Abstract

To the Editor: Heinisch et al reported that acute infusion of B-type natriuretic peptide (NP) enhances the initial glucose distribution, resulting in a decrease of postload glucose concentrations by beta cell-independent mechanisms in healthy individuals [1]. This study added to growing evidence regarding a close pathophysiological link between NPs and metabolic traits in obesity, type 2 diabetes and associated diseases [2]. The mechanisms by which NP regulates glucose metabolism are not fully understood, but a reciprocal relationship between glucose regulation and NP has been suggested in type 2 diabetes and cardiovascular diseases (CVDs) [1, 2]. In addition, we and others observed the same type of relations between insulin and NP in obesity [3, 4]. Previous large-cohort observations such as the Study to Prevent NIDDM (STOP-NIDDM) [5, 6] indicate that reduction of postprandial glucose load may be involved in the prevention of both type 2 diabetes and incident hypertension, pointing to a potential ‘bi-directional relationship’

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