Publications by authors named "Monique Cristine Oliveira"
Cerebral ischemia-induced hyperglycemia has been reported to accentuate neurological damage following focal or global cerebral ischemia. Hyperglycemia found in rats following focal brain ischemia occurs in the first 24 h and has been claimed to be caused by increased liver gluconeogenesis and insulin resistance. However, liver gluconeogenesis and the mechanisms leading to hyperglycemia after global cerebral ischemia remain uncertain.
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- Severe rheumatoid cachexia leads to notable loss of muscle and fat mass in advanced rheumatoid arthritis patients, increasing the risk of cardiovascular diseases.
- Circulating levels of triglycerides (TG) and free fatty acids (FFA) are not well-defined in severe arthritis, prompting a study to explore lipid profiles and liver metabolism in arthritic rats.
- Findings show reduced TG and cholesterol levels in the serum and liver of arthritic rats, alongside higher FFA levels, indicating alterations in lipid metabolism driven by increased oxidation and reduced fatty acid synthesis in the arthritic liver.
Estrogen deficiency is associated with aging and increases the incidence of metabolic syndrome and hypertension. In this study, the effects of tibolone, a synthetic steroid, on the cardiovascular system, liver lipid metabolism, and redox status were evaluated, in ovariectomized (OVX) rats with renovascular hypertension (two-kidneys, one-clip, OVX + 2K1C). This study encompassed direct measurements of mean arterial pressure , plasma biochemical analysis, liver lipid contents, and assessments of the mitochondrial and peroxisomal β-oxidation capacities.
View Article and Find Full Text PDFLiver mitochondrial function and redox status in an experimental model of non-alcoholic fatty liver disease induced by monosodium L-glutamate in rats.
Exp Mol Pathol
December 2011
Article Synopsis
- The study aimed to explore the role of mitochondrial dysfunction in non-alcoholic fatty liver disease (NAFLD) using a rat model of obesity induced by monosodium L-glutamate (MSG).
- Results showed that liver mitochondria from these obese rats had increased fatty acid β-oxidation and oxidising capacity for succinate without impairing oxidative phosphorylation efficiency.
- The overall findings suggested that mitochondrial dysfunction does not contribute to liver fat accumulation in this model, and enhancements in specific enzyme activities may help defend against oxidative stress.
Article Synopsis
- The study examines how fat accumulation in the liver affects calcium movement and the liver's response to the hormone phenylephrine in obese rats.
- Researchers used rats with MSG-induced obesity to analyze calcium uptake in liver cells, finding reduced calcium absorption in the livers of obese rats due to decreased enzyme activity.
- Despite having similar glycogen levels, obese rat livers released more glucose in reaction to phenylephrine, suggesting altered metabolic responses linked to higher intracellular calcium levels.