Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0011860 (type 2 diabetes)
 57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A number of disease states, including type 2 diabetes (T2D), are associated with an increased risk of pulmonary infection. Glucagon-like peptide-1 (GLP-1) receptor agonists are used to treat T2D and exert anti-inflammatory actions through a single, well-defined GLP-1 receptor (GLP-1R). Although highly expressed in the lung, little is known about the role of the GLP-1R in the context of pulmonary inflammation. Here we examined the consequences of gain or loss of GLP-1R activity in infectious and noninfectious lung inflammation. We studied wild-type mice treated with a GLP-1R agonist, and Glp1r-/- mice, in the setting of bleomycin-induced noninfectious lung injury and influenza virus infection. Loss of the GLP-1R attenuated the severity of bleomycin-induced lung injury, whereas activation of GLP-1R signaling increased pulmonary inflammation via the sympathetic nervous system. In contrast, GLP-1R agonism reduced the pathogen load in mice with experimental influenza virus infection in association with increased expression of intracellular interferon-inducible GTPases. Notably, the GLP-1 receptor agonist liraglutide improved the survival rate after influenza virus infection. Our results reveal context-dependent roles for the GLP-1 system in the response to lung injury. Notably, the therapeutic response of GLP-1R agonism in the setting of experimental influenza virus infection may have relevance for ongoing studies of GLP-1R agonism in people with T2D susceptible to viral lung injury.
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PMID:GLP-1 Receptor Signaling Differentially Modifies the Outcomes of Sterile vs Viral Pulmonary Inflammation in Male Mice. 3312 41

Diabetic ketoacidosis is typically associated with type I diabetes mellitus, but it can be associated with type II diabetes mellitus under the conditions of extreme stress or as a presenting manifestation of ketosis-prone type II diabetes mellitus. A 38-year-old prediabetic male presented to the emergency room with hyperglycemia six weeks after recovery from coronavirus disease 2019 (COVID-19) pneumonia. Laboratory results showed severe hyperglycemia, metabolic acidosis, positive ketones in urine and blood, and elevated fasting C- peptide level. COVID-19 polymerase chain reaction (PCR) was negative, and immunoglobulin G (IgG) antibodies were positive. The workup was completely unremarkable for acute infection. Hemoglobin A1C increased from 6.1% to 10.8% within six weeks. The mechanism by which COVID-19 infection may trigger the onset of full-blown diabetes mellitus remains unknown. Viral infection may cause the direct destruction of pancreatic beta cells or trigger the changes in the body that induce the state of insulin resistance. Antibodies against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection may cross-react or interfere with the functioning of endogenous insulin. The association between type II diabetes and COVID-19 infections needs additional investigations to ascertain the exact mechanism by which COVID-19 infection triggers the onset of full-blown diabetes mellitus.
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PMID:Onset of Ketosis-Prone Diabetes in the Setting of COVID-19 Infection. 3315 47

Nuclear factor erythroid 2-related factor 2 (Nrf2) is an essential transcription factor that maintains the cell's redox balance state and reduces inflammation in different adverse stresses. Under the oxidative stress, Nrf2 is separated from Kelch-like ECH-associated protein 1 (Keap1), which is a key sensor of oxidative stress, translocated to the nucleus, interacts with the antioxidant response element (ARE) in the target gene, and then activates the transcriptional pathway to ameliorate the cellular redox condition. Curcumin is a yellow polyphenolic curcuminoid from Curcuma longa (turmeric) that has revealed a broad spectrum of bioactivities, including antioxidant, anti-inflammatory, anti-tumor, and anti-viral activities. Curcumin significantly increases the nuclear expression levels and promotes the biological effects of Nrf2 via the interaction with Cys151 in Keap1, which makes it a marvelous therapeutic candidate against a broad range of oxidative stress-related diseases, including type 2 diabetes (T2D), neurodegenerative diseases (NDs), cardiovascular diseases (CVDs), cancers, viral infections, and more recently SARS-CoV-2. Currently, the multifactorial property of the diseases and lack of adequate medical treatment, especially in viral diseases, result in developing new strategies to finding potential drugs. Curcumin potentially opens up new views as possible Nrf2 activator. However, its low bioavailability that is due to low solubility and low stability in the physiological conditions is a significant challenge in the field of its efficient and effective utilization in medicinal purposes. In this review, we summarized recent studies on the potential effect of curcumin to activate Nrf2 as the design of potential drugs for a viral infection like SARS-Cov2 and acute and chronic inflammation diseases in order to improve the cells' protection.
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PMID:Anti-Viral Potential and Modulation of Nrf2 by Curcumin: Pharmacological Implications. 3329 60


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