Abstract
First seen as a storage organ, the white adipose tissue (WAT) is now considered as an endocrine organ. WAT can produce an array of bioactive factors known as adipokines acting at physiological level and playing a vital role in energy metabolism as well as in immune response. The global effect of adipokines in metabolic activities is well established, but their impact on the physiology and the pathophysiology of the central nervous system (CNS) remains poorly defined. Adipokines are not only produced by the WAT but can also be expressed in the CNS where receptors for these factors are present. When produced in periphery and to affect the CNS, these factors may either cross the blood brain barrier (BBB) or modify the BBB physiology by acting on cells forming the BBB. Adipokines could regulate neuroinflammation and oxidative stress which are two major physiological processes involved in neurodegeneration and are associated with many chronic neurodegenerative diseases. In this review, we focus on four important adipokines (leptin, resistin, adiponectin, and TNFα) and one lipokine (lysophosphatidic acid—LPA) associated with autotaxin, its producing enzyme. Their potential effects on neurodegeneration and brain repair (neurogenesis) will be discussed. Understanding and regulating these adipokines could be an interesting lead to novel therapeutic strategy in order to counteract neurodegenerative disorders and/or promote brain repair.
Highlights
Obesity and type 2 diabetes mellitus (T2DM) are main health issues in our modern societies and constitute very important public health challenges [1,2,3]
While the causal nature of all the processes leading to neurodegeneration has not been definitively established, it is widely accepted that neuroinflammation and oxidative stress responses occur with clinical manifestation of the disease
We described the impact of proinflammatory adipokines (TNFα and leptin) on brain homeostasis and functions
Summary
Obesity and type 2 diabetes mellitus (T2DM) are main health issues in our modern societies and constitute very important public health challenges [1,2,3]. One result from excess body weight and physical inactivity is the dramatic development of type 2 diabetes that WHO has predicted to be the seventh leading cause of death in. An increasing number of data recently highlights that metabolic syndrome, notably obesity and type 2 diabetes, are correlated with an increased risk to develop dementia and/or neurodegenerative diseases such as AD, as well as neurological and neurovascular disorders [8,9,10,11]. Breaking the paradigm, recent studies show that underweight people (BMI < 20 kg/m2) display higher risk of dementia while very obese people (BMI > 40 kg/m2) have lower dementia risk than healthy weight people [15]. It has been suggested that the misexpression of adipose-derived factors called adipokines or adipocytokines may disrupt directly or indirectly brain homeostasis and functions
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