Liraglutide is a glucagon-like peptide-1 analog with pharmacokinetic properties suitable for once-daily administration approved by the Food and Drug Administration for the treatment of patients with type 2 diabetes. Clinical trial data from large, controlled studies demonstrate the safety and efficacy of liraglutide in terms of hemoglobin A(1c) (HbA(1c)) reduction, reductions in body weight, and the drug's low risk for hypoglycemic events when used as monotherapy. Liraglutide has been studied as monotherapy and in combination with metformin, glimepiride, and rosiglitazone for the treatment of type 2 diabetes. Additionally, comparative data with insulin glargine and exenatide therapy are available from Phase III trials. Once-daily administration may provide a therapeutic advantage for liraglutide over twice-daily exenatide, with similar improvements in HbA(1c) and body weight observed when liraglutide was compared with exenatide. The glucose-dependent mechanism of insulin release with incretin analog therapy holds potential clinical significance in the management of postprandial hyperglycemic excursions, with minimal risk of hypoglycemia when used with non-secretagogue medications. Data to date on patient-reported outcomes with liraglutide treatment are encouraging. The most common adverse events associated with liraglutide therapy are dose-dependent nausea, vomiting, and diarrhea. Diligent postmarketing surveillance to elucidate the risk of pancreatitis and medullary thyroid carcinoma in a heterogeneous population are likely warranted.
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J Microbiol Immunol Infect
January 2025
Institute of Clinical Medicine, College of Medicine, National Cheng Kung University, Tainan, 70101, Taiwan; Department of Pediatrics, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan, 70101, Taiwan. Electronic address:
Background: COVID-19 mRNA vaccines have demonstrated 95 % efficacy in the general population. However, their immunogenicity in adolescents with Type 1 Diabetes (T1D), who exhibit weaken immune responses, remains insufficiently explored.
Methods: Longitudinal analysis of innate immune responses following PRR-agonists and BNT162b2 vaccine stimulations, along with S-specific antibody responses, memory T cell recall responses, and RNA-sequencing were assessed in eight T1D adolescents and 16 healthy controls at six different timepoints.
Cell Signal
January 2025
Department of Endocrinology, The Third Xiangya Hospital, Central South University, 410007 Changsha, Hunan, China. Electronic address:
Type 1 diabetes (T1D) is an autoimmune disease characterized by hyperglycemia caused by the destruction of insulin-producing β cells. Viral infection is an important environmental factor which is associated with the islet autoimmunity in genetically susceptible individuals. Loss of β-cells and triggering of insulitis following viral infection could result from several non-exclusive mechanisms.
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January 2025
Kaiser Permanente Washington Health Research Institute, 1730 Minor Ave, Seattle, WA 98101, USA.
Ecotoxicol Environ Saf
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Department of Occupational and Environmental Health, School of Public Health, Dalian Medical University, No. 9 West Section Lvshun South Road, Dalian 116044, China; Global Health Research Center, Dalian Medical University, No. 9 West Section Lvshun South Road, Dalian 116044, China. Electronic address:
Sodium arsenite (NaAsO), the most common form of inorganic arsenic prevalent in the environment, has been closely linked to islet β-cell dysfunction, a critical pathological hallmark of type 2 diabetes (T2D). Even though apoptosis plays a pivotal role in arsenic-induced islet β-cell dysfunction, the explicit underlying mechanisms remain elusive. Here, we have identified that the SET-Rac1 signaling pathway is instrumental in the apoptosis and dysfunction of islet β-cells induced by NaAsO.
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December 2024
Department of Plastic and Cosmetic Surgery, The Second Affiliated Hospital of Army Medical University, Chongqing 400038, China. Electronic address:
The chronic diabetic wounds represented by diabetes foot ulcers (DFUs) are a worldwide challenge. Excessive production of reactive oxygen species (ROS) and persistent inflammation caused by the impaired phenotype switch of macrophages from M1 to M2 during wound healing are the main culprits of non-healing diabetic wounds. Therefore, an injectable DMM/GelMA hydrogel as a promising wound dressing was designed to regulate the mitochondrial metabolism of macrophages via inhibiting succinate dehydrogenase (SDH) activity and to promote macrophage repolarization towards M2 type.
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