Hypothalamic Inflammation and Glioses as Aetiopathogenetic Factor in High Fat Diet Induced Obesity and Various Therapeutic Options to Resolve it.
Feeding HFD to rodents triggers inflammation and gliosis in the arcuate nucleus located in the mediobasal hypothalamus (MBH), even before obesity occurs9,12 and eventually reduces proopiomelanocortin cell number. Even though evidence exists from animal studies, the significance of this hypothalamic glioses in humans had largely been unknown.
Data from recent studies suggests that neuronal inflammation may be a downstream event during DIO, with recruitment and activation of hypothalamic glial cells being more proximal response to HFD exposure. This gliosis process involves accumulation and multiplication of activated microglia and astrocytes in the region of MBH. Various studies have implicated microglia in the development of diet-induced inflammatory signals along with metabolic dysfunction, but a similar role for astrocytes is not clear. Buckman demonstrated a modest role of astrocytic inflammation to caloric intake on the first day of HFD feeding but there was no analysis of susceptibility to DIO.
There are abundant astrocytes throughout the CNS and involved in many fundamental processes like synaptic transmission, neurovascular coupling, and blood-brain barrier maintenance.30 Additionally, astrocytes participate in CNS immune responses, when they take an activated phenotype having raised GFAP expression and release of proinflammatory cytokines which can enhance neurotoxicity and neurodegenerative disease progression. Hence, astrocytes have the basic requirement to affect energy homeostasis regulation in health and disease. MBH astrocytes modulate feeding behavior on pharmacological activation and show dynamic responses to circulating signals of nutrient availability like insulin and leptin.
Obes Res Open J. 2017; 4(2): 44-60.doi: 10.17140/OROJ-4-132