Effects of type 2 diabetes on insulin secretion, insulin action, glucose effectiveness, and postprandial glucose metabolism

Ananda Basu, Chiara Dalla Man, Rita Basu, Gianna Toffolo, Claudio Cobelli, Robert A. Rizza

Research output: Contribution to journalArticle

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Abstract

OBJECTIVE - In this study, we sought to determine whether postprandial insulin secretion, insulin action, glucose effectiveness, and glucose turnover were abnormal in type 2 diabetes. RESEARCH DESIGN AND METHODS - Fourteen subjects with type 2 diabetes and 11 nondiabetic subjects matched for age, weight, and BMI underwent a mixed-meal test using the triple-tracer technique. Indexes of insulin secretion, insulin action, and glucose effectiveness were assessed using the oral "minimal" and C-peptide models. RESULTS - Fasting and postprandial glucose concentrations were higher in the diabetic than nondiabetic subjects. Although peak insulin secretion was delayed (P < 0.001) and lower (P < 0.05) in type 2 diabetes, the integrated total postprandial insulin response did not differ between groups. Insulin action, insulin secretion, disposition indexes, and glucose effectiveness all were lower (P < 0.05) in diabetic than in nondiabetic subjects. Whereas the rate of meal glucose appearance did not differ between groups, the percent suppression of endogenous glucose production (EGP) was slightly delayed and the increment in glucose disappearance was substantially lower (P < 0.01) in diabetic subjects during the first 3 h after meal ingestion. Together, these defects resulted in an excessive rise in postprandial glucose concentrations in the diabetic subjects. CONCLUSIONS - When measured using methods that avoid non-steady-state error, the rate of appearance of ingested glucose was normal and suppression of EGP was only minimally impaired. However, when considered in light of the prevailing glucose concentration, both were abnormal. In contrast, rates of postprandial glucose disappearance were substantially decreased due to defects in insulin secretion, insulin action, and glucose effectiveness.

Original languageEnglish (US)
Pages (from-to)866-872
Number of pages7
JournalDiabetes Care
Volume32
Issue number5
DOIs
StatePublished - May 2009

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Type 2 Diabetes Mellitus
Insulin
Glucose
Meals
C-Peptide
Fasting
Research Design
Eating

ASJC Scopus subject areas

  • Internal Medicine
  • Endocrinology, Diabetes and Metabolism
  • Advanced and Specialized Nursing

Cite this

Effects of type 2 diabetes on insulin secretion, insulin action, glucose effectiveness, and postprandial glucose metabolism. / Basu, Ananda; Dalla Man, Chiara; Basu, Rita; Toffolo, Gianna; Cobelli, Claudio; Rizza, Robert A.

In: Diabetes Care, Vol. 32, No. 5, 05.2009, p. 866-872.

Research output: Contribution to journalArticle

Basu, Ananda ; Dalla Man, Chiara ; Basu, Rita ; Toffolo, Gianna ; Cobelli, Claudio ; Rizza, Robert A. / Effects of type 2 diabetes on insulin secretion, insulin action, glucose effectiveness, and postprandial glucose metabolism. In: Diabetes Care. 2009 ; Vol. 32, No. 5. pp. 866-872.
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AU - Toffolo, Gianna

AU - Cobelli, Claudio

AU - Rizza, Robert A.

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AB - OBJECTIVE - In this study, we sought to determine whether postprandial insulin secretion, insulin action, glucose effectiveness, and glucose turnover were abnormal in type 2 diabetes. RESEARCH DESIGN AND METHODS - Fourteen subjects with type 2 diabetes and 11 nondiabetic subjects matched for age, weight, and BMI underwent a mixed-meal test using the triple-tracer technique. Indexes of insulin secretion, insulin action, and glucose effectiveness were assessed using the oral "minimal" and C-peptide models. RESULTS - Fasting and postprandial glucose concentrations were higher in the diabetic than nondiabetic subjects. Although peak insulin secretion was delayed (P < 0.001) and lower (P < 0.05) in type 2 diabetes, the integrated total postprandial insulin response did not differ between groups. Insulin action, insulin secretion, disposition indexes, and glucose effectiveness all were lower (P < 0.05) in diabetic than in nondiabetic subjects. Whereas the rate of meal glucose appearance did not differ between groups, the percent suppression of endogenous glucose production (EGP) was slightly delayed and the increment in glucose disappearance was substantially lower (P < 0.01) in diabetic subjects during the first 3 h after meal ingestion. Together, these defects resulted in an excessive rise in postprandial glucose concentrations in the diabetic subjects. CONCLUSIONS - When measured using methods that avoid non-steady-state error, the rate of appearance of ingested glucose was normal and suppression of EGP was only minimally impaired. However, when considered in light of the prevailing glucose concentration, both were abnormal. In contrast, rates of postprandial glucose disappearance were substantially decreased due to defects in insulin secretion, insulin action, and glucose effectiveness.

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