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

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

Author Masi, Laureane Nunes Google Scholar
Martins, Amanda Roque Google Scholar
Crisma, Amanda Rabello Google Scholar
do Amaral, Catia Lira Google Scholar
Davanso, Mariana Rodrigues Google Scholar
Afonso Serdan, Tamires Duarte Google Scholar
Cavalcante da Cunha de Sa, Roberta Dourado Autor UNIFESP Google Scholar
Cruz, Maysa Mariana Autor UNIFESP Google Scholar
Cardoso Alonso-Vale, Maria Isabel Autor UNIFESP Google Scholar
Torres, Rosngela Pavan Google Scholar
Mancini-Filho, Jorge Google Scholar
Bertaglia Pereira, Joice Naiara Google Scholar
da Silva Righetti, Marta Maria Google Scholar
Liberti, Edson Aparecido Google Scholar
Hirabara, Sandro Massao Google Scholar
Curi, Rui Google Scholar
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-alpha 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-1 beta, 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.
xmlui.dri2xhtml.METS-1.0.item-coverage London
Language English
Sponsor CAPES
CNPq
FAPESP
Guggenheim Foundation
Grant number CAPES
CNPq
FAPESP
Guggenheim Foundation
Date 2017
Published in Scientific Reports. London, v. 7, p. -, 2017.
ISSN 2045-2322 (Sherpa/Romeo, impact factor)
Publisher Nature Publishing Group
Extent -
Origin http://dx.doi.org/10.1038/s41598-017-04308-1
Access rights ACESSO ABERTO
Type Article
Web of Science ID WOS:000403840000009
URI https://repositorio.unifesp.br/handle/11600/53643

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