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Insulin Augmentation of Glucose-Stimulated Insulin Secretion Is Impaired in Insulin-Resistant Humans
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| Zeitschriftentitel: | Diabetes |
|---|---|
| Personen und Körperschaften: | , , , , , |
| In: | Diabetes, 61, 2012, 2, S. 301-309 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
American Diabetes Association
|
| Schlagwörter: |
| author_facet |
Halperin, Florencia Lopez, Ximena Manning, Raquel Kahn, C. Ronald Kulkarni, Rohit N. Goldfine, Allison B. Halperin, Florencia Lopez, Ximena Manning, Raquel Kahn, C. Ronald Kulkarni, Rohit N. Goldfine, Allison B. |
|---|---|
| author |
Halperin, Florencia Lopez, Ximena Manning, Raquel Kahn, C. Ronald Kulkarni, Rohit N. Goldfine, Allison B. |
| spellingShingle |
Halperin, Florencia Lopez, Ximena Manning, Raquel Kahn, C. Ronald Kulkarni, Rohit N. Goldfine, Allison B. Diabetes Insulin Augmentation of Glucose-Stimulated Insulin Secretion Is Impaired in Insulin-Resistant Humans Endocrinology, Diabetes and Metabolism Internal Medicine |
| author_sort |
halperin, florencia |
| spelling |
Halperin, Florencia Lopez, Ximena Manning, Raquel Kahn, C. Ronald Kulkarni, Rohit N. Goldfine, Allison B. 0012-1797 1939-327X American Diabetes Association Endocrinology, Diabetes and Metabolism Internal Medicine http://dx.doi.org/10.2337/db11-1067 <jats:sec> <jats:title /> <jats:p>Type 2 diabetes (T2D) is characterized by insulin resistance and pancreatic β-cell dysfunction, the latter possibly caused by a defect in insulin signaling in β-cells. We hypothesized that insulin’s effect to potentiate glucose-stimulated insulin secretion (GSIS) would be diminished in insulin-resistant persons. To evaluate the effect of insulin to modulate GSIS in insulin-resistant compared with insulin-sensitive subjects, 10 participants with impaired glucose tolerance (IGT), 11 with T2D, and 8 healthy control subjects were studied on two occasions. The insulin secretory response was assessed by the administration of dextrose for 80 min following a 4-h clamp with either saline infusion (sham) or an isoglycemic-hyperinsulinemic clamp using B28-Asp-insulin (which can be distinguished immunologically from endogenous insulin) that raised insulin concentrations to high physiologic concentrations. Pre-exposure to insulin augmented GSIS in healthy persons. This effect was attenuated in insulin-resistant cohorts, both those with IGT and those with T2D. Insulin potentiates glucose-stimulated insulin secretion in insulin-resistant subjects to a lesser degree than in normal subjects. This is consistent with an effect of insulin to regulate β-cell function in humans in vivo with therapeutic implications.</jats:p> </jats:sec> Insulin Augmentation of Glucose-Stimulated Insulin Secretion Is Impaired in Insulin-Resistant Humans Diabetes |
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| title |
Insulin Augmentation of Glucose-Stimulated Insulin Secretion Is Impaired in Insulin-Resistant Humans |
| title_unstemmed |
Insulin Augmentation of Glucose-Stimulated Insulin Secretion Is Impaired in Insulin-Resistant Humans |
| title_full |
Insulin Augmentation of Glucose-Stimulated Insulin Secretion Is Impaired in Insulin-Resistant Humans |
| title_fullStr |
Insulin Augmentation of Glucose-Stimulated Insulin Secretion Is Impaired in Insulin-Resistant Humans |
| title_full_unstemmed |
Insulin Augmentation of Glucose-Stimulated Insulin Secretion Is Impaired in Insulin-Resistant Humans |
| title_short |
Insulin Augmentation of Glucose-Stimulated Insulin Secretion Is Impaired in Insulin-Resistant Humans |
| title_sort |
insulin augmentation of glucose-stimulated insulin secretion is impaired in insulin-resistant humans |
| topic |
Endocrinology, Diabetes and Metabolism Internal Medicine |
| url |
http://dx.doi.org/10.2337/db11-1067 |
| publishDate |
2012 |
| physical |
301-309 |
| description |
<jats:sec>
<jats:title />
<jats:p>Type 2 diabetes (T2D) is characterized by insulin resistance and pancreatic β-cell dysfunction, the latter possibly caused by a defect in insulin signaling in β-cells. We hypothesized that insulin’s effect to potentiate glucose-stimulated insulin secretion (GSIS) would be diminished in insulin-resistant persons. To evaluate the effect of insulin to modulate GSIS in insulin-resistant compared with insulin-sensitive subjects, 10 participants with impaired glucose tolerance (IGT), 11 with T2D, and 8 healthy control subjects were studied on two occasions. The insulin secretory response was assessed by the administration of dextrose for 80 min following a 4-h clamp with either saline infusion (sham) or an isoglycemic-hyperinsulinemic clamp using B28-Asp-insulin (which can be distinguished immunologically from endogenous insulin) that raised insulin concentrations to high physiologic concentrations. Pre-exposure to insulin augmented GSIS in healthy persons. This effect was attenuated in insulin-resistant cohorts, both those with IGT and those with T2D. Insulin potentiates glucose-stimulated insulin secretion in insulin-resistant subjects to a lesser degree than in normal subjects. This is consistent with an effect of insulin to regulate β-cell function in humans in vivo with therapeutic implications.</jats:p>
</jats:sec> |
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| author | Halperin, Florencia, Lopez, Ximena, Manning, Raquel, Kahn, C. Ronald, Kulkarni, Rohit N., Goldfine, Allison B. |
| author_facet | Halperin, Florencia, Lopez, Ximena, Manning, Raquel, Kahn, C. Ronald, Kulkarni, Rohit N., Goldfine, Allison B., Halperin, Florencia, Lopez, Ximena, Manning, Raquel, Kahn, C. Ronald, Kulkarni, Rohit N., Goldfine, Allison B. |
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| description | <jats:sec> <jats:title /> <jats:p>Type 2 diabetes (T2D) is characterized by insulin resistance and pancreatic β-cell dysfunction, the latter possibly caused by a defect in insulin signaling in β-cells. We hypothesized that insulin’s effect to potentiate glucose-stimulated insulin secretion (GSIS) would be diminished in insulin-resistant persons. To evaluate the effect of insulin to modulate GSIS in insulin-resistant compared with insulin-sensitive subjects, 10 participants with impaired glucose tolerance (IGT), 11 with T2D, and 8 healthy control subjects were studied on two occasions. The insulin secretory response was assessed by the administration of dextrose for 80 min following a 4-h clamp with either saline infusion (sham) or an isoglycemic-hyperinsulinemic clamp using B28-Asp-insulin (which can be distinguished immunologically from endogenous insulin) that raised insulin concentrations to high physiologic concentrations. Pre-exposure to insulin augmented GSIS in healthy persons. This effect was attenuated in insulin-resistant cohorts, both those with IGT and those with T2D. Insulin potentiates glucose-stimulated insulin secretion in insulin-resistant subjects to a lesser degree than in normal subjects. This is consistent with an effect of insulin to regulate β-cell function in humans in vivo with therapeutic implications.</jats:p> </jats:sec> |
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| spelling | Halperin, Florencia Lopez, Ximena Manning, Raquel Kahn, C. Ronald Kulkarni, Rohit N. Goldfine, Allison B. 0012-1797 1939-327X American Diabetes Association Endocrinology, Diabetes and Metabolism Internal Medicine http://dx.doi.org/10.2337/db11-1067 <jats:sec> <jats:title /> <jats:p>Type 2 diabetes (T2D) is characterized by insulin resistance and pancreatic β-cell dysfunction, the latter possibly caused by a defect in insulin signaling in β-cells. We hypothesized that insulin’s effect to potentiate glucose-stimulated insulin secretion (GSIS) would be diminished in insulin-resistant persons. To evaluate the effect of insulin to modulate GSIS in insulin-resistant compared with insulin-sensitive subjects, 10 participants with impaired glucose tolerance (IGT), 11 with T2D, and 8 healthy control subjects were studied on two occasions. The insulin secretory response was assessed by the administration of dextrose for 80 min following a 4-h clamp with either saline infusion (sham) or an isoglycemic-hyperinsulinemic clamp using B28-Asp-insulin (which can be distinguished immunologically from endogenous insulin) that raised insulin concentrations to high physiologic concentrations. Pre-exposure to insulin augmented GSIS in healthy persons. This effect was attenuated in insulin-resistant cohorts, both those with IGT and those with T2D. Insulin potentiates glucose-stimulated insulin secretion in insulin-resistant subjects to a lesser degree than in normal subjects. This is consistent with an effect of insulin to regulate β-cell function in humans in vivo with therapeutic implications.</jats:p> </jats:sec> Insulin Augmentation of Glucose-Stimulated Insulin Secretion Is Impaired in Insulin-Resistant Humans Diabetes |
| spellingShingle | Halperin, Florencia, Lopez, Ximena, Manning, Raquel, Kahn, C. Ronald, Kulkarni, Rohit N., Goldfine, Allison B., Diabetes, Insulin Augmentation of Glucose-Stimulated Insulin Secretion Is Impaired in Insulin-Resistant Humans, Endocrinology, Diabetes and Metabolism, Internal Medicine |
| title | Insulin Augmentation of Glucose-Stimulated Insulin Secretion Is Impaired in Insulin-Resistant Humans |
| title_full | Insulin Augmentation of Glucose-Stimulated Insulin Secretion Is Impaired in Insulin-Resistant Humans |
| title_fullStr | Insulin Augmentation of Glucose-Stimulated Insulin Secretion Is Impaired in Insulin-Resistant Humans |
| title_full_unstemmed | Insulin Augmentation of Glucose-Stimulated Insulin Secretion Is Impaired in Insulin-Resistant Humans |
| title_short | Insulin Augmentation of Glucose-Stimulated Insulin Secretion Is Impaired in Insulin-Resistant Humans |
| title_sort | insulin augmentation of glucose-stimulated insulin secretion is impaired in insulin-resistant humans |
| title_unstemmed | Insulin Augmentation of Glucose-Stimulated Insulin Secretion Is Impaired in Insulin-Resistant Humans |
| topic | Endocrinology, Diabetes and Metabolism, Internal Medicine |
| url | http://dx.doi.org/10.2337/db11-1067 |