Alteration in the number of neuronal and non-neuronal cells in mouse models of obesity.
Mayara M AndradeCaroline FernandesLeticia Forny-GermanoRafaella A GonçalvesMichelle GomesEmily Castro-FonsecaAngela M Ramos-LoboFernanda Tovar-MollCarlos Humberto Andrade-MoraesJose DonatoFernanda G De FelicePublished in: Brain communications (2023)
Obesity is defined as abnormal or excessive fat accumulation that may impair health and is a risk factor for developing other diseases, such as type 2 diabetes and cardiovascular disorder. Obesity is also associated with structural and functional alterations in the brain, and this condition has been shown to increase the risk of Alzheimer's disease. However, while obesity has been associated with neurodegenerative processes, its impact on brain cell composition remains to be determined. In the current study, we used the isotropic fractionator method to determine the absolute composition of neuronal and non-neuronal cells in different brain regions of the genetic mouse models of obesity Lep ob/ob and LepR Null/Null . Our results show that 10- to 12-month-old female Lep ob/ob and LepR Null/Null mice have reduced neuronal number and density in the hippocampus compared to C57BL/6 wild-type mice. Furthermore, LepR Null/Null mice have increased density of non-neuronal cells, mainly glial cells, in the hippocampus, frontal cortex and hypothalamus compared to wild-type or Lep ob/ob mice, indicating enhanced inflammatory responses in different brain regions of the LepR Null/Null model. Collectively, our findings suggest that obesity might cause changes in brain cell composition that are associated with neurodegenerative and inflammatory processes in different brain regions of female mice.
Keyphrases
- high fat diet induced
- cerebral ischemia
- insulin resistance
- wild type
- type diabetes
- induced apoptosis
- metabolic syndrome
- resting state
- weight loss
- weight gain
- functional connectivity
- white matter
- cell cycle arrest
- adipose tissue
- subarachnoid hemorrhage
- oxidative stress
- brain injury
- healthcare
- public health
- cardiovascular disease
- mouse model
- single cell
- endoplasmic reticulum stress
- gene expression
- multiple sclerosis
- mental health
- physical activity
- bone marrow
- social media
- cell death
- genome wide
- prefrontal cortex