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Beta-cell function improvement after biliopancreatic diversion in subjects with type 2 diabetes and morbid obesity.
Obesity (Silver Spring) 2010; 18(5):932-6O

Abstract

In subjects with obesity and type 2 diabetes mellitus (T2DM), biliopancreatic diversion (BPD) improves glucose stimulated insulin secretion, whereas the effects on other secretion mechanisms are still unknown. Our objective was to evaluate the early effects of BPD on nonglucose-stimulated insulin secretion. In 16 morbid obese subjects (9 with T2DM and 7 with normal fasting glucose (NFG)), we measured insulin secretion after glucose-dependent arginine stimulation test and after intravenous glucose tolerance test (IVGTT) before and 1 month after BPD. After surgery the mean weight lost was 13% in both groups. The acute insulin response during IVGTT was improved in T2DM after BDP (from 55 +/- 10 to 277 +/- 91 pmol/l, P = 0.03). A reduction of insulin response to arginine was observed in NFG, whereas opposite was found in T2DM. In particular, acute insulin response to arginine at basal glucose concentrations (AIR(basal)) was reduced but insulin response at 14 mmol/l of plasma glucose (AIR(14)) was increased. Therefore, after BPD any statistical difference in AIR(14) between NFG and T2DM disappeared (1,032 +/- 123 for NFG and 665 +/- 236 pmol/l for T2DM, P = ns). The same was observed for Slope(AIR), a measure of glucose potentiation, reduced in T2DM before BPD but increased after surgery, when no statistically significant difference resulted compared with NFG (Slope(AIR) after BPD: 78 +/- 11 in NFG and 56 +/- 18 pmol/l in T2DM, P = ns). In conclusion, in obese T2DM subjects 1 month after BPD we observed a great improvement of both glucose- and nonglucose-stimulated insulin secretions. The mechanisms by which BDP improve insulin secretion are still unknown.

Authors+Show Affiliations

Department of Endocrinology and Medicine, University of Genova, Genoa, Italy.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

20186136

Citation

Briatore, Lucia, et al. "Beta-cell Function Improvement After Biliopancreatic Diversion in Subjects With Type 2 Diabetes and Morbid Obesity." Obesity (Silver Spring, Md.), vol. 18, no. 5, 2010, pp. 932-6.
Briatore L, Salani B, Andraghetti G, et al. Beta-cell function improvement after biliopancreatic diversion in subjects with type 2 diabetes and morbid obesity. Obesity (Silver Spring). 2010;18(5):932-6.
Briatore, L., Salani, B., Andraghetti, G., Maggi, D., Adami, G. F., Scopinaro, N., & Cordera, R. (2010). Beta-cell function improvement after biliopancreatic diversion in subjects with type 2 diabetes and morbid obesity. Obesity (Silver Spring, Md.), 18(5), pp. 932-6. doi:10.1038/oby.2010.28.
Briatore L, et al. Beta-cell Function Improvement After Biliopancreatic Diversion in Subjects With Type 2 Diabetes and Morbid Obesity. Obesity (Silver Spring). 2010;18(5):932-6. PubMed PMID: 20186136.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Beta-cell function improvement after biliopancreatic diversion in subjects with type 2 diabetes and morbid obesity. AU - Briatore,Lucia, AU - Salani,Barbara, AU - Andraghetti,Gabriella, AU - Maggi,Davide, AU - Adami,Gian Franco, AU - Scopinaro,Nicola, AU - Cordera,Renzo, Y1 - 2010/02/25/ PY - 2010/2/27/entrez PY - 2010/2/27/pubmed PY - 2010/7/22/medline SP - 932 EP - 6 JF - Obesity (Silver Spring, Md.) JO - Obesity (Silver Spring) VL - 18 IS - 5 N2 - In subjects with obesity and type 2 diabetes mellitus (T2DM), biliopancreatic diversion (BPD) improves glucose stimulated insulin secretion, whereas the effects on other secretion mechanisms are still unknown. Our objective was to evaluate the early effects of BPD on nonglucose-stimulated insulin secretion. In 16 morbid obese subjects (9 with T2DM and 7 with normal fasting glucose (NFG)), we measured insulin secretion after glucose-dependent arginine stimulation test and after intravenous glucose tolerance test (IVGTT) before and 1 month after BPD. After surgery the mean weight lost was 13% in both groups. The acute insulin response during IVGTT was improved in T2DM after BDP (from 55 +/- 10 to 277 +/- 91 pmol/l, P = 0.03). A reduction of insulin response to arginine was observed in NFG, whereas opposite was found in T2DM. In particular, acute insulin response to arginine at basal glucose concentrations (AIR(basal)) was reduced but insulin response at 14 mmol/l of plasma glucose (AIR(14)) was increased. Therefore, after BPD any statistical difference in AIR(14) between NFG and T2DM disappeared (1,032 +/- 123 for NFG and 665 +/- 236 pmol/l for T2DM, P = ns). The same was observed for Slope(AIR), a measure of glucose potentiation, reduced in T2DM before BPD but increased after surgery, when no statistically significant difference resulted compared with NFG (Slope(AIR) after BPD: 78 +/- 11 in NFG and 56 +/- 18 pmol/l in T2DM, P = ns). In conclusion, in obese T2DM subjects 1 month after BPD we observed a great improvement of both glucose- and nonglucose-stimulated insulin secretions. The mechanisms by which BDP improve insulin secretion are still unknown. SN - 1930-739X UR - https://www.unboundmedicine.com/medline/citation/20186136/Beta_cell_function_improvement_after_biliopancreatic_diversion_in_subjects_with_type_2_diabetes_and_morbid_obesity_ L2 - https://doi.org/10.1038/oby.2010.28 DB - PRIME DP - Unbound Medicine ER -