Abstract
Obesity prevalence is increasing at an unprecedented rate throughout the world, and is a strong risk factor for metabolic, cardiovascular, and neurological/neurodegenerative disorders. While low-grade systemic inflammation triggered primarily by adipose tissue dysfunction is closely linked to obesity, inflammation is also observed in the brain or the central nervous system (CNS). Considering that the hypothalamus, a classical homeostatic center, and other higher cortical areas (e.g. prefrontal cortex, dorsal striatum, hippocampus, etc.) also actively participate in regulating energy homeostasis by engaging in inhibitory control, reward calculation, and memory retrieval, understanding the role of CNS oxidative stress and inflammation in obesity and their underlying mechanisms would greatly help develop novel therapeutic interventions to correct obesity and related comorbidities. Here we review accumulating evidence for the association between ER stress and mitochondrial dysfunction, the main culprits responsible for oxidative stress and inflammation in various brain regions, and energy imbalance that leads to the development of obesity. Potential beneficial effects of natural antioxidant and anti-inflammatory compounds on CNS health and obesity are also discussed.
Highlights
Obesity is considered today as a global health problem
Obesity-associated inflammation is causally linked to a host of metabolic changes, such as insulin resistance and impaired glucose metabolism that disrupt energy homeostasis [5], raising the urgency to gain a better understanding of the source(s) of inflammation and the underlying cellular/molecular mechanisms that initiate this inflammatory process
In support of this concept, high-fat diet (HFD) feeding increases brain inflammation in rats [21], and pro-inflammatory genes such as TNF-α and IL-6 are elevated in the mediobasal hypothalamus (MBH), the homeostatic brain center critical for the control of energy balance, long before they are present in liver or white adipose tissue (WAT) [22]
Summary
Obesity is considered today as a global health problem. Its prevalence stands at over 40% in the US alone, affecting more than 90 million adults and nearly 14 million children [1,2]. Given that the role of the brain is to integrate a myriad of nutrient-related signals and tightly control energy homeostasis through modulating the autonomic, endocrine, and behavioral effectors, it is reasonable to speculate that inflammation in the CNS may potentially serve as an important contributing factor to energy imbalance In support of this concept, high-fat diet (HFD) feeding increases brain inflammation in rats [21], and pro-inflammatory genes such as TNF-α and IL-6 are elevated in the mediobasal hypothalamus (MBH), the homeostatic brain center critical for the control of energy balance, long before they are present in liver or WAT [22]. We discuss current evidence on the roles of antioxidants and anti-inflammatory agents in obesity-related CNS oxidative stress and inflammation, and their potential uses to correct obesity
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