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Dipeptidyl Peptidase 4 Inhibition Increases Postprandial Norepinephrine via Substance P (NK1 Receptor) During RAAS Inhibition.

Jessica R WilsonScott Jafarian KermanScott A HubersChang YuHui NianEric GrouzmannPhilippe J EugsterDustin S MayfieldNancy J Brown
Published in: Journal of the Endocrine Society (2019)
DPP4 inhibition increases postprandial concentrations of the Y1 agonist NPY 1-36. During treatment with an ACE inhibitor or angiotensin receptor blocker, DPP4 inhibition increased postprandial norepinephrine through a substance P receptor-dependent mechanism. Increased NPY 1-36 and norepinephrine could increase risk of heart failure but did not result in higher postprandial blood pressure.
Keyphrases
  • blood glucose
  • heart failure
  • blood pressure
  • angiotensin converting enzyme
  • atrial fibrillation
  • metabolic syndrome
  • heart rate
  • weight loss