Butcher, Masaki Fujita, Frank C
The assumption driving this overlap: glutathione's role in cellular detoxification must somehow accelerate or protect against the metabolic shifts GLP-1 medications trigger
Introduction Tuberculosis (TB) is a chronic infectious disease caused by an obligate pathogen, Mycobacterium tuberculosis (Mtb), in humans ( in vitro drug resistance to not only INH and RIF, but also all fluoroquinolones and at least one injectable aminoglycoside ( The presence of a mycobacterial population with more than one bacterial phenotype has been observed in patients with TB, as indicated by bacterial populations with varying growth dynamics in sputum samples ( Mycobacterial Persisters Adapt to Stresses in the Host and Exhibit Antibiotic Tolerance Antibiotic Tolerance Host-related stresses, such as hypoxia, acidic conditions, nutrient starvation, oxidative stress, and cytokine responses, alter the metabolic state of pathogens and eventually induces a drug-tolerant phenotype termed persister ( The mechanism of antibiotic tolerance through the formation of persisters in response to a variety of stresses, including nutrient deprivation, oxidative stress, acidic environment, osmotic conditions, and host immune-mediated stresses, has been described in many pathogenic bacteria, including Escherichia coli , Staphylococcus aureus , Pseudomonas aeruginosa , and Mtb ( Mtb Adapts to Host-Mediated Stresses Through Metabolic Regulation Regulation of Transcription Factors Mtb encounters various stresses, such as acidic pH, oxidative stress, hypoxia, nutrient deprivation, and cytokine-mediated effectors, during infection
Animal toxicology studies have not revealed significant adverse effects at therapeutic dose ranges
