Adipocyte-specific deletion of PIP5K1c reduces diet-induced obesity and insulin resistance by increasing energy expenditure
Abstract Background Phosphatidylinositol 4-phosphate 5-kinase type I c (PIP5K1c) catalyses the synthesis of phospholipid phosphatidylinositol 4,5-bisphosphate (PIP2) by phosphorylating phosphatidylinositol 4 phosphate, which plays multiple roles in regulating focal adhesion formation, invasion, and...
| Main Authors: | , , , , , , , , |
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| Format: | Article |
| Language: | English |
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BMC
2022-01-01
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| Series: | Lipids in Health and Disease |
| Subjects: | |
| Online Access: | https://doi.org/10.1186/s12944-021-01616-4 |
| _version_ | 1798034516704493568 |
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| author | Guan Huang Cuishan Yang Sheng Guo Miaoling Huang Liping Deng Ying Huang Puxin Chen Feng Chen Xiaohong Huang |
| author_facet | Guan Huang Cuishan Yang Sheng Guo Miaoling Huang Liping Deng Ying Huang Puxin Chen Feng Chen Xiaohong Huang |
| author_sort | Guan Huang |
| collection | DOAJ |
| description | Abstract Background Phosphatidylinositol 4-phosphate 5-kinase type I c (PIP5K1c) catalyses the synthesis of phospholipid phosphatidylinositol 4,5-bisphosphate (PIP2) by phosphorylating phosphatidylinositol 4 phosphate, which plays multiple roles in regulating focal adhesion formation, invasion, and cell migration signal transduction cascades. Here, a new physiological mechanism of PIP5K1c in adipocytes and systemic metabolism is reported. Methods Adipose-specific conditional knockout mice were generated to delete the PIP5K1c gene in adipocytes. In addition, in vitro research investigated the effect of PIP5K1c deletion on adipogenesis. Results Deletion of PIP5K1c in adipocytes significantly alleviated high fat diet (HFD)-induced obesity, hyperlipidaemia, hepatic steatosis, and insulin resistance. PIP5K1c deficiency in adipocytes also decreased adipocyte volume in HFD-induced obese mice, whereas no significant differences were observed in body weight and adipose tissue weight under normal chow diet conditions. PIP5K1c knockout in adipocytes significantly enhanced energy expenditure, which protected mice from HFD-induced weight gain. In addition, adipogenesis was markedly impaired in mouse stromal vascular fraction (SVF) from PIP5K1c-deleted mice. Conclusion Under HFD conditions, PIP5K1c regulates adipogenesis and adipose tissue homeostasis. Together, these data indicate that PIP5K1c could be a novel potential target for regulating fat accumulation, which could provide novel insight into the treatment of obesity. |
| first_indexed | 2024-04-11T20:45:15Z |
| format | Article |
| id | doaj.art-62845a6344d846f489811ab19b06832a |
| institution | Directory Open Access Journal |
| issn | 1476-511X |
| language | English |
| last_indexed | 2024-04-11T20:45:15Z |
| publishDate | 2022-01-01 |
| publisher | BMC |
| record_format | Article |
| series | Lipids in Health and Disease |
| spelling | doaj.art-62845a6344d846f489811ab19b06832a2022-12-22T04:04:03ZengBMCLipids in Health and Disease1476-511X2022-01-0121111110.1186/s12944-021-01616-4Adipocyte-specific deletion of PIP5K1c reduces diet-induced obesity and insulin resistance by increasing energy expenditureGuan Huang0Cuishan Yang1Sheng Guo2Miaoling Huang3Liping Deng4Ying Huang5Puxin Chen6Feng Chen7Xiaohong Huang8Department of Pathology, Shenzhen Clinical Medical College, Guangzhou University of Chinese Medicine, Longgang District Central Hospital of ShenzhenDepartment of Nursing, Shenzhen Clinical Medical College, Guangzhou University of Chinese Medicine, Longgang District Central Hospital of ShenzhenDepartment of Medical Administration, Shenzhen Clinical Medical College, Guangzhou University of Chinese Medicine, Longgang District Central Hospital of ShenzhenDepartment of Metabolism and Endocrinology, Shenzhen Clinical Medical College, Guangzhou University of Chinese Medicine, Longgang District Central Hospital of ShenzhenDepartment of Metabolism and Endocrinology, Shenzhen Clinical Medical College, Guangzhou University of Chinese Medicine, Longgang District Central Hospital of ShenzhenDepartment of Metabolism and Endocrinology, Shenzhen Clinical Medical College, Guangzhou University of Chinese Medicine, Longgang District Central Hospital of ShenzhenDepartment of Metabolism and Endocrinology, Shenzhen Clinical Medical College, Guangzhou University of Chinese Medicine, Longgang District Central Hospital of ShenzhenDepartment of Plastic Surgy, Shenzhen Clinical Medical College, Guangzhou University of Chinese Medicine; Longgang District Central Hospital of ShenzhenDepartment of Nursing, Shenzhen Clinical Medical College, Guangzhou University of Chinese Medicine, Longgang District Central Hospital of ShenzhenAbstract Background Phosphatidylinositol 4-phosphate 5-kinase type I c (PIP5K1c) catalyses the synthesis of phospholipid phosphatidylinositol 4,5-bisphosphate (PIP2) by phosphorylating phosphatidylinositol 4 phosphate, which plays multiple roles in regulating focal adhesion formation, invasion, and cell migration signal transduction cascades. Here, a new physiological mechanism of PIP5K1c in adipocytes and systemic metabolism is reported. Methods Adipose-specific conditional knockout mice were generated to delete the PIP5K1c gene in adipocytes. In addition, in vitro research investigated the effect of PIP5K1c deletion on adipogenesis. Results Deletion of PIP5K1c in adipocytes significantly alleviated high fat diet (HFD)-induced obesity, hyperlipidaemia, hepatic steatosis, and insulin resistance. PIP5K1c deficiency in adipocytes also decreased adipocyte volume in HFD-induced obese mice, whereas no significant differences were observed in body weight and adipose tissue weight under normal chow diet conditions. PIP5K1c knockout in adipocytes significantly enhanced energy expenditure, which protected mice from HFD-induced weight gain. In addition, adipogenesis was markedly impaired in mouse stromal vascular fraction (SVF) from PIP5K1c-deleted mice. Conclusion Under HFD conditions, PIP5K1c regulates adipogenesis and adipose tissue homeostasis. Together, these data indicate that PIP5K1c could be a novel potential target for regulating fat accumulation, which could provide novel insight into the treatment of obesity.https://doi.org/10.1186/s12944-021-01616-4ObesityPIP5K1cAdipose tissueEnergy expenditureAdipogenesis |
| spellingShingle | Guan Huang Cuishan Yang Sheng Guo Miaoling Huang Liping Deng Ying Huang Puxin Chen Feng Chen Xiaohong Huang Adipocyte-specific deletion of PIP5K1c reduces diet-induced obesity and insulin resistance by increasing energy expenditure Lipids in Health and Disease Obesity PIP5K1c Adipose tissue Energy expenditure Adipogenesis |
| title | Adipocyte-specific deletion of PIP5K1c reduces diet-induced obesity and insulin resistance by increasing energy expenditure |
| title_full | Adipocyte-specific deletion of PIP5K1c reduces diet-induced obesity and insulin resistance by increasing energy expenditure |
| title_fullStr | Adipocyte-specific deletion of PIP5K1c reduces diet-induced obesity and insulin resistance by increasing energy expenditure |
| title_full_unstemmed | Adipocyte-specific deletion of PIP5K1c reduces diet-induced obesity and insulin resistance by increasing energy expenditure |
| title_short | Adipocyte-specific deletion of PIP5K1c reduces diet-induced obesity and insulin resistance by increasing energy expenditure |
| title_sort | adipocyte specific deletion of pip5k1c reduces diet induced obesity and insulin resistance by increasing energy expenditure |
| topic | Obesity PIP5K1c Adipose tissue Energy expenditure Adipogenesis |
| url | https://doi.org/10.1186/s12944-021-01616-4 |
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