Reduced gastric inhibitory polypeptide but normal glucagon-like peptide 1 response to oral glucose in postmenopausal women with impaired glucose tolerance

Åhrén, Bo; Larsson, Hillevi; Holst, Jens J.

doi:10.1530/eje.0.1370127

Cited by 51 publications

(39 citation statements)

References 35 publications

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“…Another explanation for the higher GLP-1 response after oral glucose vs the solid mixed meal would be an accelerated gastric emptying that has been described for early diabetic patients during a liquid meal (38,39). In line with earlier studies, GLP-1 response among persons with IH was unaltered (7,8,10,40,41). This suggests that a defect in GLP-1 secretion is unlikely to precede type 2 diabetes development, which is consistent with earlier findings among first-degree diabetes relatives, and in induced insulin resistance among healthy subjects (27,42).…”

Section: Figure 1 Glucose Insulin and Triglyceride Responses (Meangssupporting

confidence: 90%

“…Earlier studies among diabetic patients mostly report no change in GIP response after a meal or oral glucose (10,11,12,13), a higher response (7, 9, 41) or a slightly lower response (8,44). Similarly, GIP response among persons with IH has been reported unaltered (8,41), decreased (40) or increased (7). Obesity has been reported to be associated with higher GIP responses (43), but we did not find a relationship between BMI and GIP meal response.…”

Section: Figure 1 Glucose Insulin and Triglyceride Responses (Meangscontrasting

confidence: 81%

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Preserved GLP-1 and exaggerated GIP secretion in type 2 diabetes and relationships with triglycerides and ALT

Alssema

Rijkelijkhuizen²,

Holst³

et al. 2013

European Journal of Endocrinology

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Objective: To i) compare incretin responses to oral glucose and mixed meal of diabetic patients with the normoglycaemic population and ii) to investigate whether incretin responses are associated with hypertriglyceridaemia and alanine aminotransferase (ALT) as liver fat marker. Design: A population-based study. Methods: A total of 163 persons with normal glucose metabolism (NGM), 20 with intermediate hyperglycaemia and 20 with type 2 diabetes aged 40-65 years participated. Participants received a mixed meal and oral glucose load on separate occasions. Glucagon-like peptide 1 (GLP-1), glucosedependent insulinotropic polypeptide (GIP) and glucagon profiles were analysed as total area under the curve (tAUC) and incremental area under the curve. Results: In diabetic patients compared with persons with NGM, we found increased GLP-1 secretion (tAUC per hour) following oral glucose (23.2 pmol/l (95% CI 17.7-28.7) vs 18.0 (95% CI 16.9-19.1), P!0.05) but not after the mixed meal. GIP secretion among diabetic patients was increased on both occasions (82.9 pmol/l (55.9-109.8) vs 47.1 (43.8-50.4) for oral glucose and 130.6 (92.5-168.7) vs 83.2 (77.5-88.9) for mixed meal, both P!0.05). After oral glucose, GLP-1 (tAUC per hour) was inversely related to fasting triglycerides. GIP (tAUC per hour) was positively related to fasting and postprandial triglycerides. Higher fasting GIP levels were related to higher fasting and postprandial triglyceride levels and ALT. Conclusion: This study confirms that in type 2 diabetes, GLP-1 secretion is generally preserved and that GIP secretion is exaggerated. The mechanism underlying the divergent associations of GLP-1 and GIP metabolism with fat metabolism and liver fat accumulation warrants further study.

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Section: Figure 1 Glucose Insulin and Triglyceride Responses (Meangssupporting

confidence: 90%

Section: Figure 1 Glucose Insulin and Triglyceride Responses (Meangscontrasting

confidence: 81%

Preserved GLP-1 and exaggerated GIP secretion in type 2 diabetes and relationships with triglycerides and ALT

Alssema

Rijkelijkhuizen²,

Holst³

et al. 2013

European Journal of Endocrinology

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show abstract

“…Normal GLP-1 responses were reported in some subjects with impaired glucose tolerance [96,106], whereas an impairment was identified in others. However, further analysis concluded that the reductions could largely be explained by differences in BMI and/or insulin sensitivity [93,107].…”

Section: Subjects At Risk Of Developing Type 2 Diabetesmentioning

confidence: 99%

Physiology of Incretins in Health and Disease

Deacon

Åhrén²

2011

Rev Diabet Stud

112

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■ AbstractThe incretin hormones, glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1), are gut peptides which are secreted by endocrine cells in the intestinal mucosa. Their plasma concentrations increase quickly following food ingestion, and carbohydrate, fat, and protein have all been shown to stimulate GLP-1 and GIP secretion. Although neural and hormonal mechanisms have also been proposed to regulate incretin hormone secretion, direct stimulation of the enteroendocrine cells by the presence of nutrients in the intestinal lumen is probably the most important factor in humans. The actions of the incretin hormones are crucial for maintaining normal islet function and glucose homeostasis. Furthermore, it is also now being recognized that incretin hormones may have other actions in addition to their glucoregulatory effects. Studies have shown that GLP-1 and GIP levels and actions may be perturbed in disease states, but interpretation of the precise relationship between disease and incretins is difficult. The balance of evidence seems to suggest that alterations in secretion and/or action of incretin hormones arise secondarily to the development of insulin resistance, glucose intolerance, and/or increases in body weight rather than being causative factors. However, these impairments may contribute to the deterioration of glycemic control in diabetic patients.

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“…Disturbance of incretin secretion may also be present in insulin-resistant states, because a reduced GIP response after an oral glucose tolerance test has been demonstrated in middle-aged women with IGT (8). Furthermore, a reduced GLP-1 response after food intake occurs in obese individuals (9).…”

mentioning

confidence: 99%

Impaired Incretin Response After a Mixed Meal Is Associated With Insulin Resistance in Nondiabetic Men

et al. 2001

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OBJECTIVE -To investigate whether features of the insulin resistance syndrome are associated with altered incretin responses to food intake. RESEARCH DESIGN AND METHODS-From a population-based study, 35 men were recruited, representing a wide spectrum of insulin sensitivity and body weight. Each subject underwent a hyperinsulinemic-euglycemic clamp to determine insulin sensitivity. A mixed meal was given, and plasma levels of gastric inhibitory polypeptide (GIP) and glucagon-like peptide 1 (GLP-1), as well as insulin, glucagon, and glucose were measured.RESULTS -Insulin resistance was associated with impaired GIP and GLP-1 responses to a mixed meal. The total area under the curve (AUC) of the GIP response after the mixed meal was associated with insulin sensitivity (r ϭ 0.54, P Ͻ 0.01). There was a significant difference between the highest and the lowest tertile of insulin sensitivity (P Ͻ 0.05). GLP-1 levels 15 min after food intake were significantly lower in the most insulin-resistant tertile compared with the most insulin-sensitive tertile. During the first hour, the AUC of GLP-1 correlated significantly with insulin sensitivity (r ϭ 0.47, P Ͻ 0.01). Multiple linear regression analysis showed that insulin resistance, but not obesity, was an independent predictor of these decreased incretin responses.CONCLUSIONS -In insulin resistance, the GIP and GLP-1 responses to a mixed meal are impaired and are related to the degree of insulin resistance. Decreased incretin responsiveness may be of importance for the development of impaired glucose tolerance.

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Reduced gastric inhibitory polypeptide but normal glucagon-like peptide 1 response to oral glucose in postmenopausal women with impaired glucose tolerance

Cited by 51 publications

References 35 publications

Preserved GLP-1 and exaggerated GIP secretion in type 2 diabetes and relationships with triglycerides and ALT

Preserved GLP-1 and exaggerated GIP secretion in type 2 diabetes and relationships with triglycerides and ALT

Physiology of Incretins in Health and Disease

Impaired Incretin Response After a Mixed Meal Is Associated With Insulin Resistance in Nondiabetic Men

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