Glucagon-like peptide-1 response to meals and post-prandial hyperglycemia in Type 2 diabetic patients
Abstract Background: The impaired response of glucagon-like peptide-1 (GLP-1) to meals in diabetic patients can contribute to the pathogenesis of impaired insulin secretion and post-prandial hyperglycemia. This study is aimed at the assessment of the relationship between meal-induced GLP-1 and post-...
Ausführliche Beschreibung
Autor*in: |
Mannucci, E. [verfasserIn] |
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E-Artikel |
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Sprache: |
Englisch |
Erschienen: |
2009 |
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Schlagwörter: |
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Anmerkung: |
© Italian Society of Endocrinology (SIE) 2010 |
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Übergeordnetes Werk: |
Enthalten in: Journal of endocrinological investigation - [S. l.] : Springer, 1978, 33(2009), 3 vom: 11. Sept., Seite 147-150 |
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Übergeordnetes Werk: |
volume:33 ; year:2009 ; number:3 ; day:11 ; month:09 ; pages:147-150 |
Links: |
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DOI / URN: |
10.1007/BF03346573 |
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Katalog-ID: |
SPR03684537X |
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520 | |a Abstract Background: The impaired response of glucagon-like peptide-1 (GLP-1) to meals in diabetic patients can contribute to the pathogenesis of impaired insulin secretion and post-prandial hyperglycemia. This study is aimed at the assessment of the relationship between meal-induced GLP-1 and post-prandial hyperglycemia in Type 2 diabetic patients. Methods: Twenty-one drug-naïve Type 2 diabetic patients were studied. Blood glucose and active GLP-1 levels were measured 0, 30, 60, 90, and 120 min after a standard test meal. A continuous glucose monitoring (CGM) system was applied for the following 3 days. Nutrient intake at each meal was calculated on the basis of patients’ food records. For each patient, post-prandial 120-min glucose incremental area under the curve (iAUC) was included in linear regression model exploring its relationship with total energy and carbohydrate intake, and the angular coefficient for total energy (EAC) and carbohydrate (CAC) was calculated. Results: GLP-1 levels peaked 30 min after the test meal. Logarithmically transformed 60-min GLP-1 iAUC showed a significant inverse correlation with glycated hemoglobin ($ HbA_{1c} $) (p<0.01). A significant inverse correlation of 60-min GLP-1 iAUC was also observed with EAC and CAC (both p<0.01), meaning that patients with a lower GLP-1 response to the test meal had a higher increment of post-prandial glucose for each additional unit of total energy or carbohydrate intake. Conclusions: In Type 2 diabetic patients, a lower GLP-1 response to meals is associated with a higher $ HbA_{1c} $, and with a greater degree of meal-induced hyperglycemia, both in a meal test and during CGM in “real-life” conditions. | ||
650 | 4 | |a Continuous glucose monitoring system |7 (dpeaa)DE-He213 | |
650 | 4 | |a diabetes mellitus |7 (dpeaa)DE-He213 | |
650 | 4 | |a glucagon-like peptide-1 |7 (dpeaa)DE-He213 | |
650 | 4 | |a standard test meal |7 (dpeaa)DE-He213 | |
700 | 1 | |a Pala, L. |4 aut | |
700 | 1 | |a Monami, M. |4 aut | |
700 | 1 | |a Vico, L. |4 aut | |
700 | 1 | |a Bardini, G. |4 aut | |
700 | 1 | |a Dicembrini, I. |4 aut | |
700 | 1 | |a Ciani, S. |4 aut | |
700 | 1 | |a Lamanna, C. |4 aut | |
700 | 1 | |a Marchionni, N. |4 aut | |
700 | 1 | |a Rotella, C. M. |4 aut | |
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10.1007/BF03346573 doi (DE-627)SPR03684537X (SPR)BF03346573-e DE-627 ger DE-627 rakwb eng Mannucci, E. verfasserin aut Glucagon-like peptide-1 response to meals and post-prandial hyperglycemia in Type 2 diabetic patients 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Italian Society of Endocrinology (SIE) 2010 Abstract Background: The impaired response of glucagon-like peptide-1 (GLP-1) to meals in diabetic patients can contribute to the pathogenesis of impaired insulin secretion and post-prandial hyperglycemia. This study is aimed at the assessment of the relationship between meal-induced GLP-1 and post-prandial hyperglycemia in Type 2 diabetic patients. Methods: Twenty-one drug-naïve Type 2 diabetic patients were studied. Blood glucose and active GLP-1 levels were measured 0, 30, 60, 90, and 120 min after a standard test meal. A continuous glucose monitoring (CGM) system was applied for the following 3 days. Nutrient intake at each meal was calculated on the basis of patients’ food records. For each patient, post-prandial 120-min glucose incremental area under the curve (iAUC) was included in linear regression model exploring its relationship with total energy and carbohydrate intake, and the angular coefficient for total energy (EAC) and carbohydrate (CAC) was calculated. Results: GLP-1 levels peaked 30 min after the test meal. Logarithmically transformed 60-min GLP-1 iAUC showed a significant inverse correlation with glycated hemoglobin ($ HbA_{1c} $) (p<0.01). A significant inverse correlation of 60-min GLP-1 iAUC was also observed with EAC and CAC (both p<0.01), meaning that patients with a lower GLP-1 response to the test meal had a higher increment of post-prandial glucose for each additional unit of total energy or carbohydrate intake. Conclusions: In Type 2 diabetic patients, a lower GLP-1 response to meals is associated with a higher $ HbA_{1c} $, and with a greater degree of meal-induced hyperglycemia, both in a meal test and during CGM in “real-life” conditions. Continuous glucose monitoring system (dpeaa)DE-He213 diabetes mellitus (dpeaa)DE-He213 glucagon-like peptide-1 (dpeaa)DE-He213 standard test meal (dpeaa)DE-He213 Pala, L. aut Monami, M. aut Vico, L. aut Bardini, G. aut Dicembrini, I. aut Ciani, S. aut Lamanna, C. aut Marchionni, N. aut Rotella, C. M. aut Enthalten in Journal of endocrinological investigation [S. l.] : Springer, 1978 33(2009), 3 vom: 11. Sept., Seite 147-150 (DE-627)369556267 (DE-600)2119482-8 1720-8386 nnns volume:33 year:2009 number:3 day:11 month:09 pages:147-150 https://dx.doi.org/10.1007/BF03346573 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 33 2009 3 11 09 147-150 |
spelling |
10.1007/BF03346573 doi (DE-627)SPR03684537X (SPR)BF03346573-e DE-627 ger DE-627 rakwb eng Mannucci, E. verfasserin aut Glucagon-like peptide-1 response to meals and post-prandial hyperglycemia in Type 2 diabetic patients 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Italian Society of Endocrinology (SIE) 2010 Abstract Background: The impaired response of glucagon-like peptide-1 (GLP-1) to meals in diabetic patients can contribute to the pathogenesis of impaired insulin secretion and post-prandial hyperglycemia. This study is aimed at the assessment of the relationship between meal-induced GLP-1 and post-prandial hyperglycemia in Type 2 diabetic patients. Methods: Twenty-one drug-naïve Type 2 diabetic patients were studied. Blood glucose and active GLP-1 levels were measured 0, 30, 60, 90, and 120 min after a standard test meal. A continuous glucose monitoring (CGM) system was applied for the following 3 days. Nutrient intake at each meal was calculated on the basis of patients’ food records. For each patient, post-prandial 120-min glucose incremental area under the curve (iAUC) was included in linear regression model exploring its relationship with total energy and carbohydrate intake, and the angular coefficient for total energy (EAC) and carbohydrate (CAC) was calculated. Results: GLP-1 levels peaked 30 min after the test meal. Logarithmically transformed 60-min GLP-1 iAUC showed a significant inverse correlation with glycated hemoglobin ($ HbA_{1c} $) (p<0.01). A significant inverse correlation of 60-min GLP-1 iAUC was also observed with EAC and CAC (both p<0.01), meaning that patients with a lower GLP-1 response to the test meal had a higher increment of post-prandial glucose for each additional unit of total energy or carbohydrate intake. Conclusions: In Type 2 diabetic patients, a lower GLP-1 response to meals is associated with a higher $ HbA_{1c} $, and with a greater degree of meal-induced hyperglycemia, both in a meal test and during CGM in “real-life” conditions. Continuous glucose monitoring system (dpeaa)DE-He213 diabetes mellitus (dpeaa)DE-He213 glucagon-like peptide-1 (dpeaa)DE-He213 standard test meal (dpeaa)DE-He213 Pala, L. aut Monami, M. aut Vico, L. aut Bardini, G. aut Dicembrini, I. aut Ciani, S. aut Lamanna, C. aut Marchionni, N. aut Rotella, C. M. aut Enthalten in Journal of endocrinological investigation [S. l.] : Springer, 1978 33(2009), 3 vom: 11. Sept., Seite 147-150 (DE-627)369556267 (DE-600)2119482-8 1720-8386 nnns volume:33 year:2009 number:3 day:11 month:09 pages:147-150 https://dx.doi.org/10.1007/BF03346573 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 33 2009 3 11 09 147-150 |
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10.1007/BF03346573 doi (DE-627)SPR03684537X (SPR)BF03346573-e DE-627 ger DE-627 rakwb eng Mannucci, E. verfasserin aut Glucagon-like peptide-1 response to meals and post-prandial hyperglycemia in Type 2 diabetic patients 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Italian Society of Endocrinology (SIE) 2010 Abstract Background: The impaired response of glucagon-like peptide-1 (GLP-1) to meals in diabetic patients can contribute to the pathogenesis of impaired insulin secretion and post-prandial hyperglycemia. This study is aimed at the assessment of the relationship between meal-induced GLP-1 and post-prandial hyperglycemia in Type 2 diabetic patients. Methods: Twenty-one drug-naïve Type 2 diabetic patients were studied. Blood glucose and active GLP-1 levels were measured 0, 30, 60, 90, and 120 min after a standard test meal. A continuous glucose monitoring (CGM) system was applied for the following 3 days. Nutrient intake at each meal was calculated on the basis of patients’ food records. For each patient, post-prandial 120-min glucose incremental area under the curve (iAUC) was included in linear regression model exploring its relationship with total energy and carbohydrate intake, and the angular coefficient for total energy (EAC) and carbohydrate (CAC) was calculated. Results: GLP-1 levels peaked 30 min after the test meal. Logarithmically transformed 60-min GLP-1 iAUC showed a significant inverse correlation with glycated hemoglobin ($ HbA_{1c} $) (p<0.01). A significant inverse correlation of 60-min GLP-1 iAUC was also observed with EAC and CAC (both p<0.01), meaning that patients with a lower GLP-1 response to the test meal had a higher increment of post-prandial glucose for each additional unit of total energy or carbohydrate intake. Conclusions: In Type 2 diabetic patients, a lower GLP-1 response to meals is associated with a higher $ HbA_{1c} $, and with a greater degree of meal-induced hyperglycemia, both in a meal test and during CGM in “real-life” conditions. Continuous glucose monitoring system (dpeaa)DE-He213 diabetes mellitus (dpeaa)DE-He213 glucagon-like peptide-1 (dpeaa)DE-He213 standard test meal (dpeaa)DE-He213 Pala, L. aut Monami, M. aut Vico, L. aut Bardini, G. aut Dicembrini, I. aut Ciani, S. aut Lamanna, C. aut Marchionni, N. aut Rotella, C. M. aut Enthalten in Journal of endocrinological investigation [S. l.] : Springer, 1978 33(2009), 3 vom: 11. Sept., Seite 147-150 (DE-627)369556267 (DE-600)2119482-8 1720-8386 nnns volume:33 year:2009 number:3 day:11 month:09 pages:147-150 https://dx.doi.org/10.1007/BF03346573 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 33 2009 3 11 09 147-150 |
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10.1007/BF03346573 doi (DE-627)SPR03684537X (SPR)BF03346573-e DE-627 ger DE-627 rakwb eng Mannucci, E. verfasserin aut Glucagon-like peptide-1 response to meals and post-prandial hyperglycemia in Type 2 diabetic patients 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Italian Society of Endocrinology (SIE) 2010 Abstract Background: The impaired response of glucagon-like peptide-1 (GLP-1) to meals in diabetic patients can contribute to the pathogenesis of impaired insulin secretion and post-prandial hyperglycemia. This study is aimed at the assessment of the relationship between meal-induced GLP-1 and post-prandial hyperglycemia in Type 2 diabetic patients. Methods: Twenty-one drug-naïve Type 2 diabetic patients were studied. Blood glucose and active GLP-1 levels were measured 0, 30, 60, 90, and 120 min after a standard test meal. A continuous glucose monitoring (CGM) system was applied for the following 3 days. Nutrient intake at each meal was calculated on the basis of patients’ food records. For each patient, post-prandial 120-min glucose incremental area under the curve (iAUC) was included in linear regression model exploring its relationship with total energy and carbohydrate intake, and the angular coefficient for total energy (EAC) and carbohydrate (CAC) was calculated. Results: GLP-1 levels peaked 30 min after the test meal. Logarithmically transformed 60-min GLP-1 iAUC showed a significant inverse correlation with glycated hemoglobin ($ HbA_{1c} $) (p<0.01). A significant inverse correlation of 60-min GLP-1 iAUC was also observed with EAC and CAC (both p<0.01), meaning that patients with a lower GLP-1 response to the test meal had a higher increment of post-prandial glucose for each additional unit of total energy or carbohydrate intake. Conclusions: In Type 2 diabetic patients, a lower GLP-1 response to meals is associated with a higher $ HbA_{1c} $, and with a greater degree of meal-induced hyperglycemia, both in a meal test and during CGM in “real-life” conditions. Continuous glucose monitoring system (dpeaa)DE-He213 diabetes mellitus (dpeaa)DE-He213 glucagon-like peptide-1 (dpeaa)DE-He213 standard test meal (dpeaa)DE-He213 Pala, L. aut Monami, M. aut Vico, L. aut Bardini, G. aut Dicembrini, I. aut Ciani, S. aut Lamanna, C. aut Marchionni, N. aut Rotella, C. M. aut Enthalten in Journal of endocrinological investigation [S. l.] : Springer, 1978 33(2009), 3 vom: 11. Sept., Seite 147-150 (DE-627)369556267 (DE-600)2119482-8 1720-8386 nnns volume:33 year:2009 number:3 day:11 month:09 pages:147-150 https://dx.doi.org/10.1007/BF03346573 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 33 2009 3 11 09 147-150 |
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10.1007/BF03346573 doi (DE-627)SPR03684537X (SPR)BF03346573-e DE-627 ger DE-627 rakwb eng Mannucci, E. verfasserin aut Glucagon-like peptide-1 response to meals and post-prandial hyperglycemia in Type 2 diabetic patients 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Italian Society of Endocrinology (SIE) 2010 Abstract Background: The impaired response of glucagon-like peptide-1 (GLP-1) to meals in diabetic patients can contribute to the pathogenesis of impaired insulin secretion and post-prandial hyperglycemia. This study is aimed at the assessment of the relationship between meal-induced GLP-1 and post-prandial hyperglycemia in Type 2 diabetic patients. Methods: Twenty-one drug-naïve Type 2 diabetic patients were studied. Blood glucose and active GLP-1 levels were measured 0, 30, 60, 90, and 120 min after a standard test meal. A continuous glucose monitoring (CGM) system was applied for the following 3 days. Nutrient intake at each meal was calculated on the basis of patients’ food records. For each patient, post-prandial 120-min glucose incremental area under the curve (iAUC) was included in linear regression model exploring its relationship with total energy and carbohydrate intake, and the angular coefficient for total energy (EAC) and carbohydrate (CAC) was calculated. Results: GLP-1 levels peaked 30 min after the test meal. Logarithmically transformed 60-min GLP-1 iAUC showed a significant inverse correlation with glycated hemoglobin ($ HbA_{1c} $) (p<0.01). A significant inverse correlation of 60-min GLP-1 iAUC was also observed with EAC and CAC (both p<0.01), meaning that patients with a lower GLP-1 response to the test meal had a higher increment of post-prandial glucose for each additional unit of total energy or carbohydrate intake. Conclusions: In Type 2 diabetic patients, a lower GLP-1 response to meals is associated with a higher $ HbA_{1c} $, and with a greater degree of meal-induced hyperglycemia, both in a meal test and during CGM in “real-life” conditions. Continuous glucose monitoring system (dpeaa)DE-He213 diabetes mellitus (dpeaa)DE-He213 glucagon-like peptide-1 (dpeaa)DE-He213 standard test meal (dpeaa)DE-He213 Pala, L. aut Monami, M. aut Vico, L. aut Bardini, G. aut Dicembrini, I. aut Ciani, S. aut Lamanna, C. aut Marchionni, N. aut Rotella, C. M. aut Enthalten in Journal of endocrinological investigation [S. l.] : Springer, 1978 33(2009), 3 vom: 11. Sept., Seite 147-150 (DE-627)369556267 (DE-600)2119482-8 1720-8386 nnns volume:33 year:2009 number:3 day:11 month:09 pages:147-150 https://dx.doi.org/10.1007/BF03346573 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 33 2009 3 11 09 147-150 |
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Enthalten in Journal of endocrinological investigation 33(2009), 3 vom: 11. Sept., Seite 147-150 volume:33 year:2009 number:3 day:11 month:09 pages:147-150 |
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Mannucci, E. @@aut@@ Pala, L. @@aut@@ Monami, M. @@aut@@ Vico, L. @@aut@@ Bardini, G. @@aut@@ Dicembrini, I. @@aut@@ Ciani, S. @@aut@@ Lamanna, C. @@aut@@ Marchionni, N. @@aut@@ Rotella, C. M. @@aut@@ |
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This study is aimed at the assessment of the relationship between meal-induced GLP-1 and post-prandial hyperglycemia in Type 2 diabetic patients. Methods: Twenty-one drug-naïve Type 2 diabetic patients were studied. Blood glucose and active GLP-1 levels were measured 0, 30, 60, 90, and 120 min after a standard test meal. A continuous glucose monitoring (CGM) system was applied for the following 3 days. Nutrient intake at each meal was calculated on the basis of patients’ food records. For each patient, post-prandial 120-min glucose incremental area under the curve (iAUC) was included in linear regression model exploring its relationship with total energy and carbohydrate intake, and the angular coefficient for total energy (EAC) and carbohydrate (CAC) was calculated. Results: GLP-1 levels peaked 30 min after the test meal. Logarithmically transformed 60-min GLP-1 iAUC showed a significant inverse correlation with glycated hemoglobin ($ HbA_{1c} $) (p<0.01). A significant inverse correlation of 60-min GLP-1 iAUC was also observed with EAC and CAC (both p<0.01), meaning that patients with a lower GLP-1 response to the test meal had a higher increment of post-prandial glucose for each additional unit of total energy or carbohydrate intake. 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Mannucci, E. |
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Mannucci, E. misc Continuous glucose monitoring system misc diabetes mellitus misc glucagon-like peptide-1 misc standard test meal Glucagon-like peptide-1 response to meals and post-prandial hyperglycemia in Type 2 diabetic patients |
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Glucagon-like peptide-1 response to meals and post-prandial hyperglycemia in Type 2 diabetic patients Continuous glucose monitoring system (dpeaa)DE-He213 diabetes mellitus (dpeaa)DE-He213 glucagon-like peptide-1 (dpeaa)DE-He213 standard test meal (dpeaa)DE-He213 |
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Glucagon-like peptide-1 response to meals and post-prandial hyperglycemia in Type 2 diabetic patients |
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Mannucci, E. Pala, L. Monami, M. Vico, L. Bardini, G. Dicembrini, I. Ciani, S. Lamanna, C. Marchionni, N. Rotella, C. M. |
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glucagon-like peptide-1 response to meals and post-prandial hyperglycemia in type 2 diabetic patients |
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Glucagon-like peptide-1 response to meals and post-prandial hyperglycemia in Type 2 diabetic patients |
abstract |
Abstract Background: The impaired response of glucagon-like peptide-1 (GLP-1) to meals in diabetic patients can contribute to the pathogenesis of impaired insulin secretion and post-prandial hyperglycemia. This study is aimed at the assessment of the relationship between meal-induced GLP-1 and post-prandial hyperglycemia in Type 2 diabetic patients. Methods: Twenty-one drug-naïve Type 2 diabetic patients were studied. Blood glucose and active GLP-1 levels were measured 0, 30, 60, 90, and 120 min after a standard test meal. A continuous glucose monitoring (CGM) system was applied for the following 3 days. Nutrient intake at each meal was calculated on the basis of patients’ food records. For each patient, post-prandial 120-min glucose incremental area under the curve (iAUC) was included in linear regression model exploring its relationship with total energy and carbohydrate intake, and the angular coefficient for total energy (EAC) and carbohydrate (CAC) was calculated. Results: GLP-1 levels peaked 30 min after the test meal. Logarithmically transformed 60-min GLP-1 iAUC showed a significant inverse correlation with glycated hemoglobin ($ HbA_{1c} $) (p<0.01). A significant inverse correlation of 60-min GLP-1 iAUC was also observed with EAC and CAC (both p<0.01), meaning that patients with a lower GLP-1 response to the test meal had a higher increment of post-prandial glucose for each additional unit of total energy or carbohydrate intake. Conclusions: In Type 2 diabetic patients, a lower GLP-1 response to meals is associated with a higher $ HbA_{1c} $, and with a greater degree of meal-induced hyperglycemia, both in a meal test and during CGM in “real-life” conditions. © Italian Society of Endocrinology (SIE) 2010 |
abstractGer |
Abstract Background: The impaired response of glucagon-like peptide-1 (GLP-1) to meals in diabetic patients can contribute to the pathogenesis of impaired insulin secretion and post-prandial hyperglycemia. This study is aimed at the assessment of the relationship between meal-induced GLP-1 and post-prandial hyperglycemia in Type 2 diabetic patients. Methods: Twenty-one drug-naïve Type 2 diabetic patients were studied. Blood glucose and active GLP-1 levels were measured 0, 30, 60, 90, and 120 min after a standard test meal. A continuous glucose monitoring (CGM) system was applied for the following 3 days. Nutrient intake at each meal was calculated on the basis of patients’ food records. For each patient, post-prandial 120-min glucose incremental area under the curve (iAUC) was included in linear regression model exploring its relationship with total energy and carbohydrate intake, and the angular coefficient for total energy (EAC) and carbohydrate (CAC) was calculated. Results: GLP-1 levels peaked 30 min after the test meal. Logarithmically transformed 60-min GLP-1 iAUC showed a significant inverse correlation with glycated hemoglobin ($ HbA_{1c} $) (p<0.01). A significant inverse correlation of 60-min GLP-1 iAUC was also observed with EAC and CAC (both p<0.01), meaning that patients with a lower GLP-1 response to the test meal had a higher increment of post-prandial glucose for each additional unit of total energy or carbohydrate intake. Conclusions: In Type 2 diabetic patients, a lower GLP-1 response to meals is associated with a higher $ HbA_{1c} $, and with a greater degree of meal-induced hyperglycemia, both in a meal test and during CGM in “real-life” conditions. © Italian Society of Endocrinology (SIE) 2010 |
abstract_unstemmed |
Abstract Background: The impaired response of glucagon-like peptide-1 (GLP-1) to meals in diabetic patients can contribute to the pathogenesis of impaired insulin secretion and post-prandial hyperglycemia. This study is aimed at the assessment of the relationship between meal-induced GLP-1 and post-prandial hyperglycemia in Type 2 diabetic patients. Methods: Twenty-one drug-naïve Type 2 diabetic patients were studied. Blood glucose and active GLP-1 levels were measured 0, 30, 60, 90, and 120 min after a standard test meal. A continuous glucose monitoring (CGM) system was applied for the following 3 days. Nutrient intake at each meal was calculated on the basis of patients’ food records. For each patient, post-prandial 120-min glucose incremental area under the curve (iAUC) was included in linear regression model exploring its relationship with total energy and carbohydrate intake, and the angular coefficient for total energy (EAC) and carbohydrate (CAC) was calculated. Results: GLP-1 levels peaked 30 min after the test meal. Logarithmically transformed 60-min GLP-1 iAUC showed a significant inverse correlation with glycated hemoglobin ($ HbA_{1c} $) (p<0.01). A significant inverse correlation of 60-min GLP-1 iAUC was also observed with EAC and CAC (both p<0.01), meaning that patients with a lower GLP-1 response to the test meal had a higher increment of post-prandial glucose for each additional unit of total energy or carbohydrate intake. Conclusions: In Type 2 diabetic patients, a lower GLP-1 response to meals is associated with a higher $ HbA_{1c} $, and with a greater degree of meal-induced hyperglycemia, both in a meal test and during CGM in “real-life” conditions. © Italian Society of Endocrinology (SIE) 2010 |
collection_details |
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container_issue |
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title_short |
Glucagon-like peptide-1 response to meals and post-prandial hyperglycemia in Type 2 diabetic patients |
url |
https://dx.doi.org/10.1007/BF03346573 |
remote_bool |
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author2 |
Pala, L. Monami, M. Vico, L. Bardini, G. Dicembrini, I. Ciani, S. Lamanna, C. Marchionni, N. Rotella, C. M. |
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Pala, L. Monami, M. Vico, L. Bardini, G. Dicembrini, I. Ciani, S. Lamanna, C. Marchionni, N. Rotella, C. M. |
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doi_str |
10.1007/BF03346573 |
up_date |
2024-07-03T19:54:59.527Z |
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|
score |
7.400387 |