Dysregulation of mitochondrial dynamics mediated aortic perivascular adipose tissue-associated vascular reactivity impairment under excessive fructose intake

被引:1
作者
Wu, Kay L. H. [1 ,2 ]
Wu, Chih-Wei [3 ,4 ]
Chen, Lee-Wei [5 ,6 ,7 ]
Chang, Hsiao-Huang [8 ,9 ]
Cheng, Ching-Li [10 ]
Wu, Cai-Yi [3 ]
Lee, Yu-Chi [1 ]
Chen, I-Chun [1 ]
Hung, Chun-Ying [1 ]
Liu, Wen-Chung [3 ,11 ,12 ,13 ]
机构
[1] Kaohsiung Chang Gung Mem Hosp, Inst Translat Res Biomed, Kaohsiung, Taiwan
[2] Natl Tainan Inst Nursing, Dept Sr Citizen Serv, Tainan, Taiwan
[3] Kaohsiung Vet Gen Hosp, Plast Surg, Kaohsiung, Taiwan
[4] Natl Chiayi Univ, Dept Counseling, Chiayi, Taiwan
[5] Kaohsiung Vet Gen Hosp, Dept Surg, Kaohsiung, Taiwan
[6] Natl Yang Ming Chiao Tung Univ, Inst Emergency & Crit Care Med, Taipei, Taiwan
[7] Natl Sun Yat Sen Univ, Dept Biol Sci, Kaohsiung, Taiwan
[8] Taipei Med Univ, Sch Med, Dept Surg, Taipei, Taiwan
[9] Taipei Vet Gen Hosp, Dept Surg, Div Cardiovasc Surg, Taipei, Taiwan
[10] Natl Tainan Inst Nursing, Dept Nursing, Tainan, Taiwan
[11] Natl Yang Ming Univ, Sch Med, Dept Surg, Taipei, Taiwan
[12] Natl Sun Yat Sen Univ, Inst Biomed Sci, Kaohsiung, Taiwan
[13] Natl Sun Yat Sen Univ, Coll Med, Sch Med, Kaohsiung, Taiwan
关键词
High fructose diet; Perivascular adipose tissue; Adipose whitening; Mitochondrial dynamics; Vascular reactivity; COENZYME-Q10; SUPPLEMENTATION; INSULIN-RESISTANCE; ACID LEVELS; LEPTIN; HYPERTENSION; METAANALYSIS; ENDOTHELIUM; SENSITIVITY; BIOGENESIS; FUSION;
D O I
10.1186/s12986-023-00776-7
中图分类号
R15 [营养卫生、食品卫生]; TS201 [基础科学];
学科分类号
100403 ;
摘要
Excessive fructose intake presents the major risk factor for metabolic cardiovascular disease. Perivascular adipose tissue (PVAT) is a metabolic tissue and possesses a paracrine function in regulating aortic reactivity. However, whether and how PVAT alters vascular function under fructose overconsumption remains largely unknown. In this study, male Sprague-Dawley rats (8 weeks old) were fed a 60% high fructose diet (HFD) for 12 weeks. Fasting blood sugar, insulin, and triglycerides were significantly increased by HFD intake. Plasma adiponectin was significantly enhanced in the HFD group. The expression of uncoupling protein 1 (UCP1) and mitochondrial mass were reduced in the aortic PVAT of the HFD group. Concurrently, the expression of peroxisome proliferator-activated receptor-gamma coactivator 1 alpha (PGC-1 alpha) and mitochondrial transcription factor A (TFAM) were suppressed. Furthermore, decreased fusion proteins (OPA1, MFN1, and MFN2) were accompanied by increased fission proteins (FIS1 and phospho-DRP1). Notably, the upregulated alpha-smooth muscle actin (alpha-SMA) and osteocalcin in the PVAT were concurrent with the impaired reactivity of aortic contraction and relaxation. Coenzyme Q10 (Q, 10 mg/100 mL, 4 weeks) effectively reversed the aforementioned events induced by HFD. Together, these results suggested that the dysregulation of mitochondrial dynamics mediated HFD-triggered PVAT whitening to impair aortic reactivity. Fortunately, coenzyme Q10 treatment reversed HFD-induced PVAT whitening and aortic reactivity.
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页数:15
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