Postprandial oxidative stress and gastrointestinal hormones: is there a link?
Language English Country United States Media electronic-ecollection
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
25141237
PubMed Central
PMC4139261
DOI
10.1371/journal.pone.0103565
PII: PONE-D-13-44113
Knihovny.cz E-resources
- MeSH
- Diabetes Mellitus, Type 2 blood MeSH
- Gastrointestinal Hormones blood MeSH
- Insulin blood MeSH
- Blood Glucose analysis MeSH
- Fatty Acids, Nonesterified blood MeSH
- Middle Aged MeSH
- Humans MeSH
- Lipids blood MeSH
- Oxidative Stress physiology MeSH
- Postprandial Period physiology MeSH
- Check Tag
- Middle Aged MeSH
- Humans MeSH
- Male MeSH
- Female MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Gastrointestinal Hormones MeSH
- Insulin MeSH
- Blood Glucose MeSH
- Fatty Acids, Nonesterified MeSH
- Lipids MeSH
BACKGROUND: Abnormal postprandial elevation of plasma glucose and lipids plays an important role in the pathogenesis of diabetes and strongly predicts cardiovascular mortality. In patients suffering from type 2 diabetes (T2D) postprandial state is associated with oxidative stress, cardiovascular risk and, probably, with impairment of both secretion and the effect of gastrointestinal peptides. Evaluating postprandial changes of gastrointestinal hormones together with changes in oxidative stress markers may help to understand the mechanisms behind the postprandial state in diabetes as well as suggest new preventive and therapeutical strategies. METHODS: A standard meal test has been used for monitoring the postprandial concentrations of gastrointestinal hormones and oxidative stress markers in patients with T2D (n = 50) compared to healthy controls (n = 50). Blood samples were drawn 0, 30, 60, 120 and 180 minutes after the standard meal. RESULTS: Both basal and postprandial plasma concentrations of glucose and insulin proved to be significantly higher in patients with T2D, whereas plasma concentrations of ghrelin showed significantly lower values during the whole meal test. In comparison with healthy controls, both basal and postprandial concentrations of almost all other gastrointestinal hormones and lipoperoxidation were significantly increased while ascorbic acid, reduced glutathione and superoxide dismutase activity were decreased in patients with T2D. A positive relationship was found between changes in GIP and those of glucose and immunoreactive insulin in diabetic patients (p<0.001 and p<0.001, respectively) and between changes in PYY and those of glucose (p<0.01). There was a positive correlation between changes in GIP and PYY and changes in ascorbic acid in patients with T2D (p<0.05 and p<0.001, respectively). CONCLUSION/INTERPRETATION: Apart from a positive relationship of postprandial changes in GIP and PYY with changes in ascorbic acid, there was no direct link observed between gastrointestinal hormones and oxidative stress markers in diabetic patients. TRIAL REGISTRATION: ClinicalTrials.gov NCT01572402.
Faculty Hospital Pilsen Pilsen Czech Republic
Institute for Clinical and Experimental Medicine Prague Czech Republic
See more in PubMed
Bonora E, Muggeo M (2001) Postprandial blood glucose as a risk factor for cardiovascular disease in Type II diabetes: the epidemiological evidence. Diabetologia 44: 2107–2114. 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
Wajchenberg BL (2007) beta-cell failure in diabetes and preservation by clinical treatment. Endocr Rev 28: 187–218. PubMed
Drucker DJ, Sherman SI, Gorelick FS, Bergenstal RM, Sherwin RS, et al. (2010) Incretin-based therapies for the treatment of type 2 diabetes: evaluation of the risks and benefits. Diabetes Care 33: 428–433. PubMed PMC
Meier JJ, Nauck MA (2006) Incretins and the development of type 2 diabetes. Curr Diab Rep 6: 194–201. PubMed
Vilsboll T, Krarup T, Madsbad S, Holst JJ (2002) Defective amplification of the late phase insulin response to glucose by GIP in obese Type II diabetic patients. Diabetologia 45: 1111–1119. PubMed
Holst JJ, Knop FK, Vilsboll T, Krarup T, Madsbad S (2011) Loss of incretin effect is a specific, important, and early characteristic of type 2 diabetes. Diabetes Care 34 (Suppl 2) S251–257. PubMed PMC
Hamed EA, Zakary MM, Ahmed NS, Gamal RM (2011) Circulating leptin and insulin in obese patients with and without type 2 diabetes mellitus: relation to ghrelin and oxidative stress. Diabetes Res Clin Pract 94: 434–441. PubMed
Ceriello A (2012) The emerging challenge in diabetes: The “metabolic memory”. Vasc Pharmacol 57: 133–138. PubMed
Ceriello A, Bortolotti N, Motz E, Crescentini A, Lizzio S, et al. (1998) Meal-generated oxidative stress in type 2 diabetic patients. Diabetes Care 21: 1529–1533. PubMed
Sampson MJ, Gopaul N, Davies IR, Hughes DA, Carrier MJ (2002) Plasma F2 isoprostanes: direct evidence of increased free radical damage during acute hyperglycemia in type 2 diabetes. Diabetes Care 25: 537–541. PubMed
Beisswenger PJ, Howell SK, O'Dell RM, Wood ME, Touchette AD, et al. (2001) alpha-Dicarbonyls increase in the postprandial period and reflect the degree of hyperglycemia. Diabetes Care 24: 726–732. PubMed
Yokode M, 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: 720–729. 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: 31–35. PubMed
Cavalot F, Petrelli A, Traversa M, Bonomo K, Fiora E, et al. (2006) Postprandial blood glucose is a stronger predictor of cardiovascular events than fasting blood glucose in type 2 diabetes mellitus, particularly in women: lessons from the San Luigi Gonzaga Diabetes Study. J Clin Endocrinol Metab 91: 813–819. PubMed
Knop FK, Vilsboll T, Hojberg PV, Larsen S, Madsbad S, et al. (2007) The insulinotropic effect of GIP is impaired in patients with chronic pancreatitis and secondary diabetes mellitus as compared to patients with chronic pancreatitis and normal glucose tolerance. Regul Pept 144: 123–130. PubMed
Vilsboll T, Holst JJ (2004) Incretins, insulin secretion and Type 2 diabetes mellitus. Diabetologia 47: 357–366. PubMed
Alssema M, Rijkelijkhuizen JM, Holst JJ, Teerlink T, Scheffer PG, et al. (2013) Preserved GLP-1 and exaggerated GIP secretion in type 2 diabetes and relationships with triglycerides and ALT. Eur J Endocrinol 169: 421–430. PubMed
Meier JJ, Gallwitz B, Askenas M, Vollmer K, Deacon CF, et al. (2005) Secretion of incretin hormones and the insulinotropic effect of gastric inhibitory polypeptide in women with a history of gestational diabetes. Diabetologia 48: 1872–1881. PubMed
Solomon TP, Haus JM, Kelly KR, Rocco M, Kashyap SR, et al. (2010) Improved pancreatic beta-cell function in type 2 diabetic patients after lifestyle-induced weight loss is related to glucose-dependent insulinotropic polypeptide. Diabetes Care 33: 1561–1566. PubMed PMC
Flatt PR (2008) Dorothy Hodgkin Lecture 2008. Gastric inhibitory polypeptide (GIP) revisited: a new therapeutic target for obesity-diabetes? Diabet Med 25: 759–764. PubMed
Ranganath LR (2008) The entero-insular axis: implications for human metabolism. Clin Chem Lab Med 46: 43–56. PubMed
Gault VA, Irwin N, Green BD, McCluskey JT, Greer B, et al. (2005) Chemical ablation of gastric inhibitory polypeptide receptor action by daily (Pro3)GIP administration improves glucose tolerance and ameliorates insulin resistance and abnormalities of islet structure in obesity-related diabetes. Diabetes 54: 2436–2446. PubMed
Flatt PR (2007) Effective surgical treatment of obesity may be mediated by ablation of the lipogenic gut hormone gastric inhibitory polypeptide (GIP): evidence and clinical opportunity for development of new obesity-diabetes drugs? Diab Vasc Dis Res 4: 151–153. PubMed
Irwin N, Flatt PR (2009) Evidence for beneficial effects of compromised gastric inhibitory polypeptide action in obesity-related diabetes and possible therapeutic implications. Diabetologia 52: 1724–1731. PubMed
Skrha J, Hilgertova J, Jarolímkova, Kunešova M, Hill M (2010) Meal test for glucose-dependent insulinotropic peptide (GLP) in obese and type 2 diabetic patients. Physiol Res 59: 749–755. PubMed
Lutz TA (2013) The interaction of amylin with other hormones in the control of eating. Diabetes Obes Metab 15: 99–111. PubMed
Small CJ, Bloom SR (2004) Gut hormones as peripheral anti obesity targets. Curr Drug Targets CNS Neurol Disord 3: 379–388. PubMed
Ashby D, Bloom SR (2007) Recent progress in PYY research–an update report for 8th NPY meeting. Peptides 28: 198–202. PubMed
Feinle-Bisset C, 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: E948–953. PubMed
Rigamonti AE, Resnik M, Compri E, Agosti F, De Col A, et al. (2011) The cholestyramine-induced decrease of PYY postprandial response is negatively correlated with fat mass in obese women. Horm Metab Res 43: 569–573. PubMed
Mather KJ, Paradisi G, Leaming R, Hook G, Steinberg HO, et al. (2002) Role of amylin in insulin secretion and action in humans: antagonist studies across the spectrum of insulin sensitivity. Diabetes Metab Res Rev 18: 118–126. PubMed
Hou X, Sun L, Li Z, Mou H, Yu Z, et al. (2011) Associations of amylin with inflammatory markers and metabolic syndrome in apparently healthy Chinese. PLoS One 6: e24815. PubMed PMC
Kahleova H, Mari A, Nofrate V, Matoulek M, Kazdova L, et al. (2012) Improvement in beta-cell function after diet-induced weight loss is associated with decrease in pancreatic polypeptide in subjects with type 2 diabetes. J Diabetes Complications 26: 442–449. PubMed
De Vriese C, Perret J, Delporte C (2010) Focus on the short- and long-term effects of ghrelin on energy homeostasis. Nutrition 26: 579–584. PubMed
English PJ, Ashcroft A, Patterson M, Dovey TM, Halford JC, et al. (2007) Metformin prolongs the postprandial fall in plasma ghrelin concentrations in type 2 diabetes. Diabetes Metab Res Rev 23: 299–303. PubMed
Teff KL, Elliott SS, Tschop M, Kieffer TJ, Rader D, et al. (2004) Dietary fructose reduces circulating insulin and leptin, attenuates postprandial suppression of ghrelin, and increases triglycerides in women. J Clin Endocrinol Metab 89: 2963–2972. PubMed
Barazzoni R, Zanetti M, Semolic A, Cattin MR, Pirulli A, et al. (2011) High-fat diet with acyl-ghrelin treatment leads to weight gain with low inflammation, high oxidative capacity and normal triglycerides in rat muscle. PLoS One 6: e26224. PubMed PMC
Padh H, Subramoniam A, Aleo JJ (1985) Glucose inhibits cellular ascorbic acid uptake by fibroblasts in vitro. Cell Biol Int Rep 9: 531–538. PubMed
Anderson RA, Evans LM, Ellis GR, Khan N, Morris K, et al. (2006) Prolonged deterioration of endothelial dysfunction in response to postprandial lipaemia is attenuated by vitamin C in Type 2 diabetes. Diabet Med 23: 258–264. PubMed
Runchey SS, Valsta LM, Schwarz Y, Wang C, Song Y, et al. (2013) Effect of low- and high-glycemic load on circulating incretins in a randomized clinical trial. Metabolism 62: 188–195. PubMed PMC
ClinicalTrials.gov
NCT01572402