Evidence map›Paper›PMID 35834165›Full record

ArticleJournal of endocrinological investigation2022

Stachydrine alleviates lipid-induced skeletal muscle insulin resistance via AMPK/HO-1-mediated suppression of inflammation and endoplasmic reticulum stress.

T W Jung, H Kim, S Y Park, W Cho, H Oh, H J Lee, A M Abd El-Aty, A Hacimuftuoglu, J H Jeong

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Article in Journal of endocrinological investigation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed, 3 pooled it
2.4field-weighted citation impact, top 12% 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

5 citing papers in PubMed, 3 syntheses or guidelines pooled it, 18 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Host insulin resistance caused byFrontiers in cellular and infection microbiology · 2023
    Pooled it
  4. Review
  5. Article
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 at 4 institutions in 3 countries.

T W Jung *Department of Pharmacology, College of Medicine, Chung-Ang University, Seoul, Republic of Korea.
H Kim *Department of Pharmacology, College of Medicine, Chung-Ang University, Seoul, Republic of Korea.
S Y ParkDepartment of Pharmacology, College of Medicine, Chung-Ang University, Seoul, Republic of Korea.
W ChoDepartment of Pharmacology, College of Medicine, Chung-Ang University, Seoul, Republic of Korea.
H OhDepartment of Pharmacology, College of Medicine, Chung-Ang University, Seoul, Republic of Korea.
H J LeeDepartment of Anatomy and Cell Biology, Chung-Ang University Hospital, Chung-Ang University College of Medicine, Seoul, Korea.
A M Abd El-AtyDepartment of Pharmacology, Faculty of Veterinary Medicine, Cairo University, Giza, 12211, Egypt.
A HacimuftuogluDepartment of Medical Pharmacology, Medical Faculty, Ataturk University, 25240, Erzurum, Türkiye.
J H JeongDepartment of Pharmacology, College of Medicine, Chung-Ang University, Seoul, Republic of Korea. jhjeong3@cau.ac.kr.ORCID http://orcid.org/0000-0001-8257-403X
Chung-Ang University · KRAtatürk University · TRCairo University · EGChung-Ang University Hospital · KR

Funding

National Research Foundation (KR) 2021R1F1A1050004
6 · The paper itself

Abstract

objectiveInsulin resistance develops due to skeletal muscle inflammation and endoplasmic reticulum (ER) stress. Stachydrine (STA), extracted from Leonurus heterophyllus, has been shown to suppress proliferation and induce apoptosis in breast cancer cells and exert anti-inflammatory properties in the brain, heart, and liver. However, the roles of STA in insulin signaling in skeletal muscle remain unclear. Herein, we examined the impacts of STA on insulin signaling in skeletal muscle under hyperlipidemic conditions and its related molecular mechanisms.

methodsVarious protein expression levels were determined by Western blotting. Levels of mouse serum cytokines were measured by ELISA.

resultsWe found that STA-ameliorated inflammation and ER stress, leading to attenuation of insulin resistance in palmitate-treated C2C12 myocytes. STA dose-dependently enhanced AMPK phosphorylation and HO-1 expression. Administration of STA attenuated not only insulin resistance but also inflammation and ER stress in the skeletal muscle of high-fat diet (HFD)-fed mice. Additionally, STA-ameliorated glucose tolerance and insulin sensitivity, as well as serum TNFα and MCP-1, in mice fed a HFD. Small interfering (si) RNA-associated suppression of AMPK or HO-1 expression abolished the effects of STA in C2C12 myocytes.

conclusionsThese results suggest that STA activates AMPK/HO-1 signaling, resulting in reduced inflammation and ER stress, thereby improving skeletal muscle insulin resistance. Using STA as a natural ingredient, this research successfully treated insulin resistance and type 2 diabetes.

Indexed as

Diabetes Mellitus, Type 2Insulin ResistanceAMP-Activated Protein KinasesAnimalsDiet, High-FatEndoplasmic Reticulum StressGlucoseInflammationInsulinMiceMice, Inbred C57BLMuscle, SkeletalPalmitatesProlineRNATumor Necrosis Factor-alphaAMP-Activated Protein KinasesGlucoseInsulinPalmitatesProlineRNAstachydrineTumor Necrosis Factor-alphaAMPKER stressHO-1InflammationInsulin resistanceStachydrine

Identifiers

PMID35834165
OpenAlexW4285387653

What OpenQuestion holds

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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.