Evidence map›Paper›PMID 39128897›Full record

ArticleSignal transduction and targeted therapy2024

Potassium voltage-gated channel subfamily H member 2 (KCNH2) is a promising target for incretin secretagogue therapies.

Ying-Chao Yuan, Hao Wang, Ze-Ju Jiang, Chang Liu, Qi Li, Si-Rui Zhou, Jin-Kui Yang

Abstract read
In one paragraph

Article in Signal transduction and targeted therapy, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed.

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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

7 authors.

Ying-Chao Yuan *Beijing Key Laboratory of Diabetes Research and Care, Department of Endocrinology and Metabolism, Beijing Diabetes Institute, Beijing Tongren Hospital, Capital Medical University, Beijing, 100730, China.
Hao Wang *Beijing Key Laboratory of Diabetes Research and Care, Department of Endocrinology and Metabolism, Beijing Diabetes Institute, Beijing Tongren Hospital, Capital Medical University, Beijing, 100730, China. hwang@mail.ccmu.edu.cn.
Ze-Ju JiangBeijing Key Laboratory of Diabetes Research and Care, Department of Endocrinology and Metabolism, Beijing Diabetes Institute, Beijing Tongren Hospital, Capital Medical University, Beijing, 100730, China.
Chang LiuBeijing Key Laboratory of Diabetes Research and Care, Department of Endocrinology and Metabolism, Beijing Diabetes Institute, Beijing Tongren Hospital, Capital Medical University, Beijing, 100730, China.
Qi LiBeijing Key Laboratory of Diabetes Research and Care, Department of Endocrinology and Metabolism, Beijing Diabetes Institute, Beijing Tongren Hospital, Capital Medical University, Beijing, 100730, China.
Si-Rui ZhouBeijing Key Laboratory of Diabetes Research and Care, Department of Endocrinology and Metabolism, Beijing Diabetes Institute, Beijing Tongren Hospital, Capital Medical University, Beijing, 100730, China.
Jin-Kui YangBeijing Key Laboratory of Diabetes Research and Care, Department of Endocrinology and Metabolism, Beijing Diabetes Institute, Beijing Tongren Hospital, Capital Medical University, Beijing, 100730, China. jkyang@ccmu.edu.cn.ORCID 0000-0002-5430-2149

Funding

National Natural Science Foundation of China (National Science Foundation of China) 81930019Natural Science Foundation of Beijing Municipality (Beijing Natural Science Foundation) 7232232
6 · The paper itself

Abstract

Derived from enteroendocrine cells (EECs), glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic peptide (GIP) are pivotal incretin hormones crucial for blood glucose regulation. Medications of GLP-1 analogs and GLP-1 receptor activators are extensively used in the treatment of type 2 diabetes (T2D) and obesity. However, there are currently no agents to stimulate endogenous incretin secretion. Here, we find the pivotal role of KCNH2 potassium channels in the regulation of incretin secretion. Co-localization of KCNH2 with incretin-secreting EECs in the intestinal epithelium of rodents highlights its significance. Gut epithelial cell-specific KCNH2 knockout in mice improves glucose tolerance and increases oral glucose-triggered GLP-1 and GIP secretion, particularly GIP. Furthermore, KCNH2-deficient primary intestinal epithelial cells exhibit heightened incretin, especially GIP secretion upon nutrient stimulation. Mechanistically, KCNH2 knockdown in EECs leads to reduced K

Indexed as

Enteroendocrine CellsGlucagon-Like Peptide 1IncretinsAnimalsDiabetes Mellitus, Type 2ERG1 Potassium ChannelGastric Inhibitory PolypeptideHumansMiceMice, KnockoutSecretagoguesERG1 Potassium ChannelGastric Inhibitory PolypeptideGlucagon-Like Peptide 1IncretinsKCNH2 protein, humanSecretagogues

Identifiers

PMID39128897
PMCPMC11317495

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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.