AZD5423 (Standard)

Endocrine diseases often arise from disrupted hormone production, hormone signaling, or target-tissue responsiveness; for diabetes-focused endocrine disease models, insulin signaling regulates glucose uptake, hepatic glucose output, lipid metabolism, and β-cell compensation. Type 2 diabetes develops through interacting defects in insulin resistance, β-cell dysfunction, adipose inflammation, hepatic glucose overproduction, altered incretin signaling, and ectopic lipid metabolism. A major unresolved question is whether endocrine dysfunction is driven primarily by target-tissue insulin resistance, intrinsic β-cell failure, immune/inflammatory stress, or combined multi-organ failure that differs by disease stage.

Ovalbumin-induced allergic airway inflammation is a mouse model in which systemic sensitization to ovalbumin, usually with aluminum hydroxide adjuvant, is followed by airway ovalbumin challenge to induce allergic airway inflammation, eosinophil recruitment, mucus production, serum antigen-specific IgE, Th2 cytokine responses, and airway hyperresponsiveness to methacholine. The model is used to study allergen-driven airway inflammation and asthma-like immune responses, but it does not reproduce every feature of human asthma. The main readouts are bronchoalveolar lavage fluid cellularity, lung histopathology, airway hyperresponsiveness, serum OVA-specific IgE, and cytokines such as IL-4, IL-5, and IL-13 in bronchoalveolar lavage fluid or lung samples. Eosinophilia and Th2 cytokines reflect allergic type 2 inflammation, while methacholine responsiveness provides a functional airway-reactivity endpoint.