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Worsening Postural Tachycardia Syndrome Is Associated With Increased
Glucose-Dependent Insulinotropic Polypeptide Secretion.
Breier NC, Paranjape SY, Scudder S, Mehr SE, Diedrich A, Flynn CR, Okamoto LE,
Hartmann B, Gasbjerg LS, Shibao CA
Submitted Externally on 6/21/2022
Hypertension (Dallas, Tex. : 1979)
Volume : Pages
79 : e89 - e99
Postural tachycardia syndrome (POTS) is characterized by excessive upright
tachycardia and disabling presyncopal symptoms, which are exacerbated after
consuming a high-carbohydrate meal; it is unknown, however, what is the precise
underlying mechanism. We seek to investigate the effect of glucose intake on
orthostatic hemodynamic changes and gastrointestinal hormone secretion in POTS.,
Prospective, case-control study, 12 women with POTS who reported a postprandial
worsening of their POTS symptoms and 13 age-matched female controls received
75-g oral glucose and 20 mg/kg acetaminophen to assess nutrient absorption.
Hemodynamic, gastrointestinal hormone and acetaminophen levels were measured for
up to 120 minutes postingestion while supine and standing., Patients with POTS
had significant orthostatic tachycardia, 48.7±11.2 versus 23.3±8.1 bpm, P=0.012
and elevated upright norepinephrine levels, 835.2±368.4 versus 356.9±156.7
pg/mL, P=0.004. After oral glucose, upright heart rate significantly increased
in POTS, 21.2±11.9% versus 6.0±19.9%, P=0.033 with a concomitant decline in
upright stroke volume, -10.3±11.90% versus 3.3±13.7%, P=0.027; total peripheral
resistance, blood pressure and cardiac output remained unaltered. Acetaminophen
rate of appearance was similar between groups (P=0.707), indicating comparable
nutrient absorption rates. POTS had increased plasma levels of C-peptide
(P=0.001), GIP (glucose-dependent insulinotropic polypeptide; P=0.001), peptide
YY (P=0.016), and pancreatic polypeptide (P=0.04) following glucose consumption,
but only GIP had a time-dependent association with the worsening upright
tachycardia and stroke volume fall., The glucose-induced worsening orthostatic
tachycardia in POTS was associated with a decline in SV; these changes occurred
while GIP, a splanchnic vasodilator, was maximally elevated.
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Financial support for this work was provided by the NIDDK Mouse Metabolic Phenotyping Centers (National MMPC, RRID:SCR_008997,
) under the MICROMouse Program, grants DK076169.
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