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高脂肪饮食与甜炼乳联合应用可加重二者分别对小鼠引起的炎症和胰岛素抵抗。

Combination of a high-fat diet with sweetened condensed milk exacerbates inflammation and insulin resistance induced by each separately in mice.

机构信息

Interdisciplinary Post-graduate Program in Health Sciences, Cruzeiro of Sul University, Sao Paulo, Brazil.

Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, Brazil.

出版信息

Sci Rep. 2017 Jun 21;7(1):3937. doi: 10.1038/s41598-017-04308-1.

Abstract

Obesogenic diets increase body weight and cause insulin resistance (IR), however, the association of these changes with the main macronutrient in the diet remains to be elucidated. Male C57BL/6 mice were fed with: control (CD), CD and sweetened condensed milk (HS), high-fat (HF), and HF and condensed milk (HSHF). After 2 months, increased body weight, glucose intolerance, adipocyte size and cholesterol levels were observed. As compared with CD, HS ingested the same amount of calories whereas HF and HSHF ingested less. HS had increased plasma AST activity and liver type I collagen. HF caused mild liver steatosis and hepatocellular damage. HF and HSHF increased LDL-cholesterol, hepatocyte and adipocyte hypertrophy, TNF-α by macrophages and decreased lipogenesis and adiponectin in adipose tissue (AT). HSHF exacerbated these effects, increasing IR, lipolysis, mRNA expression of F4/80 and leptin in AT, Tlr-4 in soleus muscle and IL-6, IL-1β, VCAM-1, and ICAM-1 protein in AT. The three obesogenic diets induced obesity and metabolic dysfunction. HS was more proinflammatory than the HF and induced hepatic fibrosis. The HF was more detrimental in terms of insulin sensitivity, and it caused liver steatosis. The combination HSHF exacerbated the effects of each separately on insulin resistance and AT inflammatory state.

摘要

致肥饮食会增加体重并导致胰岛素抵抗(IR),然而,饮食中的主要宏量营养素与这些变化的关联仍有待阐明。雄性 C57BL/6 小鼠分别喂食以下饮食:对照饮食(CD)、CD 和甜炼乳(HS)、高脂肪饮食(HF)和 HF 和炼乳(HSHF)。两个月后,观察到体重增加、葡萄糖耐量受损、脂肪细胞增大和胆固醇水平升高。与 CD 相比,HS 摄入了相同量的热量,而 HF 和 HSHF 摄入的热量较少。HS 增加了血浆天冬氨酸氨基转移酶(AST)活性和肝脏 I 型胶原。HF 导致轻度肝脂肪变性和肝细胞损伤。HF 和 HSHF 增加了 LDL-胆固醇、肝细胞和脂肪细胞肥大、巨噬细胞产生的肿瘤坏死因子-α(TNF-α),并减少了脂肪组织(AT)中的脂肪生成和脂联素。HSHF 加剧了这些效应,增加了胰岛素抵抗、脂肪分解、AT 中 F4/80 和瘦素的 mRNA 表达、比目鱼肌中的 Tlr-4 以及 AT 中的 IL-6、IL-1β、VCAM-1 和 ICAM-1 蛋白。这三种致肥饮食均可诱导肥胖和代谢功能障碍。HS 比 HF 更具炎症性,并诱导肝纤维化。HF 在胰岛素敏感性方面的损害更大,且导致肝脂肪变性。HSHF 加剧了每种饮食单独对胰岛素抵抗和 AT 炎症状态的影响。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e44/5479812/4498a01595c9/41598_2017_4308_Fig1_HTML.jpg

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