Evidence map›Paper›PMID 38936893›Full record

ArticleIn vivo (Athens, Greece)

Depression Exacerbates Hepatic Steatosis in C57BL/6J Mice by Activating the Hypothalamic-Pituitary-Adrenal Axis.

Mingli Su, Zheng Yan, Ying Wang, Jiacheng Cai, Jia Dong, Jia Luo, Dahua Chen, Aiming Liu, Hua Ye

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in In vivo (Athens, Greece). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
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

4 citing papers in PubMed.

  1. 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.

Mingli SuDepartment of Gastroenterology, the Affiliated Lihuili Hospital, Ningbo University, Ningbo, P.R. China.
Zheng YanZhejiang Key Laboratory of Pathophysiology, Department of Physiology and Pharmacology, Health Science Center, Ningbo University, Ningbo, P.R. China.
Ying WangZhejiang Key Laboratory of Pathophysiology, Department of Physiology and Pharmacology, Health Science Center, Ningbo University, Ningbo, P.R. China.
Jiacheng CaiZhejiang Key Laboratory of Pathophysiology, Department of Physiology and Pharmacology, Health Science Center, Ningbo University, Ningbo, P.R. China.
Jia DongZhejiang Key Laboratory of Pathophysiology, Department of Physiology and Pharmacology, Health Science Center, Ningbo University, Ningbo, P.R. China.
Jia LuoZhejiang Key Laboratory of Pathophysiology, Department of Physiology and Pharmacology, Health Science Center, Ningbo University, Ningbo, P.R. China.
Dahua ChenDepartment of Gastroenterology, the Affiliated Lihuili Hospital, Ningbo University, Ningbo, P.R. China.
Aiming LiuZhejiang Key Laboratory of Pathophysiology, Department of Physiology and Pharmacology, Health Science Center, Ningbo University, Ningbo, P.R. China liuaiming@nbu.edu.cn.
Hua YeDepartment of Gastroenterology, the Affiliated Lihuili Hospital, Ningbo University, Ningbo, P.R. China; yh-med@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND/

aimDepression is associated with metabolic disorders, including non-alcoholic fatty liver disease (NAFLD). However, the mechanisms underlying the interaction between them are still poorly known. MATERIALS AND

methodsIn this study, mice on a choline deficiency, L-amino acid-defined, high-fat diet (CDAHFD) developing steatosis were challenged with chronic restraint stress (CRS), a protocol widely used to induce depression. The development of depression and steatosis was evaluated using histopathology analysis, ELISA, q-PCR and Western Blot.

resultsThe contribution of the activated HPA axis to hepatic steatosis progress was fully established, which was validated using a hepatocyte model. Histopathological and biochemical analysis indicated that steatosis was exacerbated by CRS challenge, and behavioral tests indicated that the mice developed depression. Among the screened endocrinal pathways, the hypothalamic-pituitary-adrenal (HPA) axis was significantly activated and the synergistic effect of CDAHFD and CRS in activating the HPA axis was observed. In the hypothalamus, expression of corticotropin-releasing hormone (CRH) was increased by 86% and the protein levels of hypothalamic CRH were upregulated by 25% to 33% by CRS treatment. Plasma CRH levels were elevated by 45-56% and plasma adrenocorticotropic hormone (ACTH) levels were elevated by 29-58% by CRS treatment. In the liver, target genes of the HPA axis were activated, accompanied by disruption of the lipid metabolism and progression of steatohepatitis. The lipid metabolism in the Hepa1-6 cell line treated with endogenous corticosterone (CORT) was in accordance with the aforementioned in vivo responses.

conclusionDepression aggravated hepatic steatosis in CDAHFD-fed mice by activating the HPA axis. The risk of NAFLD development should be fully considered in depressive patients and improvement of psychotic disorders could be an etiological treatment strategy for them.

Indexed as

DepressionDisease Models, AnimalHypothalamo-Hypophyseal SystemNon-alcoholic Fatty Liver DiseasePituitary-Adrenal SystemAdrenocorticotropic HormoneAnimalsCorticosteroneCorticotropin-Releasing HormoneDiet, High-FatFatty LiverLiverMaleMiceMice, Inbred C57BLAdrenocorticotropic HormoneCorticosteroneCorticotropin-Releasing HormoneCDAHFDCRSDepressionHPA axissteatosis

Identifiers

PMID38936893
PMCPMC11215574

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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.