It's more than mechanics: the case for metabolic endpoints in airways disease

<title>Extract</title> Metabolic dysfunction, including insulin resistance and hyperglycaemia, has been found to contribute independently to airway inflammation, impaired lung mechanics, and altered immune responses in the lungs (figure 1). [1–7] Insulin resistance and compensatory hyperinsulinaemia can directly alter airway biology, including promoting airway smooth muscle proliferation and contractility, airway hyperresponsiveness, impaired beta-agonist responses, airway remodelling and inflammation.