Publications by authors named "Joao A Duarte"
Purpose: Recent literature has documented the relationship between fears of compassion and disordered eating attitudes and behaviours. However, research on the processes underlying this association is still in the early stages. As such, this study tested a mediator model where insecure striving and inflexible eating (i.
View Article and Find Full Text PDFCytosolic phosphoenolpyruvate carboxykinase as a cataplerotic pathway in the small intestine.
Am J Physiol Gastrointest Liver Physiol
August 2018
Article Synopsis
- - PEPCK is an enzyme in the liver and kidney involved in gluconeogenesis, with lesser roles in fatty acid and amino acid metabolism occurring in the small intestine, although its exact function there has been unclear.
- - Creating a mouse model lacking intestinal PEPCK revealed that while gluconeogenesis was abolished, blood sugar levels remained stable, suggesting its limited role in glucose regulation.
- - The knockout mice displayed reduced fat absorption and altered amino acid profiles, indicating that intestinal PEPCK primarily contributes to digesting dietary fats and processing amino acids rather than glucose production.
Article Synopsis
- - Mitochondria play a vital role in respiration and are particularly important in the liver for processes like gluconeogenesis, but during nonalcoholic fatty liver disease (NAFLD), they can produce reactive oxygen species (ROS) that harm liver cells and contribute to inflammation and insulin resistance.
- - Studies in mice showed that increased fatty acid delivery led to greater oxidative metabolism, which in turn elevated stress and inflammation, while knockout of a specific enzyme (Pck1) reduced these negative effects, indicating a strong link between metabolic processes and oxidative damage.
- - Using metformin to lower oxidative metabolism in the liver normalized the associated anabolic pathways and reduced inflammation, linking oxidative stress in human NAFLD cases to metabolic changes from high
Article Synopsis
- Intracellular lipids play a significant role in obesity-related diseases, and a new NMR method allows for quick lipidomic analysis alongside measurements of lipid synthesis pathways.
- The study used deuterated water to track lipid fluxes through processes like de novo lipogenesis and fatty acid synthesis in mice on different diets.
- Results showed that while high-fat diet mice increased certain lipid synthesis rates, de novo lipogenesis was low, indicating that most liver triglycerides came from reesterifying existing lipids rather than being newly created.
Background & Aims: Hepatic gluconeogenesis helps maintain systemic energy homeostasis by compensating for discontinuities in nutrient supply. Liver-specific deletion of cytosolic phosphoenolpyruvate carboxykinase (PEPCK-C) abolishes gluconeogenesis from mitochondrial substrates, deregulates lipid metabolism and affects TCA cycle. While the mouse liver almost exclusively expresses PEPCK-C, humans equally present a mitochondrial isozyme (PEPCK-M).
View Article and Find Full Text PDFColesevelam suppresses hepatic glycogenolysis by TGR5-mediated induction of GLP-1 action in DIO mice.
Am J Physiol Gastrointest Liver Physiol
February 2013
Bile acid sequestrants are nonabsorbable resins designed to treat hypercholesterolemia by preventing ileal uptake of bile acids, thus increasing catabolism of cholesterol into bile acids. However, sequestrants also improve hyperglycemia and hyperinsulinemia through less characterized metabolic and molecular mechanisms. Here, we demonstrate that the bile acid sequestrant, colesevelam, significantly reduced hepatic glucose production by suppressing hepatic glycogenolysis in diet-induced obese mice and that this was partially mediated by activation of the G protein-coupled bile acid receptor TGR5 and glucagon-like peptide-1 (GLP-1) release.
View Article and Find Full Text PDFBackground And Purpose: Blockade of adenosine A(2A) receptors (A(2A)R) affords robust neuroprotection in a number of brain conditions, although the mechanisms are still unknown. A likely candidate mechanism for this neuroprotection is the control of neuroinflammation, which contributes to the amplification of neurodegeneration, mainly through the abnormal release of pro-inflammatory cytokines such as interleukin(IL)-1β. We investigated whether A(2A)R controls the signaling of IL-1β and its deleterious effects in cultured hippocampal neurons.
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