Abstract P407: Increased Secretion Of Glucose Dependent Insulinotropic Polypeptide Is Associated With Postprandial Hypotension In Patients With Parkinson Disease

Abstract

Postprandial hypotension (PPH) is highly prevalent in Parkinson Disease (PD) and is defined as a sudden and substantial decrease (>20 mm Hg or >10 mm hg) in blood pressure within two hours after ingesting a meal. This condition is associated with syncope and falls. Eating a meal induces significant blood sequestration in the splanchnic circulation through the release of gastrointestinal (GI) hormones. Patients with autonomic dysfunction cannot compensate for these hemodynamic changes, which results in PPH. The purpose of this study is to evaluate if increased secretion of GI hormones, including glucose-dependent insulinotropic polypeptide (GIP), a strong splanchnic vasodilator, contributes to PPH in those with PD. We enrolled 11 PD patients, seven with PPH (PPH+) (age 69±7.65 years old, 72% males, Unified Parkinson’s Disease Rating Scale 29±18.9) and four without PPH (PPH-) (age 67±1.71 years, 75% males, UPDRS 20±15.30). PD PPH+ patients had evidence of autonomic impairment and orthostatic hypotension as defined by a change in systolic blood pressure, (-57±29.23 vs. -7±17.66 mm Hg in PPH). Blood pressure, heart rate, and blood GIP levels were measured before and at 5, 10, 15, 30, 60, 90, 120 min timepoints after 75 gr oral glucose in supine position. There was a time-dependent decrease in blood pressure with a nadir at 30 min (-17±14.30 mmHg vs. -5±17.26 in PPH-). In PD PPH+, peak GIP secretion also occurred at 30 min post-glucose ingestion (315.3±297.9 vs. 69.1±34.8 pmol/L in PPH-). PD PPH+ patients had a greater secretion of C-peptide (2141±1017.81 vs.1540.56±428.77 pmol/L in PPH-) and insulin (1477.78±1572.80 vs. 351.09±141.53 pmol/L in PPH-). These initial results show excessive GIP secretion in PD patients with PPH, suggesting that GIP may contribute to its pathophysiology.