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天然甜味剂和人工甜味剂与高脂肪饮食均可改变大鼠脂肪组织中差异味觉受体、胰岛素和 TLR4 介导的炎症通路。

Natural and Artificial Sweeteners and High Fat Diet Modify Differential Taste Receptors, Insulin, and TLR4-Mediated Inflammatory Pathways in Adipose Tissues of Rats.

机构信息

Departamento de Fisiología de la Nutrición, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, México City 14080, Mexico.

出版信息

Nutrients. 2019 Apr 19;11(4):880. doi: 10.3390/nu11040880.

DOI:10.3390/nu11040880
PMID:31010163
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6520815/
Abstract

It is difficult to know if the cause for obesity is the type of sweetener, high fat (HF) content, or the combination of sweetener and fat. The purpose of the present work was to study different types of sweeteners; in particular, steviol glycosides (SG), glucose, fructose, sucrose, brown sugar, honey, SG + sucrose (SV), and sucralose on the functionality of the adipocyte. Male Wistar rats were fed for four months with different sweeteners or sweetener with HF added. Taste receptors T1R2 and T1R3 were differentially expressed in the tongue and intestine by sweeteners and HF. The combination of fat and sweetener showed an additive effect on circulating levels of GIP and GLP-1 except for honey, SG, and brown sugar. In adipose tissue, sucrose and sucralose stimulated TLR4, and c-Jun N-terminal (JNK). The combination of HF with sweeteners increased NFκB, with the exception of SG and honey. Honey kept the insulin signaling pathway active and the smallest adipocytes in white (WAT) and brown (BAT) adipose tissue and the highest expression of adiponectin, PPARγ, and UCP-1 in BAT. The addition of HF reduced mitochondrial branched-chain amino transferase (BCAT2) branched-chain keto acid dehydrogenase E1 (BCKDH) and increased branched chain amino acids (BCAA) levels by sucrose and sucralose. Our data suggests that the consumption of particular honey maintained functional adipocytes despite the consumption of a HF diet.

摘要

很难确定肥胖的原因是甜味剂的类型、高脂肪(HF)含量还是甜味剂和脂肪的组合。本研究的目的是研究不同类型的甜味剂;特别是甜菊糖苷(SG)、葡萄糖、果糖、蔗糖、红糖、蜂蜜、SG+蔗糖(SV)和三氯蔗糖对脂肪细胞功能的影响。雄性 Wistar 大鼠用不同的甜味剂或添加 HF 的甜味剂喂养四个月。甜味剂和 HF 使舌和肠中味觉受体 T1R2 和 T1R3 呈现不同的表达。除了蜂蜜、SG 和红糖外,脂肪和甜味剂的组合对循环 GIP 和 GLP-1 水平表现出相加作用。在脂肪组织中,蔗糖和三氯蔗糖刺激 TLR4 和 c-Jun N 末端(JNK)。除了 SG 和蜂蜜外,HF 与甜味剂的组合增加了 NFκB。蜂蜜使胰岛素信号通路保持活跃,并使白色(WAT)和棕色(BAT)脂肪组织中的脂肪细胞最小化,BAT 中的脂联素、PPARγ 和 UCP-1 表达最高。HF 的添加降低了蔗糖和三氯蔗糖的支链氨基酸转移酶(BCAT2)支链酮酸脱氢酶 E1(BCKDH)和支链氨基酸(BCAA)水平。我们的数据表明,尽管食用高脂肪饮食,但某些蜂蜜的消耗可以维持功能性脂肪细胞。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/14ff/6520815/a7d996a2aaf3/nutrients-11-00880-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/14ff/6520815/b130a3a75cb7/nutrients-11-00880-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/14ff/6520815/eb4822973e9a/nutrients-11-00880-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/14ff/6520815/82ce420c6c9f/nutrients-11-00880-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/14ff/6520815/80dc3e71442c/nutrients-11-00880-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/14ff/6520815/0f14e29956bb/nutrients-11-00880-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/14ff/6520815/a7d996a2aaf3/nutrients-11-00880-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/14ff/6520815/b130a3a75cb7/nutrients-11-00880-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/14ff/6520815/eb4822973e9a/nutrients-11-00880-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/14ff/6520815/82ce420c6c9f/nutrients-11-00880-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/14ff/6520815/80dc3e71442c/nutrients-11-00880-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/14ff/6520815/0f14e29956bb/nutrients-11-00880-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/14ff/6520815/a7d996a2aaf3/nutrients-11-00880-g006.jpg

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