh Affiliated Hospital, Sun Yat-Sen University, Shenzhen, 518107, China.
Z YeThe Seventh Affiliated Hospital, Sun Yat-Sen University, Shenzhen, 518107, China.
J HuThe Seventh Affiliated Hospital, Sun Yat-Sen University, Shenzhen, 518107, China.
G ZhangThe Seventh Affiliated Hospital, Sun Yat-Sen University, Shenzhen, 518107, China.
H ChenThe Seventh Affiliated Hospital, Sun Yat-Sen University, Shenzhen, 518107, China.
Z YeThe Seventh Affiliated Hospital, Sun Yat-Sen University, Shenzhen, 518107, China.
Y HeSchool of Public Health, Sun Yat-Sen University, Guangzhou, 510080, China. heyun_jane@163.com.
J QinThe Seventh Affiliated Hospital, Sun Yat-Sen University, Shenzhen, 518107, China. qjian@mail.sysu.edu.cn.ORCID http://orcid.org/0000-0001-7113-555X
Sun Yat-sen University · CNPeking University Shenzhen Hospital · CN

Funding

National Natural Science Foundation of China 81874498Science and Technology Program of Guangzhou 201903010044Shenzhen Healthcare Research Project SZLY2018002Traditional Chinese Medicine Research Project of Guangming District GM2019020022
6 · The paper itself

Abstract

purposeThe effects of calorie restriction (CR) on gut microbiota and the mechanism of CR ameliorating hyperglycemia in streptozotocin (STZ)-induced T2DM model rats were explored.

methodsHigh-fat diet and STZ injection were applied to induce T2DM model rats. Rats were divided into the following three groups: the control-diet ad libitum group, the T2DM model group fed with ad libitum diet, and the T2DM group fed with 30% restriction diet. 16S rRNA sequencing was used to determine the bacterial communities. Lipopolysaccharide (LPS)-binding protein (LBP), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) were measured.

resultsGlucose tolerance and insulin sensitivity were improved by CR, as well as the levels of fasting and random plasma glucose. Besides, CR not only modulated the overall structure of gut microbiota but also had selective enrichment in anti-inflammatory bacteria such as Lachnospiraceae_NK4A136_group, Ruminococcaceae_9, Allobaculum, Alistipes, and Oscillibacter, and decreased pro-inflammatory pathogenic bacteria such as Bacteroides, Lachnoclostridium, and Bifidobacterium. Tax4Fun indicated that CR could regulate related functional pathways such as lipopolysaccharide biosynthesis, and the plasma levels of LBP, IL-6, and TNF-α were markedly reduced by CR, suggesting the mechanism of CR ameliorating hyperglycemia may associate with the modulation of disordered gut microbiota and the reduction of metabolic endotoxemia and inflammation.

conclusionCR could ameliorate hyperglycemia, the mechanism of which may associate with the alteration of the overall structure of gut microbiota, restoration of disordered microbiota function, and the downregulation of metabolic endotoxemia and inflammation in diabetic rats.

Indexed as

Diabetes Mellitus, ExperimentalDiabetes Mellitus, Type 2EndotoxemiaGastrointestinal MicrobiomeHyperglycemiaAnimalsBacteriaCaloric RestrictionDiet, High-FatInflammationInterleukin-6LipopolysaccharidesObesityRatsRNA, Ribosomal, 16STumor Necrosis Factor-alphaInterleukin-6LipopolysaccharidesRNA, Ribosomal, 16STumor Necrosis Factor-alphaCalorie restrictionGut microbiotaMetabolic endotoxemiaType 2 diabetes mellitus

Identifiers

PMID36219316
OpenAlexW4304194195

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.