Acute exposure to high-fat diets increases hepatic expression of genes related to cell repair and remodeling in female rats.

High-fat diets (HFD) promote the development of both obesity and fatty liver disease through the up-regulation of hepatic lipogenesis. Insulin resistance, a hallmark of both conditions, causes dysfunctional fuel partitioning and increases in lipogenesis. Recent work has demonstrated that systemic insulin resistance occurs in as little as the first 72 hours of an HFD, suggesting the potential for hepatic disruption with HFD at this time point.

Comparison of DEXA and QMR for assessing fat and lean body mass in adult rats.

There are several techniques used to measure body composition in experimental models including dual energy X-ray absorptiometry (DEXA) and quantitative magnetic resonance (QMR). DEXA/QMR data have been compared in mice, but have not been compared previously in rats. The goal of this study was to compare DEXA and QMR data in rats.

Manganese exposure inhibits the clearance of extracellular GABA and influences taurine homeostasis in the striatum of developing rats.

Manganese (Mn) accumulation in the brain has been shown to alter the neurochemistry of the basal ganglia. Mn-induced alterations in dopamine biology are fairly well understood, but recently more evidence has emerged characterizing the role of γ-aminobutyric acid (GABA) in this dysfunction. The purpose of this study was to determine if the previously observed Mn-induced increase in extracellular GABA (GABA(EC)) was due to altered GABA transporter (GAT) function, and whether Mn perturbs other amino acid neurotransmitters, namely taurine and glycine (known modulators of GABA).

Iron chelator deferoxamine alters iron-regulatory genes and proteins and suppresses osteoblast phenotype in fetal rat calvaria cells.

There are few studies describing the extent to which low iron status affects osteoblastogenesis, despite evidence that iron deficiency produces adverse effects on bone density. The purpose of this study was to evaluate alterations in intracellular iron status by measuring iron-regulated gene and protein expression and to describe development of osteoblast phenotype in primary cells treated with iron chelator deferoxamine (DFOM) during differentiation. Using the well-described fetal rat calvaria model, cells were incubated with 0-8 microM DFOM throughout differentiation (confluence to day (D) 21), or only during early differentiation (confluence to D13-15) or late differentiation (D13-15 to D21).

Extracellular norepinephrine, norepinephrine receptor and transporter protein and mRNA levels are differentially altered in the developing rat brain due to dietary iron deficiency and manganese exposure.

Manganese (Mn) is an essential trace element, but overexposure is characterized by Parkinson's like symptoms in extreme cases. Previous studies have shown that Mn accumulation is exacerbated by dietary iron deficiency (ID) and disturbances in norepinephrine (NE) have been reported. Because behaviors associated with Mn neurotoxicity are complex, the goal of this study was to examine the effects of Mn exposure and ID-associated Mn accumulation on NE uptake in synaptosomes, extracellular NE concentrations, and expression of NE transport and receptor proteins.

Manganese exposure alters extracellular GABA, GABA receptor and transporter protein and mRNA levels in the developing rat brain.

Unlike other essential trace elements (e.g., zinc and iron) it is the toxicity of manganese (Mn) that is more common in human populations than its deficiency.

Inhibition of DAT function attenuates manganese accumulation in the globus pallidus.

Manganese (Mn) is an essential nutrient, though exposure to high concentrations may result in neurotoxicity characterized by alterations in dopamine neurobiology. To date, it remains elusive how and why Mn targets dopaminergic neurons although recently the role of the dopamine transporter has been suggested. Our primary goal of this study was to examine the potential roles of the monoamine transporters, dopamine transporter (DAT), serotonin transporter (SERT) and norepinephrine transporter (NET), in neuronal Mn transport.

Brain manganese accumulation is inversely related to gamma-amino butyric acid uptake in male and female rats.

Iron (Fe) is an essential trace metal involved in numerous cellular processes. Iron deficiency (ID) is reported as the most prevalent nutritional problem worldwide. Increasing evidence suggests that ID is associated with altered neurotransmitter metabolism and a risk factor for manganese (Mn) neurotoxicity.