GPIHBP1 increase accounts for rheumatic arthritis-related hypotriglyceridemia by facilitating lipids uptake of white adipose tissues
Abstract Background Metabolism alteration is a common complication of rheumatic arthritis (RA). This work investigated the reason behind RA-caused triglyceride (TG) changes. Methods Fresh RA patients’ whole blood was transfused into NOD-SCID mice. Metabolism-regulatory tissues were examined after sa...
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BMC
2025-01-01
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| Series: | Arthritis Research & Therapy |
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| Online Access: | https://doi.org/10.1186/s13075-025-03483-1 |
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| author | Meng-Ke Song Meng-Fan Gu Ling Liu Lian-Jun He Peng Ye Kui Yang Dan-Dan Wang Opeyemi Joshua Olatunji Qin Yin Jian Zuo |
| author_facet | Meng-Ke Song Meng-Fan Gu Ling Liu Lian-Jun He Peng Ye Kui Yang Dan-Dan Wang Opeyemi Joshua Olatunji Qin Yin Jian Zuo |
| author_sort | Meng-Ke Song |
| collection | DOAJ |
| description | Abstract Background Metabolism alteration is a common complication of rheumatic arthritis (RA). This work investigated the reason behind RA-caused triglyceride (TG) changes. Methods Fresh RA patients’ whole blood was transfused into NOD-SCID mice. Metabolism-regulatory tissues were examined after sacrifice. To verify the findings, tissues of the rats with long-lasting adjuvant-induced arthritis (AIA) were analyzed. Some rats were injected with human plasma and GPIHBP1, and their blood TG was monitored. Various cells were stimulated by cytokines or rheumatic subjects’ serum. Some pre-adipocytes were cultured by human serum or in the presence of HUVEC cells and GPIHBP1. Results TG decrease occurred in blood and white adipose tissues (WAT) of the RA blood-transfused NOD-SCID mice and chronic AIA rats. Fatty acids (FA) oxidation in muscles was accelerated a bit, while TG catabolism status in their livers was varied. TNF-α, IL-1β, IL-6 and RA/AIA serum promoted expression of TG utilization-related enzymes and FA uptake transporters in pre-adipocytes, but barely affected LPL. Mild IL-6 stimulus promoted GPIHBP1 release of HUVEC cells. GPIHBP1 was increased in RA serum. This change can decrease blood TG in rats, which was overshadowed by an injection of excessive GPIHBP1. RA serum slightly inhibited LPL secretion in pre-adipocytes. Both HUVEC cells co-culture and GPIHBP1 supplement reduced LPL distribution on pre-adipocytes, and eliminated LPL activity difference between normal and RA serum-treated cells. No TG uptake difference was observed in these circumstances. Conclusion RA-associated inflammation induces GPIHBP1 secretion of endothelial cells, which facilitates blood TG hydrolysis and uptake to compensate the loss in WAT. |
| format | Article |
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| institution | Kabale University |
| issn | 1478-6362 |
| language | English |
| publishDate | 2025-01-01 |
| publisher | BMC |
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| series | Arthritis Research & Therapy |
| spelling | doaj-art-dae60d90e651409c894df2f9e20a0dfc2025-01-26T12:46:05ZengBMCArthritis Research & Therapy1478-63622025-01-0127111510.1186/s13075-025-03483-1GPIHBP1 increase accounts for rheumatic arthritis-related hypotriglyceridemia by facilitating lipids uptake of white adipose tissuesMeng-Ke Song0Meng-Fan Gu1Ling Liu2Lian-Jun He3Peng Ye4Kui Yang5Dan-Dan Wang6Opeyemi Joshua Olatunji7Qin Yin8Jian Zuo9Xin’an Medicine Research Center, the First Affiliated Hospital of Wannan Medical College (Yijishan Hospital)Xin’an Medicine Research Center, the First Affiliated Hospital of Wannan Medical College (Yijishan Hospital)Department of Pharmacy, the Second Affiliated Hospital of Wannan Medical CollegePrecision Medicine Centre, the First Affiliated Hospital of Wannan Medical College (Yijishan Hospital)Xin’an Medicine Research Center, the First Affiliated Hospital of Wannan Medical College (Yijishan Hospital)Xin’an Medicine Research Center, the First Affiliated Hospital of Wannan Medical College (Yijishan Hospital)Department of Pharmacy, the Second Affiliated Hospital of Wannan Medical CollegeAfrican Genome Center, Mohammed VI Polytechnic UniversityDepartment of Pharmacy, the Second Affiliated Hospital of Wannan Medical CollegeXin’an Medicine Research Center, the First Affiliated Hospital of Wannan Medical College (Yijishan Hospital)Abstract Background Metabolism alteration is a common complication of rheumatic arthritis (RA). This work investigated the reason behind RA-caused triglyceride (TG) changes. Methods Fresh RA patients’ whole blood was transfused into NOD-SCID mice. Metabolism-regulatory tissues were examined after sacrifice. To verify the findings, tissues of the rats with long-lasting adjuvant-induced arthritis (AIA) were analyzed. Some rats were injected with human plasma and GPIHBP1, and their blood TG was monitored. Various cells were stimulated by cytokines or rheumatic subjects’ serum. Some pre-adipocytes were cultured by human serum or in the presence of HUVEC cells and GPIHBP1. Results TG decrease occurred in blood and white adipose tissues (WAT) of the RA blood-transfused NOD-SCID mice and chronic AIA rats. Fatty acids (FA) oxidation in muscles was accelerated a bit, while TG catabolism status in their livers was varied. TNF-α, IL-1β, IL-6 and RA/AIA serum promoted expression of TG utilization-related enzymes and FA uptake transporters in pre-adipocytes, but barely affected LPL. Mild IL-6 stimulus promoted GPIHBP1 release of HUVEC cells. GPIHBP1 was increased in RA serum. This change can decrease blood TG in rats, which was overshadowed by an injection of excessive GPIHBP1. RA serum slightly inhibited LPL secretion in pre-adipocytes. Both HUVEC cells co-culture and GPIHBP1 supplement reduced LPL distribution on pre-adipocytes, and eliminated LPL activity difference between normal and RA serum-treated cells. No TG uptake difference was observed in these circumstances. Conclusion RA-associated inflammation induces GPIHBP1 secretion of endothelial cells, which facilitates blood TG hydrolysis and uptake to compensate the loss in WAT.https://doi.org/10.1186/s13075-025-03483-1Rheumatic arthritisLipids paradoxVascular endothelial cellAdipocyteCD36IL-6 |
| spellingShingle | Meng-Ke Song Meng-Fan Gu Ling Liu Lian-Jun He Peng Ye Kui Yang Dan-Dan Wang Opeyemi Joshua Olatunji Qin Yin Jian Zuo GPIHBP1 increase accounts for rheumatic arthritis-related hypotriglyceridemia by facilitating lipids uptake of white adipose tissues Arthritis Research & Therapy Rheumatic arthritis Lipids paradox Vascular endothelial cell Adipocyte CD36 IL-6 |
| title | GPIHBP1 increase accounts for rheumatic arthritis-related hypotriglyceridemia by facilitating lipids uptake of white adipose tissues |
| title_full | GPIHBP1 increase accounts for rheumatic arthritis-related hypotriglyceridemia by facilitating lipids uptake of white adipose tissues |
| title_fullStr | GPIHBP1 increase accounts for rheumatic arthritis-related hypotriglyceridemia by facilitating lipids uptake of white adipose tissues |
| title_full_unstemmed | GPIHBP1 increase accounts for rheumatic arthritis-related hypotriglyceridemia by facilitating lipids uptake of white adipose tissues |
| title_short | GPIHBP1 increase accounts for rheumatic arthritis-related hypotriglyceridemia by facilitating lipids uptake of white adipose tissues |
| title_sort | gpihbp1 increase accounts for rheumatic arthritis related hypotriglyceridemia by facilitating lipids uptake of white adipose tissues |
| topic | Rheumatic arthritis Lipids paradox Vascular endothelial cell Adipocyte CD36 IL-6 |
| url | https://doi.org/10.1186/s13075-025-03483-1 |
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