Acute and sustained inflammation and metabolic dysfunction induced by high refined carbohydrate‐containing diet in mice

Abstract

Objective The effects of high‐refined carbohydrate‐containing diet (HC) on inflammatory parameters and metabolic disarrangement of adipose tissue are poorly understood. The aim of this study was to evaluate the timing and progression of metabolic and inflammatory dysfunction induced by HC diet in mice. Design and Methods BALB/c mice were fed chow or HC diet for 1 and 3 days, 1, 2, 4, 6, 8, 10, and 12 weeks. Results Animals given HC diet exhibited acute and sustained increase in visceral adiposity, glucose intolerance, low insulin sensitivity, hyperlipemia, acute increase in mRNA expression of ACC, LPL, PPARγ, SREBP‐1, and ChREBP and altered circulating levels of adiponectin, resistin, and leptin. There was leucocyte rolling and adhesion on adipose tissue microvessels already at 3 days and until 8 weeks of HC diet. Adipose tissue of mice had increased number of macrophages (M1 and M2), lymphocytes (CD8+ and CD4+Foxp3+), and neutrophils (GR1+) already at 3 days after initiation of HC diet. Overall, concentration of cytokines and chemokines, TNF‐α, IL‐6, IL‐10, TGF‐β1, CCL2, and CXCL1, in adipose tissue was elevated throughout the experimental period. Levels of IL‐10 and TGF‐β1 tended to reach baseline levels at 12 weeks of HC diet. Conclusions We describe a novel murine model of fat pad expansion induced by HC diet that is characterized by early onset and sustained adipose tissue inflammation and metabolic disarrangement. The acute inflammatory response in adipose tissue occurs very early and is sustained, suggesting that adipose tissue inflammation is a homeostatic mechanism to regulate nutrient overload and adipose expansion.

Antihyperlipidemic and antihyperglycemic effects of the Brazilian salsaparrilhas Smilax brasiliensis Spreng. (Smilacaceae) and Herreria salsaparrilha Mart. (Agavaceae) in mice treated with a high-refined-carbohydrate containing diet

“…Many authors have shown that saponins can also reduce triglycerides in plasma, but the mechanism is not yet elucidated (Ebaid et al, 2006;Francis, Kerem, Makkar, & Becker, 2002;Gee & Johnson, 1988;Han et al, 2006;Milgate & Roberts, 1995;Oakenfull, 2001;Uemura et al, 2011;Wang et al, 2012). Previous studies in rats and BALB/c mice showed an increase in visceral fat after a long-term diet high in refined carbohydrates (Fortino et al, 2007;Oliveira et al, 2013). In our experiments, the animals fed the HC diet had a higher adiposity index, compared to the control animals, as expected.…”

“…Studies have shown that a long-term diet rich in carbohydrates (HC) is associated with increased visceral adiposity, minor oral glucose tolerance, lower insulin sensitivity and dyslipidemia, among other metabolic disorders (Ferreira, Mario, Porto, Andrade, & Botion, 2011;Lasker, Evans, & Layman, 2008;Oliveira et al, 2013). These conditions strongly influence the development of chronic diseases such as obesity, metabolic syndrome and cardiovascular diseases (Bressan, Hermsdorff, Zulet, & Martínez, 2009;Fortino, Lombardo, & Chicco, 2007;Oliveira, Versiani, Oliveira, Teixeira, & Brandão, 2014).…”

Trials of Diets for Treatment of Diabetes : A comparison of diets for treatment of type 2 diabetes, aspects on long and short term effects

“…Several mechanistic studies have reported that exposure to carbohydrates induces a pro-inflammatory response [73][74][75] . The type of carbohydrate may have a major influence on inflammation 76,77 . Also the nature of dietary fats can modulate inflammation.…”

Platelet-activating factor modulates fat storage in the liver induced by a high-refined carbohydrate-containing diet

“…The experimental protocol has been approved by the "Ethics Committee in Animal Experimentation at the Universidade Federal de Minas Gerais" (protocols: 84/2009 and 60/2010). In a first set of experiments, BALB/c mice were fed standard laboratory chow (LABINA ® ) or a high refined carbohydratecontaining (HC) diet as previously described [17] for the indicated periods in Results section. In a second set of experiments, we used a model of inflammatory hyporesponsiveness to analyze the effect of inflammation on liver steatosis and damage.…”