Insulinresistenz

Zusammenfassung

Insulinresistenz bedeutet eine gestörte Wirkung von Insulin. Diese kann durch eine verminderte Sensitivität, Responsivität oder Sensitivität plus Responsivität charakterisiert sein. Insulinresistenz kann physiologisch (z. B. in der Pubertät) auftreten oder Teil der Pathophysiologie sein (z. B. bei Diabetes mellitus Typ 2). Die Erfassung der Insulinwirkung ist methodisch aufwendig, klinische Surrogate (wie der Plasmainsulinspiegel) zeigen eine hohe Varianz und weite Normalbereiche. Neben biologischen Faktoren sind Körperzusammensetzung, Alter und Fitness wesentliche Determinanten der Insulinwirkung. Die viszeralen Fettdepots und ektope Fette in Muskel und Leber zeigen eine enge und inverse Beziehung zur Insulinwirkung. Allerdings erklären sie die Insulinresistenz nur anteilig. Neue Konzepte der Insulinresistenz berücksichtigen neben den klassischen Determinanten endokrine Faktoren (z. B. Leptin), die Inflammation im Fettgewebe und Schädigungen von Zellorganellen wie der Mitochondrien und des endoplasmatischen Retikulums. Die Behandlung der Insulinresistenz wird diese Erkenntnisse zukünftig neben den traditionellen Ansätzen (wie die Gewichtsreduktion) berüksichtigen müssen.

Abstract

Insulin resistance is characterised by reduced insulin action. It is characterised by reduced insulin sensitivity, responsivity or both. Insulin resistance can occur physiologically (eg during puberty) or is part of pathophysiology (eg in diabetes mellitus type 2). Methodologically assessment of insulin resistance is cumbersome. Clinical characterisation (eg hyperinsulinemia) by proxies of insulin resistance is limited by high intra-individual variation and lack of suitable normal ranges. Besides biological factors body composition, fitness and age are considered to be the major determinants of insulin action. Visceral fat as well as ectopic fat in skeletal muscle and liver show inverse association with insulin action. In addition to these classical determinants hormones (eg leptin), inflammation and disturbancies in organelle function (eg mitochondria and endoplasmatic reticulum) add to insulin resistance. Future treatments of insulin resistance has to take into account these new concepts in pathophysiology.

Schlüsselwörter

Glukoseverbrauch - Glukoseproduktion - Glukosetoleranz - Insulinsekretion - Insulinsensitivität - Insulinresponsivität

Key words

glucose utilisation - glucose production - glucose tolerance - insulin secretion - insulin sensitivity - insulin responsivity

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