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The Brains Behind SGLT2 Inhibition

Control of the central nervous regulation of eating behavior and further body functions by administration of drugs is a long-lasting dream in clinical research (1). In their study, Kullmann et al. (2) investigated whether the beneficial effects of empagliflozin from the new class of sodium–glucose transport protein 2 (SGLT2) inhibitors may in part be mediated by central nervous action. Drugs of the SGLT2 class recently yielded an unprecedented series of clinical trial results, which very quickly led to changes of guidelines in diabetology and cardiology. However, mechanisms of how these drugs work are not yet fully understood, and even initially believed concepts are now in doubt (3). This makes it even more important to gain further insight into SGLT2 action in the human body, especially exploring new mechanistic pathways not yet considered. In their study, the authors hypothesized that the SGLT2 inhibitor molecule would help restore insulin action in the brain (Table 1) and consequently induce favorable effects in the periphery. This is an intriguing assumption, as the focus of most studies investigating SGLT2 inhibitor action so far has been the renal effects, with the drug class’s main property being reducing the body’s glucose and fluid load (5).

…. more: Diabetes Journals (ADA) (Quelle/Source)

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