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L-精氨酸通过调节瘦素和增强高脂喂养雄性Wistar大鼠的PIK3活性来减轻心脏脂质和葡萄糖积累。

L-arginine mitigates cardiac lipid and glucose accumulation through leptin modulation and enhancement of PIK3 activities in high fat-fed male Wistar rats.

作者信息

Oyabambi Adewumi Oluwafemi, Bamidele Olubayode, Aindero Blessing Boluwatife, Awolola Adeoba Mobolaji

机构信息

Department of Physiology, Faculty of Basic Medical Sciences, College of Health Sciences, University of Ilorin, Ilorin, Nigeria.

Physiology Programme, Department of Physiology, College of Health Sciences, Bowen University, P.M.B. 284, Iwo, Osun State, Nigeria.

出版信息

Nutr Metab (Lond). 2024 Dec 4;21(1):103. doi: 10.1186/s12986-024-00852-6.

DOI:10.1186/s12986-024-00852-6
PMID:39633392
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11616303/
Abstract

BACKGROUND AND AIM

Insulin resistance and other metabolic risk factors are associated with increased cardiovascular diseases in animals fed with high fat diets (HFD). L-arginine is a semi-essential amino acid produced both endogenously and taken in the diet as supplements. It has been documented to possess antioxidant and anti-inflammatory properties and has been considered a plausible candidate for the management of metabolic disorders. Therefore, this study is aimed to determine the effects of L-arginine on lipid dysregulation and insulin resistance in high fat-fed male Wistar rats.

METHODS AND RESULTS

Twenty-four (24) male Wistar rats randomly selected into 4 groups, mean weight 110 ± 5 and, (n = 6) were fed rat chow + distilled water (vehicle); CTR, rat chow + L-arginine (150 mg/kg), HFD + vehicle, HFD + L-Arginine (150 mg/kg) for 6 weeks. The animals were anesthetized with 50 mg/kg pentobarbital sodium intraperitoneally, blood sample was taken via cardiac puncture and thereafter collected into a heparinized tube. Data were expressed as means ± SEM. HFD increased body weight gain, serum Insulin, Homeostasis model assessment of insulin resistance (HOMA-IR), area under the curve (AUC), leptin, Lipoprotein(a) or Lp(a), triglyceride-glucose index (TYG), triglycerides (TG), free fatty acids (FFAs), total cholesterol (TC), low density lipoprotein (LDL-C), TC/HDL-C, Log TG/HDL-C, TC-HDL-C)/HDL-C but decreased phospoinositide-3-kinase (PIK3) when compared with control. L-arginine, resulted in significant reduction in weight gain, fasting blood sugar (FBS), insulin, AUC, HOMA-IR, leptin, while increasing PIK3, Lp(a), TG, TC and FFA when compared with HFD.

CONCLUSION

The amelioration of lipid and glucose accumulation by L-arginine supplementation in high fat diet-fed male Wistar rats is accompanied by reduced leptin levels and PIK3 augmentation.

摘要

背景与目的

在高脂饮食(HFD)喂养的动物中,胰岛素抵抗和其他代谢危险因素与心血管疾病的增加有关。L-精氨酸是一种半必需氨基酸,可内源性产生并作为饮食补充剂摄入。已有文献证明它具有抗氧化和抗炎特性,并被认为是治疗代谢紊乱的一个合理候选物。因此,本研究旨在确定L-精氨酸对高脂喂养的雄性Wistar大鼠脂质代谢失调和胰岛素抵抗的影响。

方法与结果

将24只雄性Wistar大鼠随机分为4组,平均体重110±5,每组6只,分别喂食大鼠饲料+蒸馏水(载体);对照组,大鼠饲料+L-精氨酸(150mg/kg),高脂饮食+载体,高脂饮食+L-精氨酸(150mg/kg),持续6周。用50mg/kg戊巴比妥钠腹腔注射麻醉动物,通过心脏穿刺采集血样,然后收集到肝素化管中。数据以平均值±标准误表示。与对照组相比,高脂饮食增加了体重增加、血清胰岛素、胰岛素抵抗的稳态模型评估(HOMA-IR)、曲线下面积(AUC)、瘦素、脂蛋白(a)或Lp(a)、甘油三酯-葡萄糖指数(TYG)、甘油三酯(TG)、游离脂肪酸(FFA)、总胆固醇(TC)、低密度脂蛋白(LDL-C)、TC/HDL-C、Log TG/HDL-C、(TC-HDL-C)/HDL-C,但降低了磷酸肌醇-3-激酶(PIK3)。与高脂饮食组相比,L-精氨酸导致体重增加、空腹血糖(FBS)、胰岛素、AUC、HOMA-IR、瘦素显著降低,同时增加了PIK3、Lp(a)、TG、TC和FFA。

结论

在高脂饮食喂养的雄性Wistar大鼠中,补充L-精氨酸改善脂质和葡萄糖积累的同时伴随着瘦素水平降低和PIK3增加。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a091/11616303/08f30b39b597/12986_2024_852_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a091/11616303/e29f974024ca/12986_2024_852_Fig1_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a091/11616303/f8bb3def2b63/12986_2024_852_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a091/11616303/08f30b39b597/12986_2024_852_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a091/11616303/e29f974024ca/12986_2024_852_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a091/11616303/6b72d143b651/12986_2024_852_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a091/11616303/5026243486dd/12986_2024_852_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a091/11616303/64b11020c93f/12986_2024_852_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a091/11616303/f8bb3def2b63/12986_2024_852_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a091/11616303/08f30b39b597/12986_2024_852_Fig6_HTML.jpg

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