Parasympathetic Blockade Attenuates Augmented Pancreatic Polypeptide but Not Insulin Secretion in Pima Indians

Barbora Vozarova De Courten, Christian Weyer, Norbert Stefan, Mark Horton, Angelo DelParigi, Peter J Havel, Clifton Bogardus, P. Antonio Tataranni

Research output: Contribution to journalArticle

23 Citations (Scopus)

Abstract

There is evidence from animal models of obesity and type 2 diabetes that increased parasympathetic vagal input to the pancreas contributes to hyperinsulinemia. Compared with Caucasians, Pima Indians have a high risk of type 2 diabetes and exhibit marked hyperinsulinemia and elevated plasma levels of pancreatic polypeptide (PP), an islet hormone considered a surrogate marker of parasympathetic nervous system (PNS) drive to the pancreas. To test if hyperinsulinemia in Pima Indians is due to increased vagal input to the β-cell, we examined the effect of PNS blockade in 17 Caucasian (aged 35 ± 8 years, body fat 23 ± 7% [mean ± SD]) and 17 Pima Indian males (aged 28 ± 8 years, body fat 29 ± 5%) with normal glucose tolerance. Each participant underwent four consecutive standardized liquid meal tests (64% carbohydrate, 22% fat, and 14% protein) during which a primed infusion of atropine was administered for 120 min at the following doses: 0, 2.5, 5, and 10 μg · kg fat-free mass (FFM)-1 · h-1. Areas under the curve for early (AUC0-30 min) and total (AUC0-120 min) post prandial insulin and PP secretory responses were calculated. Early postprandial insulin and PP secretory responses were higher in Pima Indians compared with those of Caucasians (both P = 0.01). Secretion of insulin and PP was inhibited by atropine (both P < 0.001). Increasing doses of atropine attenuated the ethnic difference in PP (P = 0.01) but not in early insulin secretory responses (P = 0.6), an effect that was not due to differences in gastric emptying rate (acetaminophen test) and/or circulating glucose. Similar results were observed for total secretory responses. These results confirm that compared with Caucasians, Pima Indians have an exaggerated PNS drive to pancreatic F-cells that secrete PP. However, the hyperinsulinemia of this population does not appear to be due to increased vagal input to pancreatic β-cells.

Original languageEnglish (US)
Pages (from-to)663-671
Number of pages9
JournalDiabetes
Volume53
Issue number3
DOIs
StatePublished - Mar 2004

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Potassium Iodide
Pancreatic Polypeptide
Hyperinsulinism
Parasympathetic Nervous System
Insulin
Atropine
Type 2 Diabetes Mellitus
Meals
Adipose Tissue
Pancreas
Pancreatic Polypeptide-Secreting Cells
Fats
Glucose
Gastric Emptying
Acetaminophen
Islets of Langerhans
Area Under Curve
Animal Models
Obesity
Biomarkers

ASJC Scopus subject areas

  • Internal Medicine
  • Endocrinology, Diabetes and Metabolism

Cite this

De Courten, B. V., Weyer, C., Stefan, N., Horton, M., DelParigi, A., Havel, P. J., ... Tataranni, P. A. (2004). Parasympathetic Blockade Attenuates Augmented Pancreatic Polypeptide but Not Insulin Secretion in Pima Indians. Diabetes, 53(3), 663-671. https://doi.org/10.2337/diabetes.53.3.663

Parasympathetic Blockade Attenuates Augmented Pancreatic Polypeptide but Not Insulin Secretion in Pima Indians. / De Courten, Barbora Vozarova; Weyer, Christian; Stefan, Norbert; Horton, Mark; DelParigi, Angelo; Havel, Peter J; Bogardus, Clifton; Tataranni, P. Antonio.

In: Diabetes, Vol. 53, No. 3, 03.2004, p. 663-671.

Research output: Contribution to journalArticle

De Courten, BV, Weyer, C, Stefan, N, Horton, M, DelParigi, A, Havel, PJ, Bogardus, C & Tataranni, PA 2004, 'Parasympathetic Blockade Attenuates Augmented Pancreatic Polypeptide but Not Insulin Secretion in Pima Indians', Diabetes, vol. 53, no. 3, pp. 663-671. https://doi.org/10.2337/diabetes.53.3.663
De Courten, Barbora Vozarova ; Weyer, Christian ; Stefan, Norbert ; Horton, Mark ; DelParigi, Angelo ; Havel, Peter J ; Bogardus, Clifton ; Tataranni, P. Antonio. / Parasympathetic Blockade Attenuates Augmented Pancreatic Polypeptide but Not Insulin Secretion in Pima Indians. In: Diabetes. 2004 ; Vol. 53, No. 3. pp. 663-671.
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