TY - JOUR
T1 - Beta-cell sensitivity to glucose is impaired after gastric bypass surgery
AU - Salehi, Marzieh
AU - Gastaldelli, Amalia
AU - D'Alessio, David A.
N1 - Funding Information:
This work was supported by grants from the National Institute of Health, DK105379 (M. S.), DK083554 (M. S.) and D. K.101991 (D. D.) and in part by the National Center for Advancing Translational Sciences, National Institute of Health grant 8 UL1 TR000077.
PY - 2018/4
Y1 - 2018/4
N2 - Aims: Patients who have undergone Roux-en-Y gastric bypass surgery (GB) have exaggerated postprandial insulin secretion, which has been attributed to increased meal glucose appearance and enhanced incretin effect. Here, we sought to determine β-cell glucose sensitivity in the absence of meal stimulation and insulinotropic gut factors. Materials and methods: A total of 12 non-diabetic subjects with prior GB, and 7 matched non-surgical control subjects with normal glucose tolerance were studied. Blood glucose and insulin secretion rates were measured during a graded glucose infusion at increasing and then decreasing rates. Insulin sensitivity (SI) and glucose effectiveness (SG) were determined by the minimal model. Results: GB subjects had SI comparable to that of control subjects. GB subjects had relative hyperglycaemia during the highest dose of glucose infusion associated with significantly reduced β-cell glucose sensitivity throughout both step-up (GB: 34 ± 6, CN: 82 ± 9 pmol min−1 mM−1 L, P <.0001) and step-down (GB: 31 ± 6, CN: 74 ± 9 pmol min−1 mM−1 L, P <.0001) phases of the glucose infusion. GB subjects also had reduced SG (GB: 0.04 ± 0.00, CN: 0.07 ± 0.01 min−1, P =.004). Conclusion: In the absence of enteric stimuli, β-cell sensitivity to changes in glycaemia is blunted among individuals with GB, indicating a significant shift in a fundamental property of β-cell function several years after surgery.
AB - Aims: Patients who have undergone Roux-en-Y gastric bypass surgery (GB) have exaggerated postprandial insulin secretion, which has been attributed to increased meal glucose appearance and enhanced incretin effect. Here, we sought to determine β-cell glucose sensitivity in the absence of meal stimulation and insulinotropic gut factors. Materials and methods: A total of 12 non-diabetic subjects with prior GB, and 7 matched non-surgical control subjects with normal glucose tolerance were studied. Blood glucose and insulin secretion rates were measured during a graded glucose infusion at increasing and then decreasing rates. Insulin sensitivity (SI) and glucose effectiveness (SG) were determined by the minimal model. Results: GB subjects had SI comparable to that of control subjects. GB subjects had relative hyperglycaemia during the highest dose of glucose infusion associated with significantly reduced β-cell glucose sensitivity throughout both step-up (GB: 34 ± 6, CN: 82 ± 9 pmol min−1 mM−1 L, P <.0001) and step-down (GB: 31 ± 6, CN: 74 ± 9 pmol min−1 mM−1 L, P <.0001) phases of the glucose infusion. GB subjects also had reduced SG (GB: 0.04 ± 0.00, CN: 0.07 ± 0.01 min−1, P =.004). Conclusion: In the absence of enteric stimuli, β-cell sensitivity to changes in glycaemia is blunted among individuals with GB, indicating a significant shift in a fundamental property of β-cell function several years after surgery.
KW - gastric bypass surgery
KW - glucose tolerance
KW - β-cell glucose sensitivity
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U2 - 10.1111/dom.13165
DO - 10.1111/dom.13165
M3 - Article
C2 - 29152839
AN - SCOPUS:85038233479
VL - 20
SP - 872
EP - 878
JO - Diabetes, Obesity and Metabolism
JF - Diabetes, Obesity and Metabolism
SN - 1462-8902
IS - 4
ER -