<scp>GLP</scp>‐1 and peptide <scp>YY</scp> secretory response after fat load is impaired by insulin resistance, impaired fasting glucose and type 2 diabetes in morbidly obese subjects

Fernández‐García, José Carlos; Murri, Mora; Coín‐Aragüez, Leticia; Bekay, Rajaa El; Tinahones, Francisco J.

doi:10.1111/cen.12221

Cited by 25 publications

(21 citation statements)

References 41 publications

(78 reference statements)

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“…In the T2D patients, the V-meal resulted in a larger release of GLP-1 and GIP than the M-meal. This result is in accordance with a study suggesting that the GLP-1 response after fat intake is impaired in T2D patients [37]. In contrast, in healthy individuals, the GLP-1 and GIP responses after ingestion of the V-meal were smaller than after the M-meal.…”

Section: Discussionsupporting

confidence: 93%

“…This result was not detected in our diabetic group of patients; their postprandial response with respect to both peptides was significantly higher after the V-meal. Similarly, a previous study suggested that both insulin resistance and abnormal glucose metabolism impaired the PYY response to fat intake [37]. To the best of our knowledge, this is the first report of the different secretory responses of PP after both isocaloric meals in T2D patients compared with healthy controls.…”

Section: Discussionsupporting

confidence: 70%

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Differential Acute Postprandial Effects of Processed Meat and Isocaloric Vegan Meals on the Gastrointestinal Hormone Response in Subjects Suffering from Type 2 Diabetes and Healthy Controls: A Randomized Crossover Study

et al. 2014

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BackgroundThe intake of meat, particularly processed meat, is a dietary risk factor for diabetes. Meat intake impairs insulin sensitivity and leads to increased oxidative stress. However, its effect on postprandial gastrointestinal hormone (GIH) secretion is unclear. We aimed to investigate the acute effects of two standardized isocaloric meals: a processed hamburger meat meal rich in protein and saturated fat (M-meal) and a vegan meal rich in carbohydrates (V-meal). We hypothesized that the meat meal would lead to abnormal postprandial increases in plasma lipids and oxidative stress markers and impaired GIH responses.MethodsIn a randomized crossover study, 50 patients suffering from type 2 diabetes (T2D) and 50 healthy subjects underwent two 3-h meal tolerance tests. For statistical analyses, repeated-measures ANOVA was performed.ResultsThe M-meal resulted in a higher postprandial increase in lipids in both groups (p<0.001) and persistent postprandial hyperinsulinemia in patients with diabetes (p<0.001). The plasma glucose levels were significantly higher after the V-meal only at the peak level. The plasma concentrations of glucose-dependent insulinotropic peptide (GIP), peptide tyrosine-tyrosine (PYY) and pancreatic polypeptide (PP) were higher (p<0.05, p<0.001, p<0.001, respectively) and the ghrelin concentration was lower (p<0.001) after the M-meal in healthy subjects. In contrast, the concentrations of GIP, PYY and PP were significantly lower after the M-meal in T2D patients (p<0.001). Compared with the V-meal, the M-meal was associated with a larger increase in lipoperoxidation in T2D patients (p<0.05).Conclusion/InterpretationOur results suggest that the diet composition and the energy content, rather than the carbohydrate count, should be important considerations for dietary management and demonstrate that processed meat consumption is accompanied by impaired GIH responses and increased oxidative stress marker levels in diabetic patients.Trial RegistrationClinicalTrials.gov NCT01572402

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Section: Discussionsupporting

confidence: 93%

Section: Discussionsupporting

confidence: 70%

Differential Acute Postprandial Effects of Processed Meat and Isocaloric Vegan Meals on the Gastrointestinal Hormone Response in Subjects Suffering from Type 2 Diabetes and Healthy Controls: A Randomized Crossover Study

et al. 2014

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“…Several studies reported a reduced postprandial GLP-1 response in obese or insulin-resistant participants (42–45). By comparing the net iAUCs between the normal-weight and obese groups, we could not identify a significant difference in the GLP-1 response at any of the caloric doses investigated.…”

Section: Discussionmentioning

confidence: 99%

A Dose-Response Strategy Reveals Differences between Normal-Weight and Obese Men in Their Metabolic and Inflammatory Responses to a High-Fat Meal

Schwander

Kopf-Bolanz

Buri

et al. 2014

The Journal of Nutrition

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A dose-response strategy may not only allow investigation of the impact of foods and nutrients on human health but may also reveal differences in the response of individuals to food ingestion based on their metabolic health status. In a randomized crossover study, we challenged 19 normal-weight (BMI: 20–25 kg/m2) and 18 obese (BMI: >30 kg/m2) men with 500, 1000, and 1500 kcal of a high-fat (HF) meal (60.5% energy from fat). Blood was taken at baseline and up to 6 h postprandially and analyzed for a range of metabolic, inflammatory, and hormonal variables, including plasma glucose, lipids, and C-reactive protein and serum insulin, glucagon-like peptide-1, interleukin-6 (IL-6), and endotoxin. Insulin was the only variable that could differentiate the postprandial response of normal-weight and obese participants at each of the 3 caloric doses. A significant response of the inflammatory marker IL-6 was only observed in the obese group after ingestion of the HF meal containing 1500 kcal [net incremental AUC (iAUC) = 22.9 ± 6.8 pg/mL × 6 h, P = 0.002]. Furthermore, the net iAUC for triglycerides significantly increased from the 1000 to the 1500 kcal meal in the obese group (5.0 ± 0.5 mmol/L × 6 h vs. 6.0 ± 0.5 mmol/L × 6 h; P = 0.015) but not in the normal-weight group (4.3 ± 0.5 mmol/L × 6 h vs. 4.8 ± 0.5 mmol/L × 6 h; P = 0.31). We propose that caloric dose-response studies may contribute to a better understanding of the metabolic impact of food on the human organism. This study was registered at clinicaltrials.gov as NCT01446068.

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“…In morbidly obese patients, an oral fat load (60 g fat – 12 g saturated, 35.25 g monounsaturated and 12.75 g polyunsaturated) increased GLP‐1 secretion in normal fasting glucose with low insulin‐resistant subjects but not in normal fasting glucose with high insulin resistance, impaired fasting glucose or type 2 diabetic subjects (Fernandez‐Garcia et al . ). Furthermore, in healthy human volunteers, saturated, monounsaturated or polyunsaturated fatty acids ingestion increased plasma GLP‐1 concentration over 300 min with the largest increase induced by monounsaturated fatty acids and the least increase by saturated fatty acid (Beysen et al .…”

Section: Expression Secretion and Metabolism Of Glp‐1mentioning

confidence: 97%

“…) but fat‐induced GLP‐1 secretion is diminished (Fernandez‐Garcia et al . ). Leptin and insulin are both GLP‐1 secretagogues, and resistance to either hormone is known to inhibit GLP‐1 secretion (Anini and Brubaker, , Lim et al .…”

Section: Expression Secretion and Metabolism Of Glp‐1mentioning

confidence: 97%

Mechanisms for the cardiovascular effects of glucagon-like peptide-1

Poudyal

2015

Acta Physiol

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Over the past three decades, at least 10 hormones secreted by the enteroendocrine cells have been discovered, which directly affect the cardiovascular system through their innate receptors expressed in the heart and blood vessels or through a neural mechanism. Glucagon-like peptide-1 (GLP-1), an important incretin, is perhaps best studied of these gut-derived hormones with important cardiovascular effects. In this review, I have discussed the mechanism of GLP-1 release from the enteroendocrine L-cells and its physiological effects on the cardiovascular system. Current evidence suggests that GLP-1 has positive inotropic and chronotropic effects on the heart and may be important in preserving left ventricular structure and function by direct and indirect mechanisms. The direct effects of GLP-1 in the heart may be mediated through GLP-1R expressed in atria as well as arteries and arterioles in the left ventricle and mainly involve in the activation of multiple pro-survival kinases and enhanced energy utilization. There is also good evidence to support the involvement of a second, yet to be identified, GLP-1 receptor. Further, GLP-1(9-36)amide, which was previously thought to be the inactive metabolite of the active GLP-1(7-36)amide, may also have direct cardioprotective effects. GLP-1's action on GLP-1R expressed in the central nervous system, kidney, vasculature and the pancreas may indirectly contribute to its cardioprotective effects.

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GLP‐1 and peptide YY secretory response after fat load is impaired by insulin resistance, impaired fasting glucose and type 2 diabetes in morbidly obese subjects

Abstract: These results suggest that in morbidly obese subjects, both insulin resistance and abnormal glucose metabolism (IFG or T2D) impair the GLP-1 and PYY response to fat load. The implications of this attenuated enteroendocrine response should be elucidated by further studies.

Cited by 25 publications

References 41 publications

Differential Acute Postprandial Effects of Processed Meat and Isocaloric Vegan Meals on the Gastrointestinal Hormone Response in Subjects Suffering from Type 2 Diabetes and Healthy Controls: A Randomized Crossover Study

Differential Acute Postprandial Effects of Processed Meat and Isocaloric Vegan Meals on the Gastrointestinal Hormone Response in Subjects Suffering from Type 2 Diabetes and Healthy Controls: A Randomized Crossover Study

A Dose-Response Strategy Reveals Differences between Normal-Weight and Obese Men in Their Metabolic and Inflammatory Responses to a High-Fat Meal

Mechanisms for the cardiovascular effects of glucagon-like peptide-1

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