Evidence map›Paper›PMID 36195912›Full record

ArticleJournal of translational medicine2022

CTRP1 prevents high fat diet-induced obesity and improves glucose homeostasis in obese and STZ-induced diabetic mice.

Mingzhi Ren, Jianfei Pan, Xueying Yu, Kaile Chang, Xiaopeng Yuan, Chunbo Zhang

Open access · goldAbstract read
In one paragraph

Article in Journal of translational medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 16% 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

14 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 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

6 authors at 1 institution in 1 country.

Mingzhi Ren *School of Pharmacy, Nanchang University, Nanchang, 330031, Jiangxi, China.
Jianfei Pan *School of Pharmacy, Nanchang University, Nanchang, 330031, Jiangxi, China.
Xueying Yu *School of Pharmacy, Nanchang University, Nanchang, 330031, Jiangxi, China.
Kaile ChangSchool of Pharmacy, Nanchang University, Nanchang, 330031, Jiangxi, China.
Xiaopeng YuanSchool of Pharmacy, Nanchang University, Nanchang, 330031, Jiangxi, China.
Chunbo ZhangSchool of Pharmacy, Nanchang University, Nanchang, 330031, Jiangxi, China. cbzhang@ncu.edu.cn.ORCID 0000-0001-9618-9415
Nanchang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundC1q/tumor necrosis factor-related protein 1 (CTRP1) is an adipokine secreted by adipose tissue, related to chondrocyte proliferation, inflammation, and glucose homeostasis. However, the therapeutic effects on metabolic disorders and the underlying mechanism were unclear. Here, we investigated the functions and mechanisms of CTRP1 in treating obesity and diabetes.

methodsThe plasmid containing human CTRP1 was delivered to mice by hydrodynamic injection, which sustained expression of CTRP1 in the liver and high protein level in the blood. High-fat diet (HFD) fed mice and STZ-induced diabetes model were used to study the effects of CTRP1 on obesity, glucose homeostasis, insulin resistance, and hepatic lipid accumulation. The lipid accumulation in liver and adipose tissue, glucose tolerance, insulin sensitivity, food intake, and energy expenditure were detected by H&E staining, Oil-Red O staining, glucose tolerance test, insulin tolerance test, and metabolic cage, respectively. The metabolic-related genes and signal pathways were determined using qPCR and western blotting.

resultsWith high blood circulation, CTRP1 prevented obesity, hyperglycemia, insulin resistance, and fatty liver in HFD-fed mice. CTRP1 also improved glucose metabolism and insulin resistance in obese and STZ-induced diabetic mice. The metabolic cage study revealed that CTRP1 reduced food intake and enhanced energy expenditure. The mechanistic study demonstrated that CTRP1 upregulated the protein level of leptin in blood, thermogenic gene expression in brown adipose tissue, and the gene expression responsible for lipolysis and glycolysis in white adipose tissue (WAT). CTRP1 also downregulated the expression of inflammatory genes in WAT. Overexpression of CTRP1 activated AMPK and PI3K/Akt signaling pathways and inhibited ERK signaling pathway.

conclusionThese results demonstrate that CTRP1 could improve glucose homeostasis and prevent HFD-induced obesity and fatty liver through upregulating the energy expenditure and reducing food intake, suggesting CTRP1 may serve as a promising target for treating metabolic diseases.

Indexed as

Diabetes Mellitus, ExperimentalFatty LiverInsulin ResistanceInsulinsAdipokinesAdipose Tissue, BrownAMP-Activated Protein KinasesAnimalsComplement C1qDiet, High-FatGlucoseHomeostasisHumansLeptinLipidsMiceAdipokinesAMP-Activated Protein KinasesC1QTNF1 protein, humanComplement C1qGlucoseInsulinsLeptinLipidsPhosphatidylinositol 3-KinasesProteinsProto-Oncogene Proteins c-aktTumor Necrosis FactorsCTRP1Fatty liverGlucose homeostasisHydrodynamic gene delivery

Identifiers

PMID36195912
PMCPMC9533627
OpenAlexW4301185400

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.