Evidence map›Paper›PMID 37337224›Full record

ArticleBMC complementary medicine and therapies2023

Tianhuang formula regulates adipocyte mitochondrial function by AMPK/MICU1 pathway in HFD/STZ-induced T2DM mice.

Duosheng Luo, Yaru Zhao, Zhaoyan Fang, Yating Zhao, Yi Han, Jingyu Piao, Xianglu Rong, Jiao Guo

Open access · goldAbstract read
In one paragraph

Article in BMC complementary medicine and therapies, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

7 citing papers in PubMed, 11 citations in OpenAlex.

  1. Review
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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

8 authors at 4 institutions in 1 country.

Duosheng Luo *Guangdong Metabolic Diseases Research Center of Integrated Chinese and Western Medicine; Key Laboratory of Glucolipid Metabolic Disorder, Ministry of Education of China; Institute of Chinese Medicine, Guangdong Pharmaceutical University, Guangzhou Higher Education Mega Center; Guangdong TCM Key Laboratory for Metabolic Diseases, 280 Wai Huan Dong Road, Guangzhou, 510006, China.
Yaru Zhao *Guangdong Metabolic Diseases Research Center of Integrated Chinese and Western Medicine; Key Laboratory of Glucolipid Metabolic Disorder, Ministry of Education of China; Institute of Chinese Medicine, Guangdong Pharmaceutical University, Guangzhou Higher Education Mega Center; Guangdong TCM Key Laboratory for Metabolic Diseases, 280 Wai Huan Dong Road, Guangzhou, 510006, China.
Zhaoyan Fang *Guangdong Metabolic Diseases Research Center of Integrated Chinese and Western Medicine; Key Laboratory of Glucolipid Metabolic Disorder, Ministry of Education of China; Institute of Chinese Medicine, Guangdong Pharmaceutical University, Guangzhou Higher Education Mega Center; Guangdong TCM Key Laboratory for Metabolic Diseases, 280 Wai Huan Dong Road, Guangzhou, 510006, China.
Yating ZhaoGuangdong Metabolic Diseases Research Center of Integrated Chinese and Western Medicine; Key Laboratory of Glucolipid Metabolic Disorder, Ministry of Education of China; Institute of Chinese Medicine, Guangdong Pharmaceutical University, Guangzhou Higher Education Mega Center; Guangdong TCM Key Laboratory for Metabolic Diseases, 280 Wai Huan Dong Road, Guangzhou, 510006, China.
Yi HanGuangdong Metabolic Diseases Research Center of Integrated Chinese and Western Medicine; Key Laboratory of Glucolipid Metabolic Disorder, Ministry of Education of China; Institute of Chinese Medicine, Guangdong Pharmaceutical University, Guangzhou Higher Education Mega Center; Guangdong TCM Key Laboratory for Metabolic Diseases, 280 Wai Huan Dong Road, Guangzhou, 510006, China.
Jingyu PiaoGuangdong Metabolic Diseases Research Center of Integrated Chinese and Western Medicine; Key Laboratory of Glucolipid Metabolic Disorder, Ministry of Education of China; Institute of Chinese Medicine, Guangdong Pharmaceutical University, Guangzhou Higher Education Mega Center; Guangdong TCM Key Laboratory for Metabolic Diseases, 280 Wai Huan Dong Road, Guangzhou, 510006, China.
Xianglu RongGuangdong Metabolic Diseases Research Center of Integrated Chinese and Western Medicine; Key Laboratory of Glucolipid Metabolic Disorder, Ministry of Education of China; Institute of Chinese Medicine, Guangdong Pharmaceutical University, Guangzhou Higher Education Mega Center; Guangdong TCM Key Laboratory for Metabolic Diseases, 280 Wai Huan Dong Road, Guangzhou, 510006, China.
Jiao GuoGuangdong Metabolic Diseases Research Center of Integrated Chinese and Western Medicine; Key Laboratory of Glucolipid Metabolic Disorder, Ministry of Education of China; Institute of Chinese Medicine, Guangdong Pharmaceutical University, Guangzhou Higher Education Mega Center; Guangdong TCM Key Laboratory for Metabolic Diseases, 280 Wai Huan Dong Road, Guangzhou, 510006, China. gyguoyz@163.com.
Key Laboratory of Guangdong Province · CNGuangdong Pharmaceutical University · CNGuangzhou University of Chinese Medicine · CNIntegrated Chinese Medicine (China) · CN

Funding

Duosheng Luo 82074210Jiao Guo 81830113
6 · The paper itself

Abstract

backgroundTianhuang formula (THF) is a Chinese medicine prescription that is patented and clinically approved, and has been shown to improve energy metabolism, but the underlying mechanism remains poorly understood. The purpose of this study is to clarify the potential mechanisms of THF in the treatment of type 2 diabetes mellitus (T2DM).

methodsA murine model of T2DM was induced by high-fat diet (HFD) feeding combined with low-dose streptozocin (STZ) injections, and the diabetic mice were treated with THF by gavaging for consecutive 10 weeks. Fasting blood glucose (FBG), serum insulin, blood lipid, mitochondrial Ca

resultsTHF restored impaired glucose tolerance and insulin resistance in diabetic mice. Serum levels of lipids were significantly decreased, as well as fasting blood glucose and insulin in THF-treated mice. THF regulated

conclusionsThese results demonstrated that THF ameliorated glucose and lipid metabolism disorders in T2DM mice through the improvement of AMPK/MICU1 pathway-dependent mitochondrial function in adipose tissue.

Indexed as

Diabetes Mellitus, ExperimentalDiabetes Mellitus, Type 2Insulin ResistanceAdenosine TriphosphateAdipocytesAMP-Activated Protein KinasesAnimalsBlood GlucoseCalcium-Binding ProteinsDiet, High-FatDrugs, Chinese HerbalInsulinMiceMitochondriaMitochondrial Membrane Transport ProteinsAdenosine TriphosphateAMP-Activated Protein KinasesBlood GlucoseCalcium-Binding ProteinsDrugs, Chinese HerbalInsulinMICU1 protein, mouseMitochondrial Membrane Transport ProteinstianhuangAdipose tissueAMPKMICU1Mitochondrial functionType 2 diabetes mellitus

Identifiers

PMID37337224
PMCPMC10278277
OpenAlexW4381252050

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.