Rationale for timely insulin therapy in Type 2 diabetes within the framework of individualised treatment: 2020 update

Abstract: Type 2 diabetes is characterised by chronic hyperglycaemia and variable degrees of insulin deficiency and resistance. Hyperglycaemia and elevated fatty acids exert harmful effects on β-cell function, regeneration and apoptosis (gluco-lipotoxicity). Furthermore, chronic hyperglycaemia triggers a vicious cycle of insulin resistance, low-grade inflammation and a cascade of pro-atherogenic processes. Thus, timely near to normal glucose control is of utmost importance in the management of type 2 diabetes and prevention of micro- and macroangiopathy. The majority of patients are multimorbid and obese, with critical comorbidities such as cardiovascular disease, heart failure and chronic kidney disease. Recently published guidelines therefore recommend patient-centred risk/benefit-balanced use of oral glucose-lowering drugs or a glucagon-like peptide 1 (GLP-1) receptor agonist, or switching to insulin with glycated haemoglobin (HbA1c) out of target. This article covers the indications of early insulin treatment to prevent diabetes-related complications, particularly in subgroups with severe insulin deficit, and to achieve recovery of residual β-cell function. Furthermore, the individualised, risk/benefit-balanced, timely initiation of insulin as second and third option is analysed. Timely insulin initiation may prevent diabetes progression, reduce diabetes-related complications and has less serious adverse effects. Basal insulin is the preferred option in most clinical situations with consequences of undertreatment of chronic hyperglycaemia

Standort
Deutsche Nationalbibliothek Frankfurt am Main
Umfang
Online-Ressource
Sprache
Englisch
Anmerkungen
Diabetes therapy. - 11, 8 (2020) , 1645-1666, ISSN: 1869-6961

Schlagwort
Individualisierte Medizin
Erwarteter Nutzen
Muskelatrophie
Diabetes mellitus Typ 2
Hypoglykämie

Ereignis
Veröffentlichung
(wo)
Freiburg
(wer)
Universität
(wann)
2020
Urheber

DOI
10.1007/s13300-020-00855-5
URN
urn:nbn:de:bsz:25-freidok-1667306
Rechteinformation
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Letzte Aktualisierung
14.08.2025, 10:48 MESZ

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  • 2020

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