The role of AEBP1 in sex-specific diet-induced obesity.

Obesity is an important risk factor for heart disease, diabetes, and certain cancers, but the molecular basis for obesity is poorly understood. The transcriptional repressor AEBP1, which functions as a negative regulator of PTEN through a protein-protein interaction, is highly expressed in the stromal compartment of adipose tissues, including proliferative preadipocytes, and its expression is abolished in terminally differentiated, nonproliferative adipocytes. Here we show that transgenic overexpression of AEBP1 during adipogenesis coupled with a high-fat diet (HFD) resulted in massive obesity in female transgenic (AEBP1(TG)) mice via adipocyte hyperplasia.

Nitric oxide mediates an LPS-induced depression of cytochrome P450 (CYP1A) activity in astrocytes.

During inflammatory responses in the brain, the expression of cytochrome P450 isoforms in the CNS are modulated and the capacity of the brain to metabolize drugs and to synthesize or degrade certain endogenous chemicals and drugs is diminished. While this response can be attributed in part, to the production and action of cytokines within the brain, it is also likely that other inflammatory mediators play an integral role. This paper investigates a potential role for nitric oxide (NO) in the loss of cytochrome P450 (CYP1A) in the brain during inflammation.

The role of cytokines in the depression of CYP1A activity using cultured astrocytes as an in vitro model of inflammation in the central nervous system.

The interaction and modulation of hepatic cytochrome P450 enzymes by infection and inflammation has been well described both in clinical settings and in animal models. Recent evidence found that inflammation in the central nervous system (CNS) leads to alterations in cytochrome P450 activity in both brain and liver. The bacterial endotoxin lipopolysaccharide (LPS) was used to induce an inflammatory response in cultured astrocytes as a model of CNS inflammation.