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F&M-M36 通过β3-肾上腺素能受体/UCP1 信号减轻代谢综合征的风险因素并促进内脏脂肪褐变。

F&M-M36 Mitigates Risk Factors of Metabolic Syndrome and Promotes Visceral Fat Browning through β3-Adrenergic Receptor/UCP1 Signaling.

机构信息

Department of NEUROFARBA, Section of Pharmacology and Toxicology, University of Florence, Viale Pieraccini 6, 50139 Florence, Italy.

Enteric Neuroscience Program, Department of Medicine, Section of Gastroenterology and Hepatology, Mayo Clinic, Rochester, MN 55905, USA.

出版信息

Mar Drugs. 2023 May 17;21(5):303. doi: 10.3390/md21050303.

DOI:10.3390/md21050303
PMID:37233497
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10222845/
Abstract

Pre-metabolic syndrome (pre-MetS) may represent the best transition phase to start treatments aimed at reducing cardiometabolic risk factors of MetS. In this study, we investigated the effects of the marine microalga F&M-M36 () on cardiometabolic components of pre-MetS and its underlying mechanisms. Rats were fed a standard (5% fat) or a high-fat diet (20% fat) supplemented or not with 5% of or fenofibrate (100 mg/Kg) for 3 months. Like fenofibrate, decreased blood triglycerides ( < 0.01) and glucose levels ( < 0.01), increased fecal lipid excretion ( < 0.05) and adiponectin ( < 0.001) without affecting weight gain. Unlike fenofibrate, did not increase liver weight and steatosis, reduced renal fat ( < 0.05), diastolic ( < 0.05) and mean arterial pressure ( < 0.05). In visceral adipose tissue (VAT), , but not fenofibrate, increased the β3-adrenergic receptor (β3ADR) ( < 0.05) and Uncoupling protein 1 (UCP-1) ( < 0.001) while both induced glucagon-like peptide-1 receptor (GLP1R) protein expression ( < 0.001) and decreased interleukin (IL)-6 and IL-1β gene expression ( < 0.05). Pathway analysis on VAT whole-gene expression profiles showed that up-regulated energy-metabolism-related genes and down-regulated inflammatory and autophagy pathways. The multitarget activity of suggests that this microalga could be useful in mitigating risk factors of MetS.

摘要

预代谢综合征(pre-MetS)可能代表着开始治疗以降低代谢综合征心血管代谢风险因素的最佳过渡阶段。在这项研究中,我们研究了海洋微藻 F&M-M36()对 pre-MetS 的心血管代谢成分的影响及其潜在机制。大鼠喂食标准(5%脂肪)或高脂肪饮食(20%脂肪),并补充或不补充 5%的或非诺贝特(100mg/Kg),为期 3 个月。与非诺贝特一样,降低了血液甘油三酯(<0.01)和血糖水平(<0.01),增加了粪便脂质排泄(<0.05)和脂联素(<0.001),而体重增加不受影响。与非诺贝特不同,不增加肝脏重量和脂肪变性,减少肾脏脂肪(<0.05),降低舒张(<0.05)和平均动脉压(<0.05)。在内脏脂肪组织(VAT)中,与非诺贝特不同,增加了β3-肾上腺素能受体(β3ADR)(<0.05)和解偶联蛋白 1(UCP-1)(<0.001),而两者均诱导胰高血糖素样肽-1 受体(GLP1R)蛋白表达(<0.001)并降低白细胞介素(IL)-6 和白细胞介素(IL)-1β基因表达(<0.05)。VAT 全基因表达谱的通路分析表明,增加了与能量代谢相关的基因,并下调了炎症和自噬途径。的多靶点活性表明,这种微藻可用于减轻代谢综合征的风险因素。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/20e6/10222845/ae99ac773b91/marinedrugs-21-00303-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/20e6/10222845/f2c751fdd476/marinedrugs-21-00303-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/20e6/10222845/ffc5a3491edc/marinedrugs-21-00303-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/20e6/10222845/f6da12165c45/marinedrugs-21-00303-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/20e6/10222845/ae99ac773b91/marinedrugs-21-00303-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/20e6/10222845/f2c751fdd476/marinedrugs-21-00303-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/20e6/10222845/ffc5a3491edc/marinedrugs-21-00303-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/20e6/10222845/f6da12165c45/marinedrugs-21-00303-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/20e6/10222845/ae99ac773b91/marinedrugs-21-00303-g004.jpg

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