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Influence of Mitochondrial NAD(P) + Transhydrogenase (NNT) on Hypothalamic Inflammation and Metabolic Dysfunction Induced by a High-Fat Diet in Mice.
Horm Metab Res
October 2024
Department of Pathology, State University of Campinas (UNICAMP), Campinas, Brazil.
Article Synopsis
- The study investigates the role of the mitochondrial protein NNT in obesity-related metabolic issues, using a specific mouse model lacking NNT genetic material.
- Unlike previous studies, this research utilized a high-fat diet (45% calories from fat) that better represents typical fat-rich diets compared to the usual 60%.
- Results show that mice without NNT gained less weight on a high-fat diet but had poorer glucose tolerance, while also revealing an increase in brown adipose tissue mass and inflammatory markers in the hypothalamus associated with diet-induced inflammation.
NOD alleles at Idd1 and Idd2 loci drive exocrine pancreatic inflammation.
Immunogenetics
December 2024
Département de microbiologie, infectiologie et immunologie, Université de Montréal, Montréal, QC, Canada.
Non-obese diabetic (NOD) mice spontaneously develop autoimmune diabetes and have enabled the identification of several loci associated with diabetes susceptibility, termed insulin-dependent diabetes (Idd). The generation of congenic mice has allowed the characterization of the impact of several loci on disease susceptibility. For instance, NOD.
View Article and Find Full Text PDFDeficiency of interleukin-1 receptor antagonist in mice differentially affects bone properties under different genomic backgrounds.
Sci Rep
August 2024
Department of Orthopaedic Surgery and Biomedical Engineering, University of Tennessee Health Science Center, Memphis, TN, 38163, USA.
When IL-1 receptor antagonist (IL-1rn) is knocked out, mice have shown strain background dependent and major QTL regulated susceptibility to spontaneously inflammatory arthritis disease (SAD). The impact on bone properties resulting from the interactions of IL-1rn, genomic background strains, and the QTL locus, is unknown. Bone properties in the four specifically bred mouse strains with mutation of IL-1rn and variations in genomic components were investigated with high-resolution MicroCT and genomic analytical tools.
View Article and Find Full Text PDFEpilepsy and sudden unexpected death in epilepsy in a mouse model of human -linked developmental and epileptic encephalopathy.
Brain Commun
October 2023
Department of Pharmacology, University of Michigan Medical School, Ann Arbor, MI 48109, USA.
Voltage-gated sodium channel β1 subunits are essential proteins that regulate excitability. They modulate sodium and potassium currents, function as cell adhesion molecules and regulate gene transcription following regulated intramembrane proteolysis. Biallelic pathogenic variants in , encoding β1, are linked to developmental and epileptic encephalopathy 52, with clinical features overlapping Dravet syndrome.
View Article and Find Full Text PDFUsing rodent data to elucidate dopaminergic mechanisms of ADHD: Implications for human personality.
Personal Neurosci
January 2024
Neurobiology Research Unit, Okinawa Institute of Science and Technology Graduate University, Okinawa, Japan.
An altered behavioral response to positive reinforcement has been proposed to be a core deficit in attention deficit hyperactivity disorder (ADHD). The spontaneously hypertensive rat (SHR), a congenic animal strain, displays a similarly altered response to reinforcement. The presence of this genetically determined phenotype in a rodent model allows experimental investigation of underlying neural mechanisms.
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