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
Jazyk angličtina Země Spojené státy americké Médium electronic-ecollection
Typ dokumentu časopisecké články, randomizované kontrolované studie, práce podpořená grantem
PubMed
25222490
PubMed Central
PMC4164634
DOI
10.1371/journal.pone.0107561
PII: PONE-D-14-19921
Knihovny.cz E-zdroje
- MeSH
- diabetes mellitus 2. typu krev patologie MeSH
- dieta veganská škodlivé účinky MeSH
- gastrointestinální hormony krev MeSH
- ghrelin krev MeSH
- glukagonu podobný peptid 1 krev MeSH
- inzulin krev MeSH
- krevní glukóza MeSH
- lidé středního věku MeSH
- lidé MeSH
- lipidy krev MeSH
- manipulace s potravinami MeSH
- maso škodlivé účinky MeSH
- postprandiální období MeSH
- triglyceridy krev MeSH
- žaludeční inhibiční polypeptid krev MeSH
- Check Tag
- lidé středního věku MeSH
- lidé MeSH
- mužské pohlaví MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- randomizované kontrolované studie MeSH
- Názvy látek
- gastrointestinální hormony MeSH
- ghrelin MeSH
- glukagonu podobný peptid 1 MeSH
- inzulin MeSH
- krevní glukóza MeSH
- lipidy MeSH
- triglyceridy MeSH
- žaludeční inhibiční polypeptid MeSH
BACKGROUND: The 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. METHODS: In 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. RESULTS: The 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/INTERPRETATION: Our 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 REGISTRATION: ClinicalTrials.gov NCT01572402.
Institute for Clinical and Experimental Medicine Prague Czech Republic
Zobrazit více v PubMed
American Diabetes Association (2013) Standards of medical care in diabetes–2013. Diabetes Care 36 Suppl 1S11–66. PubMed PMC
Savage DB, Petersen KF, Shulman GI (2007) Disordered lipid metabolism and the pathogenesis of insulin resistance. Physiol Rev 87: 507–20. PubMed PMC
Lodefalk M, Aman J, Bang P (2008) Effects of fat supplementation on glycaemic response and gastric emptying in adolescents with Type 1 diabetes. Diabet Med: 1030–5. doi:10.1111/j.1464-5491.2008.02530. PubMed
Gentilcore D, Chaikomin R, Jones KL, Russo A, Feinle-Bisset C, et al. (2006) Effects of fat on gastric emptying of and the glycemic, insulin, and incretin responses to a carbohydrate meal in type 2 diabetes. J Clin Endocrinol Metab 91: 2062–7. PubMed
Wolpert HA, Atakov-Castillo A, Smith SA, Steil GM (2013) Dietary fat acutely increases glucose concentrations and insulin requirements in patients with type 1 diabetes: implications for carbohydrate-based bolus dose calculation and intensive diabetes management. Diabetes Care 36: 810–6. PubMed PMC
Peters AL, Davidson MB (1993) Protein and fat effects on glucose responses and insulin requirements in subjects with insulin-dependent diabetes mellitus. Am J Clin Nutr 58: 555–60. PubMed
Aune D, Ursin G, Veierød MB (2009) Meat consumption and the risk of type 2 diabetes: a systematic review and meta-analysis of cohort studies. Diabetologia 52: 2277–87. PubMed
Pan A1, Sun Q, Bernstein AM, Schulze MB, Manson JE, et al (2011) Red meat consumption and risk of type 2 diabetes: 3 cohorts of US adults and an updated meta-analysis. Am J Clin Nutr 94: 1088–96. PubMed PMC
Pan A1, Sun Q, Bernstein AM, Schulze MB, Manson JE, et al (2008) Meats, processed meats, obesity, weight gain and occurrence of diabetes among adults: findings from Adventist Health Studies. Ann Nutr Metab 52: 96–104. PubMed
Ceriello A, Motz E (2004) Is oxidative stress the pathogenic mechanism underlying insulin resistance, diabetes, and cardiovascular disease? The common soil hypothesis revisited. Arterioscler Thromb Vasc Biol 24: 816–23. PubMed
Feskens EJ, Virtanen SM, Räsänen L, Tuomilehto J, Stengård J, et al. (1995) Dietary factors determining diabetes and impaired glucose tolerance. A 20-year follow-up of the Finnish and Dutch cohorts of the Seven Countries Study. Diabetes Care 18: 1104–12. PubMed
Maron DJ, Fair JM, Haskell WL (1991) Saturated fat intake and insulin resistance in men with coronary artery disease. The Stanford Coronary Risk Intervention Project Investigators and Staff Circulation 84: 2020–7. PubMed
Perez-Martinez P1, Garcia-Quintana JM, Yubero-Serrano EM, Tasset-Cuevas I, Tunez I, et al (2010) Postprandial oxidative stress is modified by dietary fat: evidence from a human intervention study. Clin Sci (Lond) 15: 251–61. PubMed
Cardona F, Túnez I, Tasset I, Montilla P, Collantes E, et al. (2008) Fat overload aggravates oxidative stress in patients with the metabolic syndrome. Eur J Clin Invest 38: 510–5. PubMed
Barnard ND1, Katcher HI, Jenkins DJ, Cohen J, Turner-McGrievy G (2009) Vegetarian and vegan diets in type 2 diabetes management. Nutr Rev 67: 255–63. PubMed
Kahleova H, Matoulek M, Malinska H, Oliyarnik O, Kazdova L, et al. (2011) Vegetarian diet improves insulin resistance and oxidative stress markers more than conventional diet in subjects with Type 2 diabetes. Diabet Med 28: 549–59. PubMed PMC
Kellar KL, Iannone MA (2002) Multiplexed microsphere-based flow cytometric assays. Exp Hematol 30: 1227–37. PubMed
Yokode M1, Kita T, Kikawa Y, Ogorochi T, Narumiya S, et al (1988) Stimulated arachidonate metabolism during foam cell transformation of mouse peritoneal macrophages with oxidized low density lipoprotein. J. Clin Invest 81: 720–9. PubMed PMC
Nakagawa K, Kanno H, Miura Y (1997) Detection and analyses of ascorbyl radical in cerebrospinal fluid and serum of acute lymphoblastic leukemia. Anal Biochem 254: 31–5. PubMed
Meloun M, Hill M, Militký J, Kupka K (2000) Transformation in the PC-aided biochemical data analysis. Clin Chem Lab Med 38: 553–9. PubMed
Nuttall FQ, Gannon MC, Wald JL, Ahmed M (1985) Plasma glucose and insulin profiles in normal subjects ingesting diets of varying carbohydrate, fat and protein content. J Am Coll Nutr 4: 437–50. PubMed
Estrich D, Ravnik A, Schlierf G, Fukayama G, Kinsell L, et al. (1967) Effects of Co-ingestion of fat and protein upon carbohydrate-induced hyperglycemia. Diabetes 16: 232–7. PubMed
Bajaj M, Suraamornkul S, Kashyap S, Cusi K, Mandarino L, et al. (2004) Sustained reduction in plasma free fatty acid concentration improves insulin action without altering plasma adipocytokine levels in subjects with strong family history of type 2 diabetes. J Clin Endocrinol Metab 89: 4649–55. PubMed
Gormsen LC, Nielsen C, Jessen N, Jørgensen JO, Møller N (2011) Time-course effects of physiological free fatty acid surges on insulin sensitivity in humans. Acta Physiol 201: 349–56. PubMed
Tolhurst G, Reimann F, Gribble FM (2012) Intestinal sensing of nutrients. Handb Exp Pharmacol 209: 309–35. PubMed
Creutzfeld W (1979) The incretin concept today. Diabetologia 16: 75–85. PubMed
Nauck MA, Homberger E, Siegel EG, Allen RC, Eaton RP, et al. (1986) Incretin effects of increasing glucose loads in man calculated from venous insulin and C-peptide responses. J Clin Endocrinol Metab 63: 492–8. PubMed
Nauck M, Stöckmann F, Ebert R, Creutzfeldt W, et al. (1986) Reduced incretin effect in type 2 (non-insulin-dependent) diabetes. Diabetologia 29: 46–52. PubMed
Knop FK, Vilsbøll T, Højberg PV, Larsen S, Madsbad S, et al. (2007) Reduced incretin effect in type 2 diabetes: cause or consequence of the diabetic state? Diabetes 56: 1951–9. PubMed
Kjems LL, Holst JJ, Vølund A, Madsbad S (2003) The influence of GLP-1 on glucose-stimulated insulin secretion: effects on beta-cell sensitivity in type 2 and nondiabetic subjects. Diabetes 52: 380–6. PubMed
Xu G1, Kaneto H, Laybutt DR, Duvivier-Kali VF, Trivedi N, et al (2007) Downregulation of GLP-1 and GIP receptor expression by hyperglycemia: possible contribution to impaired incretin effects in diabetes. Diabetes 56: 1551–8. PubMed
Kang ZF1, Deng Y, Zhou Y, Fan RR, Chan JC, et al (2013) Pharmacological reduction of NEFA restores the efficacy of incretin-based therapies through GLP-1 receptor signalling in the beta cell in mouse models of diabetes. Diabetologia 56: 423–33. PubMed PMC
Vollmer K1, Holst JJ, Baller B, Ellrichmann M, Nauck MA, et al (2008) Predictors of incretin concentrations in subjects with normal, impaired and diabetic glucose tolerance. Diabetes 57: 678–87. PubMed
Rijkelijkhuizen JM1, McQuarrie K, Girman CJ, Stein PP, Mari A, et al (2010) Effects of meal size and composition on incretin, alpha-cell, and beta-cell responses. Metabolism 59: 502–11. PubMed
Carr RD1, Larsen MO, Winzell MS, Jelic K, Lindgren O, et al (2008) Incretin and islet hormonal responses to fat and protein ingestion in healthy men. Am J Physiol Endocrinol Metab 295: E779–84. PubMed
Carrel G1, Egli L, Tran C, Schneiter P, Giusti V, et al (2011) Contributions of fat and protein to the incretin effect of a mixed meal. Am J Clin Nutr 94: 997–1003. PubMed PMC
Fernández-García JC1, Murri M, Coin-Aragüez L, Alcaide J, El Bekay R, et al (2014) 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. Clin Endocrinol (Oxf) 80: 671–6. PubMed
Meier JJ, Nauck MA (2010) Is the diminished incretin effect in type 2 diabetes just an epi-phenomenon of impaired beta-cell function? Diabetes 59: 1117–25. PubMed PMC
Calanna S1, Christensen M, Holst JJ, Laferrère B, Gluud LL, et al (2013) Secretion of glucagon-like peptide-1 in patients with type 2 diabetes mellitus: systematic review and meta-analyses of clinical studies. Diabetologia 56: 965–72. PubMed PMC
Cernea S (2011) The role of incretin therapy at different stages of diabetes. Rev Diabet Stud Fall 8: 323–38. PubMed PMC
Vilsbøll T, Krarup T, Deacon CF, Madsbad S, Holst JJ (2001) Reduced postprandial concentrations of intact biologically active glucagon-like peptide 1 in type 2 diabetic patients. Diabetes 50: 609–13. PubMed
Kim BJ1, Carlson OD, Jang HJ, Elahi D, Berry C, et al (2005) Peptide YY is secreted after oral glucose administration in a gender-specific manner. J Clin Endocrinol Metab 90: 6665–71. PubMed
Batterham RL1, Le Roux CW, Cohen MA, Park AJ, Ellis SM, et al (2003) Pancreatic polypeptide reduces appetite and food intake in humans. J Clin Endocrinol Metab 88: 3989–92. PubMed
Feinle-Bisset C1, Patterson M, Ghatei MA, Bloom SR, Horowitz M (2005) Fat digestion is required for suppression of ghrelin and stimulation of peptide YY and pancreatic polypeptide secretion by intraduodenal lipid. Am J Physiol Endocrinol Metab 289: E948–53. PubMed
Adrian TE, Ferri GL, Bacarese-Hamilton AJ, Fuessl HS, Polak JM, et al. (1985) Human distribution and release of a putative new gut hormone, peptide YY. Gastroenterology 89: 1070–7. PubMed
Wren AM1, Small CJ, Ward HL, Murphy KG, Dakin CL, et al (2000) The novel hypothalamic peptide ghrelin stimulates food intake and growth hormone secretion. Endocrinology 141: 4325–8. PubMed
Blom WA, Stafleu A, de Graaf C, Kok FJ, Schaafsma G, et al. (2005) Ghrelin response to carbohydrate-enriched breakfast is related to insulin. Am J Clin Nutr 81: 367–75. PubMed
Hagemann D1, Holst JJ, Gethmann A, Banasch M, Schmidt WE, et al (2007) Glucagon-like peptide 1 (GLP-1) suppresses ghrelin levels in humans via increased insulin secretion. Regul Pept 143: 64–8. PubMed
Ceriello A, Esposito K, Testa R, Bonfigli AR, Marra M, et al. (2011) The possible protective role of glucagon-like peptide 1 on endothelium during the meal and evidence for an “endothelial resistance” to glucagon-like peptide 1 in diabetes. Diabetes Care 34: 697–702. PubMed PMC
Goldberg T1, Cai W, Peppa M, Dardaine V, Baliga BS, et al (2004) Advanced glycoxidation end products in commonly consumed foods. J Am Diet Assoc 104: 1287–91. PubMed
Li Z1, Henning SM, Zhang Y, Zerlin A, Li L, et al (2010) Antioxidant-rich spice added to hamburger meat during cooking results in reduced meat, plasma, and urine malondialdehyde concentrations. Am J Clin Nutr 91: 1180–4. PubMed PMC
Runchey SS, Valsta LM, Schwarz Y, Wang C, Song X, et al. (2013) Effect of low- and high-glycemic load on circulating incretins in a randomized clinical trial. Metabolism 62: 188–95. PubMed PMC
ClinicalTrials.gov
NCT01572402