Mapping of Microglial Brain Region, Sex and Age Heterogeneity in Obesity.
Irina V MilanovaFelipe Corrêa da SilvaAndries KalsbeekChun-Xia YiPublished in: International journal of molecular sciences (2021)
The prevalence of obesity has increased rapidly in recent years and has put a huge burden on healthcare worldwide. Obesity is associated with an increased risk for many comorbidities, such as cardiovascular diseases, type 2 diabetes and hypertension. The hypothalamus is a key brain region involved in the regulation of food intake and energy expenditure. Research on experimental animals has shown neuronal loss, as well as microglial activation in the hypothalamus, due to dietary-induced obesity. Microglia, the resident immune cells in the brain, are responsible for maintaining the brain homeostasis and, thus, providing an optimal environment for neuronal function. Interestingly, in obesity, microglial cells not only get activated in the hypothalamus but in other brain regions as well. Obesity is also highly associated with changes in hippocampal function, which could ultimately result in cognitive decline and dementia. Moreover, changes have also been reported in the striatum and cortex. Microglial heterogeneity is still poorly understood, not only in the context of brain region but, also, age and sex. This review will provide an overview of the currently available data on the phenotypic differences of microglial innate immunity in obesity, dependent on brain region, sex and age.
Keyphrases
- type diabetes
- insulin resistance
- metabolic syndrome
- resting state
- weight loss
- white matter
- high fat diet induced
- weight gain
- cerebral ischemia
- functional connectivity
- cognitive decline
- inflammatory response
- healthcare
- cardiovascular disease
- neuropathic pain
- mild cognitive impairment
- lps induced
- adipose tissue
- lipopolysaccharide induced
- blood pressure
- skeletal muscle
- body mass index
- coronary artery disease
- cardiovascular risk factors
- subarachnoid hemorrhage
- cell proliferation
- induced apoptosis
- spinal cord injury
- endoplasmic reticulum stress
- cell death
- quality improvement
- oxidative stress
- diabetic rats
- cell cycle arrest
- mass spectrometry