Evidence mapPaperPMID 39690249Full record

ArticleDiabetologia2025

Gain of pancreatic beta cell-specific SCD1 improves glucose homeostasis by maintaining functional beta cell mass under metabolic stress.

Wenyue Yin, Suyun Zou, Min Sha, Liangjun Sun, Haoqiang Gong, Can Xiong, Xinyue Huang, Jianan Wang, Yuhan Zhang, Xirui Li and 8 more

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Article in Diabetologia, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

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2citing papers in PubMed
field-weighted citation impact
1 · What the graph read from it

What it found

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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

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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

2 citing papers in PubMed.

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4 · The record

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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

18 authors.

Wenyue Yin *Key Laboratory of Human Functional Genomics of Jiangsu Province, Nanjing Medical University, Nanjing, Jiangsu, China.
Suyun Zou *Key Laboratory of Human Functional Genomics of Jiangsu Province, Nanjing Medical University, Nanjing, Jiangsu, China.
Min Sha *Department of Central Laboratory, The Affiliated Taizhou People's Hospital of Nanjing Medical University, Taizhou School of Clinical Medicine, Taizhou, Jiangsu, China.
Liangjun SunKey Laboratory of Human Functional Genomics of Jiangsu Province, Nanjing Medical University, Nanjing, Jiangsu, China.
Haoqiang GongKey Laboratory of Human Functional Genomics of Jiangsu Province, Nanjing Medical University, Nanjing, Jiangsu, China.
Can XiongKey Laboratory of Human Functional Genomics of Jiangsu Province, Nanjing Medical University, Nanjing, Jiangsu, China.
Xinyue HuangKey Laboratory of Human Functional Genomics of Jiangsu Province, Nanjing Medical University, Nanjing, Jiangsu, China.
Jianan WangKey Laboratory of Human Functional Genomics of Jiangsu Province, Nanjing Medical University, Nanjing, Jiangsu, China.
Yuhan ZhangKey Laboratory of Human Functional Genomics of Jiangsu Province, Nanjing Medical University, Nanjing, Jiangsu, China.
Xirui LiKey Laboratory of Human Functional Genomics of Jiangsu Province, Nanjing Medical University, Nanjing, Jiangsu, China.
Jin LiangKey Laboratory of Human Functional Genomics of Jiangsu Province, Nanjing Medical University, Nanjing, Jiangsu, China.
Xiaoai ChangKey Laboratory of Human Functional Genomics of Jiangsu Province, Nanjing Medical University, Nanjing, Jiangsu, China.
Shusen WangOrgan Transplant Center, Tianjin First Central Hospital, Nankai University, Tianjin, China.
Dongming SuDepartment of Pathology, Nanjing Medical University, Nanjing, Jiangsu, China.
Wanhua GuoDepartment of Nuclear Medicine, Nanjing Tongren Hospital, School of Medicine, Southeast University, Nanjing, Jiangsu, China.
Yaqin ZhangKey Laboratory of Human Functional Genomics of Jiangsu Province, Nanjing Medical University, Nanjing, Jiangsu, China. yaqinzhang@njmu.edu.cn.ORCID http://orcid.org/0000-0003-3436-4569
Tijun WuKey Laboratory of Human Functional Genomics of Jiangsu Province, Nanjing Medical University, Nanjing, Jiangsu, China. wutijun@njmu.edu.cn.ORCID http://orcid.org/0000-0002-8788-5686
Fang ChenKey Laboratory of Human Functional Genomics of Jiangsu Province, Nanjing Medical University, Nanjing, Jiangsu, China. chenfang@njmu.edu.cn.ORCID http://orcid.org/0000-0001-7702-4244

Funding

2023 Taizhou Science and Technology Support Program (Social Development) Project TS202310National Key Research and Development Program of China 2022YFF0713005National Natural Science Foundation of China 32171116National Natural Science Foundation of China 32371168National Natural Science Foundation of China 82170810National Natural Science Foundation of China 82370803Natural Science Foundation of Jiangsu Province BK20240132the Project Foundation of Taizhou School of Clinical Medicine affiliated to Nanjing Medical University TZKY20230310
6 · The paper itself

Abstract

aims/hypothesisThe key pancreatic beta cell transcription factor v-maf musculoaponeurotic fibrosarcoma oncogene homologue A (MafA) is critical for the maintenance of mature beta cell function and phenotype. The expression levels and/or activities of MafA are reduced when beta cells are chronically exposed to diabetogenic stress, such as hyperglycaemia (i.e. glucotoxicity). Interventional targets and adjuvant therapies to abate MafA loss in beta cells may provide evidence to support the effective treatment of diabetes. In this study, we aimed to investigate the function of stearoyl-CoA desaturase 1 (SCD1) in the stabilisation of MafA expression and activity in order to maintain functional beta cell mass, with a view to suppressing the development of type 2 diabetes.

methodsSCD1 expression levels were analysed in islets obtained from humans with type 2 diabetes, hyperglycaemic db/db mice, and a high-fat diet (HFD)-induced mouse model of diabetes. Pancreatic beta cell-specific Scd1 knockin (βSCD1KI) mice were generated to study the role of SCD1 in beta cell function and identity. The protein-to-protein interactions between SCD1 and MafA were detected in MIN6 and HEK293A cells. We used experiments including chromatin immunoprecipitation, cell-based ubiquitination assay and fatty acid composition analysis to investigate the specific molecular mechanism underlying the effect of SCD1 on the restoration of MafA and beta cell function under glucotoxic conditions.

resultsSCD1 expression was reduced in beta cells of humans with type 2 diabetes and in HFD-fed and db/db mice compared with healthy controls, which was attributed to glucotoxicity-induced Scd1 promoter histone deacetylation. Gain-of-function of SCD1 in beta cells improved insulin deficiency, glucose intolerance and beta cell dedifferentiation/transdifferentiation in the HFD-induced mouse model of diabetes. Mechanistically, SCD1 directly bound to the E3 ubiquitin ligase HMG-CoA reductase degradation 1 (HRD1) and stabilised nuclear MafA through interrupting MafA-HRD1 interactions in mouse islets and MIN6 cells, which inhibited the ubiquitination-mediated degradation of MafA. Moreover, the products of SCD enzyme reactions (mainly oleic acid) also alleviated glucotoxicity-mediated oxidative stress in MIN6 cells. CONCLUSIONS/

interpretationOur findings indicate that SCD1 stabilises beta cell MafA both in desaturase-dependent and -independent manners, thus improving glucose homeostasis under metabolic stress. This provides a potential novel target for precision medicine for the treatment of diabetes.

Indexed as

GlucoseInsulin-Secreting CellsStearoyl-CoA DesaturaseStress, PhysiologicalAnimalsDiabetes Mellitus, Type 2Diet, High-FatHomeostasisHumansHyperglycemiaMaf Transcription Factors, LargeMaleMiceMice, Inbred C57BLGlucoseMaf Transcription Factors, LargeSCD1 protein, humanScd1 protein, mouseStearoyl-CoA DesaturaseBeta cell maturityDiabetesGlucotoxicityMafAOxidative stressPancreatic beta cellsSCD1

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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 Socratic graph.