Evidence map›Paper›PMID 38766434›Full record

ArticleWorld journal of diabetes2024

Estrogen restores disordered lipid metabolism in visceral fat of prediabetic mice.

Su-Huan Liu, Zhao-Shui Shangguan, Paiziliya Maitiaximu, Zhi-Peng Li, Xin-Xin Chen, Can-Dong Li

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Article in World journal of diabetes, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

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5citing papers in PubMed
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1 · What the graph read from it

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3 · Its place in the literature

Who cites it

5 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

6 authors.

Su-Huan LiuResearch Base of Chinese Medicine Syndrome, Fujian University of Traditional Chinese Medicine, Fuzhou 350122, Fujian Province, China.
Zhao-Shui ShangguanResearch Center for Translational Medicine, The First Affiliated Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen 361003, Fujian Province, China.
Paiziliya MaitiaximuResearch Center for Translational Medicine, The First Affiliated Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen 361003, Fujian Province, China.
Zhi-Peng LiResearch Center for Translational Medicine, The First Affiliated Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen 361003, Fujian Province, China.
Xin-Xin ChenResearch Center for Translational Medicine, The First Affiliated Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen 361003, Fujian Province, China.
Can-Dong LiResearch Base of Chinese Medicine Syndrome, Fujian University of Traditional Chinese Medicine, Fuzhou 350122, Fujian Province, China. fjzylcd@126.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundVisceral obesity is increasingly prevalent among adolescents and young adults and is commonly recognized as a risk factor for type 2 diabetes. Estrogen [17β-estradiol (E2)] is known to offer protection against obesity

aimTo investigate the impact of E2 on the gene expression profile within VAT of a mouse model of prediabetes.

methodsMetabolic parameters were collected, encompassing body weight, weights of visceral and subcutaneous adipose tissues (VAT and SAT), random blood glucose levels, glucose tolerance, insulin tolerance, and overall body composition. The gene expression profiles of VAT were quantified utilizing the Whole Mouse Genome Oligo Microarray and subsequently analyzed through Agilent Feature Extraction software. Functional and pathway analyses were conducted employing Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analyses, respectively.

resultsFeeding a high-fat diet (HFD) moderately increased the weights of both VAT and SAT, but this increase was mitigated by the protective effect of endogenous E2. Conversely, ovariectomy (OVX) led to a significant increase in VAT weight and the VAT/SAT weight ratio, and this increase was also reversed with E2 treatment. Notably, OVX diminished the expression of genes involved in lipid metabolism compared to HFD feeding alone, signaling a widespread reduction in lipid metabolic activity, which was completely counteracted by E2 administration. This study provides a comprehensive insight into E2's local and direct protective effects against visceral adiposity in VAT at the gene level.

conclusionIn conclusion, the present study demonstrated that the HFD-induced over-nutritional challenge disrupted the gene expression profile of visceral fat, leading to a universally decreased lipid metabolic status in E2 deficient mice. E2 treatment effectively reversed this condition, shedding light on the mechanistic role and therapeutic potential of E2 in combating visceral obesity.

Indexed as

Energy metabolismEstrogenObesity, Visceral adiposityType 2 diabetes

Identifiers

PMID38766434
PMCPMC11099359

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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.