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Calorie restriction and endurance exercise share potent anti-inflammatory function in adipose tissues in ameliorating diet-induced obesity and insulin resistance in mice.

Huang P, Li S, Shao M, Qi Q, Zhao F, You J, Mao T, Li W, Yan Z, Liu Y - Nutr Metab (Lond) (2010)

Bottom Line: The aim of this study was to directly compare the effects of CR and endurance exercise in a mouse model of diet-induced obesity and insulin resistance.CR dramatically prevented high-fat diet-induced metabolic abnormalities.CR and endurance exercise each potently suppressed the expression of inflammatory cytokines in white adipose tissues with additive effects when combined, but the effects of diet and exercise interventions in the liver were moderate to minimal.

View Article: PubMed Central - HTML - PubMed

Affiliation: Key Laboratory of Nutrition and Metabolism, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences; Graduate School of the Chinese Academy of Sciences; Chinese Academy of Sciences, 294 Taiyuan Road, Shanghai 200031, China. zhen.yan@virginia.edu.

ABSTRACT

Background: Calorie restriction (CR) and endurance exercise are known to attenuate obesity and improve the metabolic syndrome. The aim of this study was to directly compare the effects of CR and endurance exercise in a mouse model of diet-induced obesity and insulin resistance.

Methods: Adult male C57BL/6N mice were randomly assigned and subjected to one of the six interventions for 8 weeks: low-fat diet (LC, 10% fat), low-fat diet with 30% calorie restriction (LR), high-fat diet (HC, 60% fat), high-fat diet with 30% calorie restriction (HR), high-fat diet with voluntary running exercise (HE), and high-fat diet with a combination of 30% calorie restriction and exercise (HRE). The impacts of the interventions were assessed by comprehensive metabolic analyses and pro-inflammatory cytokine gene expression.

Results: Endurance exercise significantly attenuated high-fat diet-induced obesity. CR dramatically prevented high-fat diet-induced metabolic abnormalities. A combination of CR and endurance exercise further reduced obesity and insulin resistance under the condition of high-fat diet. CR and endurance exercise each potently suppressed the expression of inflammatory cytokines in white adipose tissues with additive effects when combined, but the effects of diet and exercise interventions in the liver were moderate to minimal.

Conclusions: CR and endurance exercise share a potent anti-inflammatory function in adipose tissues in ameliorating diet-induced obesity and insulin resistance.

No MeSH data available.


Related in: MedlinePlus

Selective suppression by restricted food intake versus exercise of the mRNA expression levels of inflammatory cytokines in adipose tissues. The mRNA expression levels were determined by quantitative RT-PCR for (A) osteopontin (OPN), (B) tumor necrosis factor-α (TNF-α), (C) monocyte chemoattractant protein-1 (MCP-1) and (D) interlukin-6 (IL-6) in white adipose tissues and the liver of mice subjected to food restriction versus exercise for 8 weeks. Data are shown as means ± SEM (n = 6/group). Statistical analyses were done with one-way ANOVA. *p < 0.05, **p < 0.01 vs. LC; #p < 0.05, ##p < 0.01 vs. HC; Δp < 0.05, ΔΔp < 0.01 vs. HRE; N.S.: not significant.
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Figure 6: Selective suppression by restricted food intake versus exercise of the mRNA expression levels of inflammatory cytokines in adipose tissues. The mRNA expression levels were determined by quantitative RT-PCR for (A) osteopontin (OPN), (B) tumor necrosis factor-α (TNF-α), (C) monocyte chemoattractant protein-1 (MCP-1) and (D) interlukin-6 (IL-6) in white adipose tissues and the liver of mice subjected to food restriction versus exercise for 8 weeks. Data are shown as means ± SEM (n = 6/group). Statistical analyses were done with one-way ANOVA. *p < 0.05, **p < 0.01 vs. LC; #p < 0.05, ##p < 0.01 vs. HC; Δp < 0.05, ΔΔp < 0.01 vs. HRE; N.S.: not significant.

Mentions: Obesity often leads to macrophage infiltration in adipose tissues, promoting the production of pro-inflammatory cytokines that contribute to the development of the metabolic syndrome and cardiovascular abnormalities [6]. To evaluate the physiological basis of the impact of CR and endurance exercise interventions, we measured pro-inflammatory cytokine mRNAs in the white adipose tissues as well as in the liver. Osteopontin (OPN), TNF-α, MCP-1 and IL-6 mRNAs in white adipose tissues were significantly up-regulated (2-8 fold) by high-fat diet feeding. Endurance exercise significantly reduced their levels, whereas CR brought these mRNAs to levels equal to or lower than those in mice on the low-fat diet. When CR was combined with endurance exercise, MCP-1 and IL-6 mRNAs were further reduced. On the contrary, in the liver, the induction of high-fat diet feeding on these pro-inflammatory cytokine mRNAs was much less (≤ 2-fold for OPN and TNF-α) or insignificant (MCP-1 and IL-6), and the impacts of CR and endurance exercise were moderate to minimal (Figure 6).


Calorie restriction and endurance exercise share potent anti-inflammatory function in adipose tissues in ameliorating diet-induced obesity and insulin resistance in mice.

Huang P, Li S, Shao M, Qi Q, Zhao F, You J, Mao T, Li W, Yan Z, Liu Y - Nutr Metab (Lond) (2010)

Selective suppression by restricted food intake versus exercise of the mRNA expression levels of inflammatory cytokines in adipose tissues. The mRNA expression levels were determined by quantitative RT-PCR for (A) osteopontin (OPN), (B) tumor necrosis factor-α (TNF-α), (C) monocyte chemoattractant protein-1 (MCP-1) and (D) interlukin-6 (IL-6) in white adipose tissues and the liver of mice subjected to food restriction versus exercise for 8 weeks. Data are shown as means ± SEM (n = 6/group). Statistical analyses were done with one-way ANOVA. *p < 0.05, **p < 0.01 vs. LC; #p < 0.05, ##p < 0.01 vs. HC; Δp < 0.05, ΔΔp < 0.01 vs. HRE; N.S.: not significant.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2914080&req=5

Figure 6: Selective suppression by restricted food intake versus exercise of the mRNA expression levels of inflammatory cytokines in adipose tissues. The mRNA expression levels were determined by quantitative RT-PCR for (A) osteopontin (OPN), (B) tumor necrosis factor-α (TNF-α), (C) monocyte chemoattractant protein-1 (MCP-1) and (D) interlukin-6 (IL-6) in white adipose tissues and the liver of mice subjected to food restriction versus exercise for 8 weeks. Data are shown as means ± SEM (n = 6/group). Statistical analyses were done with one-way ANOVA. *p < 0.05, **p < 0.01 vs. LC; #p < 0.05, ##p < 0.01 vs. HC; Δp < 0.05, ΔΔp < 0.01 vs. HRE; N.S.: not significant.
Mentions: Obesity often leads to macrophage infiltration in adipose tissues, promoting the production of pro-inflammatory cytokines that contribute to the development of the metabolic syndrome and cardiovascular abnormalities [6]. To evaluate the physiological basis of the impact of CR and endurance exercise interventions, we measured pro-inflammatory cytokine mRNAs in the white adipose tissues as well as in the liver. Osteopontin (OPN), TNF-α, MCP-1 and IL-6 mRNAs in white adipose tissues were significantly up-regulated (2-8 fold) by high-fat diet feeding. Endurance exercise significantly reduced their levels, whereas CR brought these mRNAs to levels equal to or lower than those in mice on the low-fat diet. When CR was combined with endurance exercise, MCP-1 and IL-6 mRNAs were further reduced. On the contrary, in the liver, the induction of high-fat diet feeding on these pro-inflammatory cytokine mRNAs was much less (≤ 2-fold for OPN and TNF-α) or insignificant (MCP-1 and IL-6), and the impacts of CR and endurance exercise were moderate to minimal (Figure 6).

Bottom Line: The aim of this study was to directly compare the effects of CR and endurance exercise in a mouse model of diet-induced obesity and insulin resistance.CR dramatically prevented high-fat diet-induced metabolic abnormalities.CR and endurance exercise each potently suppressed the expression of inflammatory cytokines in white adipose tissues with additive effects when combined, but the effects of diet and exercise interventions in the liver were moderate to minimal.

View Article: PubMed Central - HTML - PubMed

Affiliation: Key Laboratory of Nutrition and Metabolism, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences; Graduate School of the Chinese Academy of Sciences; Chinese Academy of Sciences, 294 Taiyuan Road, Shanghai 200031, China. zhen.yan@virginia.edu.

ABSTRACT

Background: Calorie restriction (CR) and endurance exercise are known to attenuate obesity and improve the metabolic syndrome. The aim of this study was to directly compare the effects of CR and endurance exercise in a mouse model of diet-induced obesity and insulin resistance.

Methods: Adult male C57BL/6N mice were randomly assigned and subjected to one of the six interventions for 8 weeks: low-fat diet (LC, 10% fat), low-fat diet with 30% calorie restriction (LR), high-fat diet (HC, 60% fat), high-fat diet with 30% calorie restriction (HR), high-fat diet with voluntary running exercise (HE), and high-fat diet with a combination of 30% calorie restriction and exercise (HRE). The impacts of the interventions were assessed by comprehensive metabolic analyses and pro-inflammatory cytokine gene expression.

Results: Endurance exercise significantly attenuated high-fat diet-induced obesity. CR dramatically prevented high-fat diet-induced metabolic abnormalities. A combination of CR and endurance exercise further reduced obesity and insulin resistance under the condition of high-fat diet. CR and endurance exercise each potently suppressed the expression of inflammatory cytokines in white adipose tissues with additive effects when combined, but the effects of diet and exercise interventions in the liver were moderate to minimal.

Conclusions: CR and endurance exercise share a potent anti-inflammatory function in adipose tissues in ameliorating diet-induced obesity and insulin resistance.

No MeSH data available.


Related in: MedlinePlus