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Chronic GIPR agonism results in pancreatic islet GIPR functional desensitisation.
Mol Metab
January 2025
Section of Endocrinology and Investigative Medicine, Imperial College London, United Kingdom. Electronic address:
Objective: There is renewed interest in targeting the glucose-dependent insulinotropic polypeptide receptor (GIPR) for treatment of obesity and type 2 diabetes. G-protein coupled receptor desensitisation is suggested to reduce the long-term efficacy of glucagon-like-peptide 1 receptor (GLP-1R) agonists and may similarly affect the efficacy of GIPR agonists. We explored the extent of pancreatic GIPR functional desensitisation with sustained agonist exposure.
View Article and Find Full Text PDFDirect Induction of Buprenorphine Extended-Release: A Case Report.
J Addict Med
December 2024
From the Integrated Psychiatry, Pain, and Addiction Service, Vancouver General Hospital, Vancouver, British Columbia, Canada (PA, JSHW, JM, MN, VWL, MJI, NM); Department of Psychiatry, University of British Columbia, Vancouver, British Columbia, Canada (PA, MN, VWL, MJI, NM); Addictions and Concurrent Disorders Research Group, Department of Psychiatry, University of British Columbia, Vancouver, British Columbia, Canada (JSHW, RMK); Substance Use Response and Facilitation Service, BC Children's Hospital, Provincial Health Services Authority, Vancouver, British Columbia, Canada (MJI); BC Mental Health & Substance Use Services, Provincial Health Services Authority, Vancouver, British Columbia, Canada (NM); Bridge, Public Health Institute, Oakland, CA (AAH); Department of Emergency Medicine, Highland General Hospital-Alameda Health System, Oakland, CA (AAH); Department of Emergency Medicine, University of California, San Francisco, CA (AAH); The C4 Foundation, Coronado, CA (RM); British Columbia Centre for Excellence in HIV/AIDS, Vancouver, British Columbia, Canada (JSGM); Department of Medicine, Faculty of Medicine, University of British Columbia, Vancouver, British Columbia, Canada (JSGM); and Pharmacokinetics Modeling and Simulation Laboratory, Faculty of Pharmaceutical Sciences, University of British Columbia, Vancouver, British Columbia, Canada (ARM).
Buprenorphine has superior safety in opioid use disorder compared with alternatives due to its action as a partial opioid agonist, which limits its ability to cause respiratory depression. There is a risk of precipitated opioid withdrawal after buprenorphine exposure in someone using full opioid agonists. Buprenorphine induction strategies that avoid precipitated withdrawal remain a crucial component for starting buprenorphine in individuals actively using opioids.
View Article and Find Full Text PDFBackground: The increased incidence of Alzheimer's disease (AD) rate represent an unmet medical need and thus critical for the development of novel molecular therapeutics. Recent work focusing on patients with apoE4 alleles has highlighted the association of brain cholesterol dysregulation with elevated pathological burden and neurodegeneration. These studies have highlighted the importance of the nuclear receptor Liver X receptor (LXR) for developing AD therapies.
View Article and Find Full Text PDFBackground: Alzheimer's disease (AD) is characterized by hallmark amyloid plaques and neurofibrillary tangles as well as by a significant loss of myelin in the cerebral cortex and other brain regions, which contributes to neurodegeneration and cognitive decline. Remyelination, of the myelin sheath by oligodendrocytes, is a process that may be impaired in neurodegenerative diseases. Depending on the severity of the disease, there occurs loss or partial damage of the myelin sheath surrounding the neuron leading to memory deficits.
View Article and Find Full Text PDFBackground: VG-3927 is a highly potent, selective, brain penetrant, oral small molecule TREM2 agonist that is currently under development for the treatment of Alzheimer's disease (AD). TREM2, a receptor expressed on microglia in the brain is critical to microglial function in health and in disease. Among microglia-associated AD risk genes, partial loss-of-function variants of TREM2 confer 2-3 fold increase in risk for developing AD, motivating efforts to identify pharmacological agonists targeting TREM2 as a therapeutic option.
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