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Parasympathetic blockade attenuates augmented pancreatic polypeptide but not insulin secretion in Pima Indians.
Diabetes. 2004 Mar; 53(3):663-71.D

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 beta-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 micro g. kg fat-free mass (FFM)(-1). h(-1). Areas under the curve for early (AUC(0-30 min)) and total (AUC(0-120 min)) postprandial 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 beta-cells.

Authors+Show Affiliations

Clinical Diabetes and Nutrition Section, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Phoenix, Arizona, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article

Language

eng

PubMed ID

14988250

Citation

Vozarova de Courten, Barbora, et al. "Parasympathetic Blockade Attenuates Augmented Pancreatic Polypeptide but Not Insulin Secretion in Pima Indians." Diabetes, vol. 53, no. 3, 2004, pp. 663-71.
Vozarova de Courten B, Weyer C, Stefan N, et al. Parasympathetic blockade attenuates augmented pancreatic polypeptide but not insulin secretion in Pima Indians. Diabetes. 2004;53(3):663-71.
Vozarova de Courten, B., Weyer, C., Stefan, N., Horton, M., DelParigi, A., Havel, P., Bogardus, C., & Tataranni, P. A. (2004). Parasympathetic blockade attenuates augmented pancreatic polypeptide but not insulin secretion in Pima Indians. Diabetes, 53(3), 663-71.
Vozarova de Courten B, et al. Parasympathetic Blockade Attenuates Augmented Pancreatic Polypeptide but Not Insulin Secretion in Pima Indians. Diabetes. 2004;53(3):663-71. PubMed PMID: 14988250.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Parasympathetic blockade attenuates augmented pancreatic polypeptide but not insulin secretion in Pima Indians. AU - Vozarova de Courten,Barbora, AU - Weyer,Christian, AU - Stefan,Norbert, AU - Horton,Mark, AU - DelParigi,Angelo, AU - Havel,Peter, AU - Bogardus,Clifton, AU - Tataranni,P Antonio, PY - 2004/2/28/pubmed PY - 2004/6/21/medline PY - 2004/2/28/entrez SP - 663 EP - 71 JF - Diabetes JO - Diabetes VL - 53 IS - 3 N2 - 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 beta-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 micro g. kg fat-free mass (FFM)(-1). h(-1). Areas under the curve for early (AUC(0-30 min)) and total (AUC(0-120 min)) postprandial 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 beta-cells. SN - 0012-1797 UR - https://www.unboundmedicine.com/medline/citation/14988250/Parasympathetic_blockade_attenuates_augmented_pancreatic_polypeptide_but_not_insulin_secretion_in_Pima_Indians_ L2 - https://diabetes.diabetesjournals.org/lookup/pmidlookup?view=long&amp;pmid=14988250 DB - PRIME DP - Unbound Medicine ER -