2019
Dipeptidyl Peptidase 4 Inhibition Increases Postprandial Norepinephrine via Substance P (NK1 Receptor) During RAAS Inhibition
Wilson JR, Kerman SJ, Hubers SA, Yu C, Nian H, Grouzmann E, Eugster PJ, Mayfield DS, Brown NJ. Dipeptidyl Peptidase 4 Inhibition Increases Postprandial Norepinephrine via Substance P (NK1 Receptor) During RAAS Inhibition. Journal Of The Endocrine Society 2019, 3: 1784-1798. PMID: 31528826, PMCID: PMC6734191, DOI: 10.1210/js.2019-00185.Peer-Reviewed Original ResearchPostprandial blood pressureDPP4 inhibitionNPY 1Blood pressureHeart failureACE inhibitionSubstance PVasoactive peptidesPostprandial glucagon-like peptide-1Substance P receptor blockadeDipeptidyl peptidase-4 inhibitorsGlucagon-like peptide-1Mixed-meal studyAngiotensin receptor blockersDouble-blind treatmentPeptidase-4 inhibitorsType 2 diabetesReceptor-dependent mechanismAntihypertensive groupNPY 3Y1 agonistRAAS inhibitionReceptor blockersReceptor blockadeACE inhibitors
2011
The renin–angiotensin–aldosterone system and glucose homeostasis
Luther JM, Brown NJ. The renin–angiotensin–aldosterone system and glucose homeostasis. Trends In Pharmacological Sciences 2011, 32: 734-739. PMID: 21880378, PMCID: PMC3223326, DOI: 10.1016/j.tips.2011.07.006.Peer-Reviewed Original ResearchConceptsAldosterone systemΒ-cellsGlucose-stimulated insulin secretionIncidence of diabetesLarge clinical trialsInduces Insulin ResistanceCultured β-cellsPancreatic β-cellsRAAS inhibitionAng IIAngiotensin IIInsulin resistanceHeart diseaseClinical trialsDiabetes progressionMineralocorticoid receptorPharmacological strategiesInsulin secretionGlucose homeostasisPancreatic isletsOxidative stressDiabetesIndependent mechanismsGlucose transportCellular level