Abstract
High-fat diet (HFD) consumption can trigger chronic inflammation in some tissues. However, it remains unclear if HFD induces chronic inflammation in the spleen. This investigation aims to address the effect of HFD consumption and exercise intervention on the level of tumor necrosis factor alpha (TNF-α) in the spleen. Rats were subjected to HFD feeding and/or moderate-intensity treadmill running. The TNF-α levels in plasma and spleen were detected by ELISA. The mass and total cell numbers of the spleen were measured. In addition, the expression of TNF-α and its relevant gene mRNAs in macrophages from the spleen were analyzed by qRT-PCR. We found that HFD consumption did not significantly affect the mass and total cell numbers of the spleen. However, HFD consumption significantly increased splenic TNF-α level, the expression of TNF-α, toll-like receptor 4, and nuclear factor κB p65 mRNAs. In contrast, the expression of nicotinic acetylcholine receptor alpha 7 subunit (α7nAChR) mRNA in macrophages was downregulated. Additionally, exercise abolished the increase in splenic TNF-α level as well as the abnormal expression of TNF-α and related gene mRNAs in macrophages in HFD-fed rats. In conclusion, our results reveal that HFD consumption increases TNF-α level in the spleen, which is along with upregulation of the expression of TLR4 and NF-κB mRNAs as well as downregulation of the expression of α7nAChR mRNA in splenic macrophages in rats. Exercise abolished detrimental effects of HFD on TNF-α level in the spleen and prevented abnormal expression of these genes in the macrophages from rat spleen.
Highlights
Excessive consumption of a high-fat diet (HFD) has been well-known to contribute to the onset or development of some metabolic diseases, including obesity, type 2 diabetes mellitus, and insulin resistances [1]
We found that HFD consumption significantly increased the expression of tumor necrosis factor alpha (TNF-a) mRNA in splenic macrophages, and significant difference in the level of TNF-a expression was detected between HFD and control groups (p < 0.0001) (Figure 2A), suggesting that HFD consumption results in lowgrade inflammation in the spleen
We found that 4-week HFD consumption significantly increased TNF-a level in rat spleen, which was accompanied by upregulating the mRNA levels of TNF-a, toll-like receptor 4 (TLR4), and nuclear factor kB (NF-kB) p65, and by downregulating the mRNA of a7nAChR in macrophages from rat spleen
Summary
Excessive consumption of a high-fat diet (HFD) has been well-known to contribute to the onset or development of some metabolic diseases, including obesity, type 2 diabetes mellitus, and insulin resistances [1]. Recent studies highlight a crucial role of chronic low-grade inflammatory process in HFD-induced adverse effects [3]. In the context of excessive consumption of HFD, it is not clear whether HFD triggers TNF-a increase in the spleen Given that both endotoxin lipopolysaccharide and fatty acids target common receptor [toll-like receptor 4 (TLR4)] [6, 7], we reason that excessive consumption of HFD may promote TNF-a production in the spleen. This investigation aims to analyze the effect of HFD consumption on TNF-a level in the plasma and the spleen. The results achieved may shed new light on the management of HFD consumption-associated diseases
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