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- Lindgren, Ola, et al.
(författare)
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Incretin Effect after Oral Amino Acid Ingestion in Humans.
- 2015
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Ingår i: Journal of Clinical Endocrinology and Metabolism. - : The Endocrine Society. - 1945-7197 .- 0021-972X. ; 100:3, s. 1172-1176
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Tidskriftsartikel (refereegranskat)abstract
- Context: The incretin effect is the augmented insulin secretion by oral versus intravenous glucose at matching glucose levels. We previously demonstrated an augmented insulin secretion when fat is given orally rather than intravenously, suggesting an incretin effect also after fat. However, whether there is an incretin effect is also present after amino acid ingestion is not known. Objective: To explore insulin secretion and islet hormones after oral and intravenous amino acid administration at matched total amino acid concentrations in healthy subjects. Design: Amino acid mixture (Vaminolac(R)) was administered orally or intravenously at a rate resulting in matching total amino acid concentrations to twelve male volunteers with age 22.5±1.4 yr and BMI 22.4±1.4 kg/m(2), who had no history of diabetes. Main outcome measures: Area under the 120 min curve (AUC) for insulin, C-peptide, glucagon, intact and total glucagon like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) and insulin secretory rate and insulin clearance. Results: Insulin, C-peptide and glucagon levels increased after both oral and intravenous administration, but insulin secretion was 25% higher after oral than after intravenous amino acid challenges (P=0.006), whereas there was no significant difference in the glucagon response. Intact and total GIP rose after oral but not after intravenous amino acid administration, whereas intact and total GLP-1 levels did not change significantly in either test. Conclusion: Oral amino acid mixture ingestion elicits a stronger insulin secretory response than intravenous amino acid at matching amino acid levels and that this is associated with increased GIP level, suggesting that an incretin effect exists also after oral amino acids, possibly mediated by GIP.
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| 2. |
- Lindgren, Ola, et al.
(författare)
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Incretin Hormone and Insulin Responses to Oral Versus Intravenous Lipid Administration in Humans.
- 2011
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Ingår i: The Journal of clinical endocrinology and metabolism. - : The Endocrine Society. - 1945-7197 .- 0021-972X. ; 96, s. 2519-2524
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Tidskriftsartikel (refereegranskat)abstract
- Context: The incretin effect is responsible for the higher insulin response to oral glucose than to iv glucose at matching glucose levels. It is not known whether this effect is restricted to glucose only. Objective: The aim of the study was to examine whether insulin and incretin hormone responses are higher after oral vs. iv challenge of a lipid emulsion with matching triglyceride levels in humans. Design, Settings, and Participants: A lipid emulsion (Intralipid) was administered orally (3 ml/kg) or iv (variable infusion rates to match triglyceride levels after oral ingestion) in healthy lean males (n = 12) at a University Clinical Research Unit. Samples were collected during 300 min. Main Outcome Measures: We measured the suprabasal area under the curve for insulin, glucagon-like peptide-1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP), and the insulin secretory rate based on C-peptide levels by deconvolution. Results: Triglyceride levels increased similarly after oral and iv lipid; also, glucose and free fatty acid levels were similar in the two tests. Oral lipid elicited a clear insulin and C-peptide response, whereas no insulin or C-peptide responses were observed during iv lipid. Total and intact GIP and GLP-1 levels both increased after oral lipid administration but were not significantly altered after iv lipid. Conclusions: At matching triglyceride levels and with no difference in glucose and free fatty acid levels, oral lipid ingestion but not iv lipid infusion elicits a clear insulin response in association with increased GIP and GLP-1 concentrations. This may suggest that the incretin hormones also contribute to the islet response to noncarbohydrate nutrients.
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