Scope: The hypothalamus is a key brain region involved in the control of feeding and energy expenditure. Hypothalamic inflammation and oxidative stress are landmarks of both obesity and aging processes, although the molecular mechanisms are still unknown. Procedures: Male Wistar rats were divided into two groups: control group, receiving standard diet CD, and treated group, receiving HFD. Both groups were treated with the appropriate diet for 1, 3, 6, 12, or 18 weeks. We investigated energy balance and body composition, as well as lipid profile, homeostatic model assessment index, and inflammatory state in serum. Furthermore, we also analyzed, at hypothalamic level, inflammation and oxidative stress, and adenosine monophosphate-dependent kinase AMPK and pAMPK expression levels. Results: Our data showed that aging and HFD induce increased energy intake and energy efficiency and decreased energy expenditure associated, at hypothalamic level, with inflammation and oxidative stress and activation of AMPK. Conclusion: Our results indicate that the age at which HFD feeding starts and the diet duration are critical in obesity development. The prolonged activation of hypothalamic AMPK may be related to the alterations in energy homeostasis. The prevalence of obesity is progressively increasing worldwide and is reaching epidemic proportions.
Because glial cells have been described as mediators of inflammatory processes in the brain, the existence of a causal link between hypothalamic inflammation and the deregulations of feeding behavior, leading to involuntary weight loss or obesity for example, has been suggested. Several inflammatory pathways that could impair the hypothalamic control of energy balance have been studied over the years such as, among others, toll-like receptors and canonical cytokines. This review discusses the different inflammatory pathways that have been identified so far in the hypothalamus in the context of feeding behavior and body weight control impairments, with a particular focus on chemokines signaling that opens a new avenue in the understanding of the major role played by inflammation in obesity. Energy balance is finely regulated via a bidirectional communication between the brain and the peripheral organs. One brain area is particularly important in this regulation: the hypothalamus. Numerous studies, based either on lesion, pharmacological, or genetic approaches, indeed confirmed this [for review see Ref. Interestingly, hypothalamic inflammation has already been linked to energy balance disruptions: high-grade hypothalamic inflammation has been associated to involuntary weight loss and, on the contrary, low-grade hypothalamic inflammation has been associated to obesity 2, 3. Importantly, these feeding behavior deregulations represent major public health issues, especially obesity. Indeed, obesity, which keeps developing since the end of the 20th century, is often associated to potentially deadly comorbidities such as diabetes, cardiovascular diseases, liver diseases, and cancers.
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