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ATP synthase inhibitory factor subunit 1 regulates islet β-cell function via repression of mitochondrial homeostasis.

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机构： [1]Division of Cardiology, Department of Internal Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China [2]Cardiovascular Center of Excellence and Department of Pharmacology, Louisiana State University Health Science Center New Orleans, New Orleans, LA, USA [3]Department of Nutrition Science, University of Alabama at Birmingham, Birmingham, AL, USA [4]Department of Molecular Bioscience, Kyoto Sangyo University, Kamigamo-Motoyama, Kyoto, Japan [5]Guangdong Metabolic Diseases Research Center of Integrated Chinese and Western Medicine, Institute of Chinese Medicine, Guangdong Pharmaceutical University, Guangzhou, China

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Mitochondrial homeostasis is crucial for the function of pancreatic β-cells. ATP synthase inhibitory factor subunit 1 (IF1) is a mitochondrial protein interacting with ATP synthase to inhibit its enzyme activity. IF1 may also play a role in maintaining ATP synthase oligomerization and mitochondrial inner membrane formation. A recent study confirmed IF1 expresses in β-cells. IF1 knockdown in cultured INS-1E β-cells enhances glucose-induced insulin release. However, the role of IF1 in islet β-cells remains little known. The present study investigates islets freshly isolated from mouse lines with global IF1 knockout (IF1-/-) and overexpression (OE). The glucose-stimulated insulin secretion was increased in islets from IF1-/- mice but decreased in islets from IF1 OE mice. Transmitted Electronic Microscopic assessment of isolated islets revealed that the number of matured insulin granules (with dense core) was relatively higher in IF1-/-, but fewer in IF1 OE islets than those of controlled islets. The mitochondrial ultrastructure within β-cells of IF1 overexpressed islets was comparable with those of wild-type mice, whereas those in IF1-/- β-cells showed increased mitochondrial mass. Mitochondrial network analysis in cultured INS-1 β-cells showed a similar pattern with an increased mitochondrial network in IF1 knockdown cells. IF1 overexpressed INS-1 β-cells showed a compromised rate of mitochondrial oxidative phosphorylation with attenuated cellular ATP content. In contrast, INS-1 cells with IF1 knockdown showed markedly increased cellular respiration with improved ATP production. These results support that IF1 is a negative regulator of insulin production and secretion via inhibiting mitochondrial mass and respiration in β-cells. Therefore, inhibiting IF1 to improve β-cell function in patients can be a novel therapeutic strategy to treat diabetes.© 2021. The Author(s), under exclusive licence to United States and Canadian Academy of Pathology.

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出版当年[2021]版：

大类 | 2 区医学

小类 | 2 区医学：研究与实验 2 区病理学

最新[2025]版：

大类 | 2 区医学

小类 | 2 区医学：研究与实验 2 区病理学

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出版当年[2020]版：

Q1 PATHOLOGY Q2 MEDICINE, RESEARCH & EXPERIMENTAL

最新[2023]版：

Q1 MEDICINE, RESEARCH & EXPERIMENTAL Q1 PATHOLOGY

影响因子： 5.1 最新[2023版] 5.2 最新五年平均 5.662 出版当年[2020版] 5.391 出版当年五年平均 4.197 出版前一年[2019版] 5.511 出版后一年[2021版]

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第一作者机构： [1]Division of Cardiology, Department of Internal Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China

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通讯作者：

通讯机构： [1]Division of Cardiology, Department of Internal Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China [3]Department of Nutrition Science, University of Alabama at Birmingham, Birmingham, AL, USA [5]Guangdong Metabolic Diseases Research Center of Integrated Chinese and Western Medicine, Institute of Chinese Medicine, Guangdong Pharmaceutical University, Guangzhou, China

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