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mice ( Briggs et al . 2010 ). However, the mechanism underlying this unresponsiveness remains to be demonstrated. Immune-cell-mediated tissue inflammation in the adipose tissue, liver, and skeletal muscle plays a critical role in the development of

Introduction Type 2 diabetes mellitus (T2DM) has been recognized as an epidemic disease with low-grade chronic inflammation as its pivotal characteristic. Epidemiological studies show that inflammatory cytokines and LPS dramatically elevated

glucotoxicity, lipotoxicity, inflammation and cellular apoptosis ( Serrano Rios 1998 ). Among these complications, DN is a leading cause of end-stage kidney diseases and is associated with increased morbidity and mortality in diabetes. Under obesity

Introduction Obesity is characterized by chronic low-grade tissue inflammation that contributes to the development of insulin resistance, metabolic syndrome, and type 2 diabetes ( Hotamisligil 2006 ). Infiltration of immune cells into peripheral

endocrine organ that is profoundly affected by exercise. Exercise lessens WAT inflammation and improves systemic metabolic health, even in the settings of obesity ( Vieira et al . 2009 a , Welly et al . 2016 ), although the mechanisms are not fully

addition, clinical data have demonstrated that male hormones are independent factors contributing to the higher male susceptibility to cardiovascular diseases ( Ling et al . 2009 ). It is important to investigate the role of androgens in inflammation owing

repair of damaged or diseased organs; they also play an important role in signaling to immune cells during inflammation ( Lingen 2001 ). Immune cells Immune cells are mediators of the host defense system and play a central role in detecting and

gram-negative bacteria, is involved in atherosclerosis. It was proposed that bacteria such as Chlamydia pneumonia and Porphyromonas gingivalis might promote atherosclerosis by activating TLR4 and TLR4-mediated inflammation via LPS. In recent years

Kumar et al. 2014 , Roseno et al. 2015 ). However, more imperative to health and metabolism is the well-documented association between long-term HFD and the generation of inflammation. For example, it is well established that feeding a saturated

of liver inflammation, liver cell necrosis (hepatocyte ballooning), and liver fibrosis, which is also termed non-alcoholic steatohepatitis (NASH). NASH is thought to be the main cause of human cryptogenic cirrhosis. Histologically, NASH is similar to