Evidence map›Paper›PMID 25713102›Full record

ArticleJournal of lipid research2015

Thyroid-stimulating hormone decreases HMG-CoA reductase phosphorylation via AMP-activated protein kinase in the liver.

Xiujuan Zhang, Yongfeng Song, Mei Feng, Xinli Zhou, Yingli Lu, Ling Gao, Chunxiao Yu, Xiuyun Jiang, Jiajun Zhao

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of lipid research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

65 citing papers in PubMed, 107 citations in OpenAlex.

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  3. Spatial AuAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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5 more citing papers are in PubMed but not listed here.

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 3 institutions in 1 country.

Xiujuan ZhangDepartments of Endocrinology, Shandong Provincial Hospital Affiliated to Shandong University, Jinan 250021, China Institute of Endocrinology and Metabolism, Shandong Academy of Clinical Medicine, Shandong Provincial Hospital Affiliated to Shandong University, Jinan 250021, China.
Yongfeng SongDepartments of Endocrinology, Shandong Provincial Hospital Affiliated to Shandong University, Jinan 250021, China Institute of Endocrinology and Metabolism, Shandong Academy of Clinical Medicine, Shandong Provincial Hospital Affiliated to Shandong University, Jinan 250021, China.
Mei FengScientific Center, Shandong Provincial Hospital Affiliated to Shandong University, Jinan 250021, China.
Xinli ZhouDepartments of Endocrinology, Shandong Provincial Hospital Affiliated to Shandong University, Jinan 250021, China Institute of Endocrinology and Metabolism, Shandong Academy of Clinical Medicine, Shandong Provincial Hospital Affiliated to Shandong University, Jinan 250021, China.
Yingli LuDepartment of Endocrinology and Metabolism, Shanghai Ninth People'sHospital Affiliated to Shanghai Jiaotong University School of Medicine, Shanghai 200011, China.
Ling GaoInstitute of Endocrinology and Metabolism, Shandong Academy of Clinical Medicine, Shandong Provincial Hospital Affiliated to Shandong University, Jinan 250021, China Scientific Center, Shandong Provincial Hospital Affiliated to Shandong University, Jinan 250021, China.
Chunxiao YuDepartments of Endocrinology, Shandong Provincial Hospital Affiliated to Shandong University, Jinan 250021, China Institute of Endocrinology and Metabolism, Shandong Academy of Clinical Medicine, Shandong Provincial Hospital Affiliated to Shandong University, Jinan 250021, China.
Xiuyun JiangDepartments of Endocrinology, Shandong Provincial Hospital Affiliated to Shandong University, Jinan 250021, China Institute of Endocrinology and Metabolism, Shandong Academy of Clinical Medicine, Shandong Provincial Hospital Affiliated to Shandong University, Jinan 250021, China.
Jiajun ZhaoDepartments of Endocrinology, Shandong Provincial Hospital Affiliated to Shandong University, Jinan 250021, China Institute of Endocrinology and Metabolism, Shandong Academy of Clinical Medicine, Shandong Provincial Hospital Affiliated to Shandong University, Jinan 250021, China.
Shandong Provincial Hospital · CNShandong University · CNShanghai Ninth People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cholesterol homeostasis is strictly regulated through the modulation of HMG-CoA reductase (HMGCR), the rate-limiting enzyme of cholesterol synthesis. Phosphorylation of HMGCR inactivates it and dephosphorylation activates it. AMP-activated protein kinase (AMPK) is the major kinase phosphorylating the enzyme. Our previous study found that thyroid-stimulating hormone (TSH) increased the hepatocytic HMGCR expression, but it was still unclear whether TSH affected hepatic HMGCR phosphorylation associated with AMPK. We used bovine TSH (bTSH) to treat the primary mouse hepatocytes and HepG2 cells with or without constitutively active (CA)-AMPK plasmid or protein kinase A inhibitor (H89), and set up the TSH receptor (Tshr)-KO mouse models. The p-HMGCR, p-AMPK, and related molecular expression were tested. The ratios of p-HMGCR/HMGCR and p-AMPK/AMPK decreased in the hepatocytes in a dose-dependent manner following bTSH stimulation. The changes above were inversed when the cells were treated with CA-AMPK plasmid or H89. In Tshr-KO mice, the ratios of liver p-HMGCR/HMGCR and p-AMPK/AMPK were increased relative to the littermate wild-type mice. Consistently, the phosphorylation of acetyl-CoA carboxylase, a downstream target molecule of AMPK, increased. All results suggested that TSH could regulate the phosphorylation of HMGCR via AMPK, which established a potential mechanism for hypercholesterolemia involved in a direct action of the TSH in the liver.

Indexed as

Adenylate KinaseAnimalsCyclic AMP-Dependent Protein KinasesHep G2 CellsHumansHydroxymethylglutaryl CoA ReductasesIsoquinolinesLiverMice, Inbred C57BLMice, KnockoutPhosphorylationProtein Processing, Post-TranslationalSulfonamidesThyrotropinAdenylate KinaseCyclic AMP-Dependent Protein KinasesHydroxymethylglutaryl CoA ReductasesIsoquinolinesN-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamideSulfonamidesThyrotropinadenosine 5′-monophosphate-activated protein kinasecholesterolhydroxy-methylglutaryl coenzyme A reductase

Identifiers

PMID25713102
PMCPMC4409286
OpenAlexW2082043462

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.