Lipocalin 2 as a Link Between Metabolic Syndrome and Neuroinflammation
Obesity and its immediate consequences, such as non-alcoholic fatty liver disease and type 2 diabetes, are associated with greater neuroinflammation and risk of dementia. Excess visceral fat tissue does its part to produce chronic inflammation throughout the body, but here researchers focus on a specific metabolic dysregulation in the liver that produces inflammation in the brain. That inflammation in turn drives a faster progression towards neurodegenerative conditions. The lesson here, as in so much of this research: don't get fat, don't stay fat. You won't like the consequences.
Researchers have revealed the cause behind the previously established link between non-alcoholic fatty liver disease (i.e., NAFLD, recently reclassified as metabolic associated fatty liver disease or MAFLD) and neurological problems. The link they discovered, the unique role of an adipokine (Lipocalin-2) in causing neuroinflammation, may explain the prevalence of neurological Alzheimer's disease-like and Parkinson's disease-like phenotypes among individuals with MAFLD.
"Lipocalin 2 is one of the important mediators exclusively produced in the liver and circulated throughout the body among those who have nonalcoholic steatohepatitis - or NASH - which is a more advanced form of MAFLD. The research is immensely significant because MAFLD patients have been shown to develop Alzheimer's and Parkinson's-like symptoms as older adults. Scientists can use these results to advance our knowledge in neuroinflammatory complications in MAFLD and develop appropriate treatments."
Ninety percent of the obese population and 40-70 percent of those with type 2 diabetes appear to have MAFLD, according to the Centers for Disease Control and Prevention. In addition to overweight/obese status and diabetes, other risk factors include high cholesterol and/or triglycerides, high blood pressure and metabolic syndrome. These individuals have a higher risk for having diseased livers, which are associated with increased lipocalin 2 - as found in the present study. The lipocalin 2 circulates throughout the body at higher levels, possibly inducing inflammation in the brain.