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肥胖诱导饮食会导致沙鼠体重增加、全身代谢改变、脂肪组织炎症、肝脂肪变性和氧化应激()。

Obesity-induced diet leads to weight gain, systemic metabolic alterations, adipose tissue inflammation, hepatic steatosis, and oxidative stress in gerbils ().

作者信息

Ventura Luciana L A, Fortes Nathália C L, Santiago Helton C, Caliari Marcelo V, Gomes Maria A, Oliveira Dirce R

机构信息

Department of Parasitologia/Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais , Belo Horizonte , Minas Gerais , Brazil.

Department of Nutrição/Escola de Enfermagem, Universidade Federal de Minas Gerais , Belo Horizonte , Minas Gerais , Brazil.

出版信息

PeerJ. 2017 Mar 2;5:e2967. doi: 10.7717/peerj.2967. eCollection 2017.

DOI:10.7717/peerj.2967
PMID:28265495
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5337087/
Abstract

BACKGROUND

Nowadays, the number of obese people in the world has reached alarming proportions. During the expansion of adipose tissue, a number of functions such as activation and release of cytokines and hormones may be affected. This leads the body to a pro-inflammatory pattern, which may affect the proper functioning of many tissues. Thus, studying the mechanisms by which obesity induces physiological disorders is necessary, and may be facilitated by the use of animal models, in particular rodents. We sought to characterize the metabolic and adipose tissue changes resulting from a diet rich in fats and simple sugars in gerbils.

METHODS

We divided 14 gerbils into two experimental groups that received a diet rich in simple carbohydrates and fats with 5,86 kcal/g (OB,  = 7) or a standard diet with 4.15 kcal/g (CT;  = 7) for 11 weeks. The animals had free access to water and food. The animal weight and food consumption were measured weekly. Blood, adipose tissue and liver of each animal were collected at the end of experiment. The following parameters were determined: cholesterol (COL), triglycerides (TGL) and glycemia (GLI) in the plasma; cytokines (IL-6, IL-10 and TNF-α) and hormones (adiponectin and leptin) in adipose tissue; activity of superoxide dismutase (SOD) and catalase (CAT), extraction and differentiation of fat and histology in liver.

RESULTS

The consumption of a diet rich in simple carbohydrates and fats led to increased total body weight and increased relative weights of liver and adipose tissue. In addition, we observed increased fasting glucose levels and circulating triglycerides, along with high TNF-α production in adipose tissue and increased total fat, cholesterol and triglyceride contents in the liver, contributing to higher intensity of hepatic steatosis. On the other hand, the animals of this group showed depletion in the enzyme activity of SOD and CAT in the liver, as well as reduction of IL-10 and adiponectin levels in adipose tissue.

DISCUSSION

High intake of saturated fat and simple carbohydrates establish the gerbil as an experimental model for the study of metabolic and hepatic abnormalities resulting from obesity.

摘要

背景

如今,全球肥胖人数已达到惊人的比例。在脂肪组织扩张过程中,细胞因子和激素的激活与释放等多种功能可能会受到影响。这会使身体呈现促炎模式,可能影响许多组织的正常功能。因此,研究肥胖诱发生理紊乱的机制很有必要,使用动物模型,特别是啮齿动物,可能会有助于这一研究。我们试图描述富含脂肪和单糖的饮食对沙鼠代谢和脂肪组织变化的影响。

方法

我们将14只沙鼠分为两个实验组,一组喂食富含单糖和脂肪的饮食,热量为5.86千卡/克(肥胖组,n = 7),另一组喂食标准饮食,热量为4.15千卡/克(对照组,n = 7),持续11周。动物可自由获取水和食物。每周测量动物体重和食物摄入量。实验结束时收集每只动物的血液、脂肪组织和肝脏。测定以下参数:血浆中的胆固醇(COL)、甘油三酯(TGL)和血糖(GLI);脂肪组织中的细胞因子(白细胞介素-6、白细胞介素-10和肿瘤坏死因子-α)和激素(脂联素和瘦素);肝脏中超氧化物歧化酶(SOD)和过氧化氢酶(CAT)的活性、脂肪的提取与分化以及组织学。

结果

食用富含单糖和脂肪的饮食导致总体重增加,肝脏和脂肪组织的相对重量增加。此外,我们观察到空腹血糖水平和循环甘油三酯升高,脂肪组织中肿瘤坏死因子-α产生增加,肝脏中总脂肪、胆固醇和甘油三酯含量增加,导致肝脂肪变性强度更高。另一方面,该组动物肝脏中SOD和CAT的酶活性降低,脂肪组织中白细胞介素-10和脂联素水平降低。

讨论

高饱和脂肪和单糖摄入量使沙鼠成为研究肥胖引起的代谢和肝脏异常的实验模型。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2bd6/5337087/1ce53c7563d7/peerj-05-2967-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2bd6/5337087/a791d90c16d8/peerj-05-2967-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2bd6/5337087/5d58ebd7e1fe/peerj-05-2967-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2bd6/5337087/7b5ffbcef443/peerj-05-2967-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2bd6/5337087/f2a9f4d6df7f/peerj-05-2967-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2bd6/5337087/1ce53c7563d7/peerj-05-2967-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2bd6/5337087/a791d90c16d8/peerj-05-2967-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2bd6/5337087/5d58ebd7e1fe/peerj-05-2967-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2bd6/5337087/7b5ffbcef443/peerj-05-2967-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2bd6/5337087/f2a9f4d6df7f/peerj-05-2967-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2bd6/5337087/1ce53c7563d7/peerj-05-2967-g005.jpg

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