STARD10 regulates human pancreatic β cell differentiation and triglyceride metabolism

The STARD10 gene encodes for a lipid transfer protein and is associated with type 2 diabetes (T2D) risk and β cell function. However, the role of STARD10 in human β cell development and function are still unclear. Here, we deleted STARD10 in human embryonic stem cells and differentiated them into β-like cells. The deletion of STARD10 reduced the formation of INS<sup>+</sup> β-like cells and proliferation. Lipidomics analyses revealed that STARD10-null β-like cells had higher triglyceride levels. Consistently, the expression levels of ETFB, which is involved in fatty acid β-oxidation, were severely reduced in STARD10-null β-like cells. STARD10-null β-like cells also had reduced glycolytic function, mitochondrial oxidative phosphorylation, and palmitate oxidation, which can likely contribute to slower proliferation and β cell dysfunction. Overall, our findings provided further insights into the role of STARD10 in human β cell development and function, and how its loss-of-function can contribute to increased T2D risk.

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Publication Details

Journal
Stem Cell Reports
Published
2026-02-12
DOI
https://doi.org/10.1016/j.stemcr.2026.102815
Primary Topic
Pancreatic function and diabetes
Type
article
Field-Weighted Citation Impact
0.00

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article

STARD10 regulates human pancreatic β cell differentiation and triglyceride metabolism

Peter I. Benke, Hwee Hui Lau, Adrian Kee Keong Teo, Federico Torta et al.
Stem Cell Reports
Pancreatic function and diabetes
article

STARD10 regulates human pancreatic β cell differentiation and triglyceride metabolism

Peter I. Benke, Hwee Hui Lau, Adrian Kee Keong Teo, Federico Torta, Shawn Hoon, Nur Shabrina Amirruddin, Sneha Muralidharan, Ming Hu, Euodia Xi Hui Lim, Guy A. Rutter, Andreas Alvin P. Soetedjo, Natasha H.J. Ng, Wei Xuan Tan
article en

Abstract

The STARD10 gene encodes for a lipid transfer protein and is associated with type 2 diabetes (T2D) risk and β cell function. However, the role of STARD10 in human β cell development and function are still unclear. Here, we deleted STARD10 in human embryonic stem cells and differentiated them into β-like cells. The deletion of STARD10 reduced the formation of INS<sup>+</sup> β-like cells and proliferation. Lipidomics analyses revealed that STARD10-null β-like cells had higher triglyceride levels. Consistently, the expression levels of ETFB, which is involved in fatty acid β-oxidation, were severely reduced in STARD10-null β-like cells. STARD10-null β-like cells also had reduced glycolytic function, mitochondrial oxidative phosphorylation, and palmitate oxidation, which can likely contribute to slower proliferation and β cell dysfunction. Overall, our findings provided further insights into the role of STARD10 in human β cell development and function, and how its loss-of-function can contribute to increased T2D risk.

Stem Cell ReportsVol. 21(3)
National University of Singapore (SG), Nanyang Technological University (SG), Genomics (United Kingdom) (GB), Signature Research (United States) (US), Imperial College London (GB), Institute of Molecular and Cell Biology (SG)
Japan Agency for Medical Research and Development, Wellcome Trust, European Federation of Pharmaceutical Industries and Associations, Duke-NUS Medical School, Diabetes UK, European Commission, National Research Foundation, National University of Singapore, Agence Nationale de la Recherche, Medical Research Council, National Medical Research Council, Institute of Molecular and Cell Biology
Good health and well-being
Openalex Percentile: Top 58%
Pancreatic function and diabetes
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