Evidence map›Paper›PMID 24644425›Full record

ArticleInternational journal of biological sciences2014

Metformin plays a dual role in MIN6 pancreatic β cell function through AMPK-dependent autophagy.

Yingling Jiang, Wei Huang, Jing Wang, Zhipeng Xu, Jieyu He, Xiaohong Lin, Zhiguang Zhou, Jingjing Zhang

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

Article in International journal of biological sciences, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
9.1field-weighted citation impact, top 2% 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

62 citing papers in PubMed, 106 citations in OpenAlex.

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  8. Characterizing poorly controlled type 2 diabetes usingMetabolomics : Official journal of the Metabolomic Society · 2024
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2 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

8 authors at 1 institution in 1 country.

Yingling Jiang1. Metabolic Syndrome Research Center and Diabetes Center, Institute of Aging and Geriatric Diseases, Key Laboratory of Diabetes Immunology, Ministry of Education, Institute of Metabolism and Endocrinology, Second Xiangya Hospital, Central South University, Changsha, Hunan, China 410011 ; 2. Endocrinology Department, Zhuzhou Central Hospital, Zhuzhou, Hunan, China 412007.
Wei Huang1. Metabolic Syndrome Research Center and Diabetes Center, Institute of Aging and Geriatric Diseases, Key Laboratory of Diabetes Immunology, Ministry of Education, Institute of Metabolism and Endocrinology, Second Xiangya Hospital, Central South University, Changsha, Hunan, China 410011.
Jing Wang1. Metabolic Syndrome Research Center and Diabetes Center, Institute of Aging and Geriatric Diseases, Key Laboratory of Diabetes Immunology, Ministry of Education, Institute of Metabolism and Endocrinology, Second Xiangya Hospital, Central South University, Changsha, Hunan, China 410011.
Zhipeng Xu1. Metabolic Syndrome Research Center and Diabetes Center, Institute of Aging and Geriatric Diseases, Key Laboratory of Diabetes Immunology, Ministry of Education, Institute of Metabolism and Endocrinology, Second Xiangya Hospital, Central South University, Changsha, Hunan, China 410011.
Jieyu He1. Metabolic Syndrome Research Center and Diabetes Center, Institute of Aging and Geriatric Diseases, Key Laboratory of Diabetes Immunology, Ministry of Education, Institute of Metabolism and Endocrinology, Second Xiangya Hospital, Central South University, Changsha, Hunan, China 410011.
Xiaohong Lin2. Endocrinology Department, Zhuzhou Central Hospital, Zhuzhou, Hunan, China 412007.
Zhiguang Zhou1. Metabolic Syndrome Research Center and Diabetes Center, Institute of Aging and Geriatric Diseases, Key Laboratory of Diabetes Immunology, Ministry of Education, Institute of Metabolism and Endocrinology, Second Xiangya Hospital, Central South University, Changsha, Hunan, China 410011.
Jingjing Zhang1. Metabolic Syndrome Research Center and Diabetes Center, Institute of Aging and Geriatric Diseases, Key Laboratory of Diabetes Immunology, Ministry of Education, Institute of Metabolism and Endocrinology, Second Xiangya Hospital, Central South University, Changsha, Hunan, China 410011.
Central South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Metformin improves insulin sensitivity in insulin sensitive tissues such as liver, muscle and fat. However, the functional roles and the underlying mechanism of metformin action in pancreatic β cells remain elusive. Here we show that, under normal growth condition, metformin suppresses MIN6 β cell proliferation and promotes apoptosis via an AMPK-dependent and autophagy-mediated mechanism. On the other hand, metformin protects MIN6 cells against palmitic acid (PA)-induced apoptosis. Our findings indicate that metformin plays a dual role in β cell survival and overdose of this anti-diabetic drug itself may lead to potential β cell toxicity.

Indexed as

AMP-Activated Protein KinasesAnimalsApoptosisAutophagyCell ProliferationCell SurvivalHypoglycemic AgentsInsulin-Secreting CellsMaleMetforminMiceMice, Inbred C57BLPalmitic AcidSignal TransductionAMP-Activated Protein KinasesHypoglycemic AgentsMetforminPalmitic AcidAMPKapoptosisautophagymetforminpancreatic β cells

Identifiers

PMID24644425
PMCPMC3957082
OpenAlexW2123838232

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.