PMID- 18329309 OWN - NLM STAT- MEDLINE DCOM- 20080806 LR - 20131121 IS - 1262-3636 (Print) IS - 1262-3636 (Linking) VI - 34 IP - 2 DP - 2008 Apr TI - Plasma 15-F2t isoprostane concentrations are increased during acute fructose loading in type 2 diabetes. PG - 148-54 LID - 10.1016/j.diabet.2007.11.003 [doi] AB - OBJECTIVE: Fructose consumption is increasing worldwide and is likely to play a role in metabolic disorders. Dietary fructose is often recommended for diabetic patients, as this form of carbohydrate leads to a lower postprandial rise in plasma glucose and insulin. However, fructose contributes to the generation of free radicals. The aim of this work was to investigate the acute effects of a fructose load in patients with type 2 diabetes mellitus (T2DM), compared with healthy controls, on several metabolic oxidative biomarkers, particularly plasma 15-F2t isoprostanes (15-F2t isoPs). RESEARCH DESIGN AND METHODS: Six T2DM patients and six healthy subjects were recruited. All patients underwent a single fructose tolerance test (75 g of anhydrous fructose). Plasma 15-F2t isoPs concentrations, plasma total antioxidant capacity (TAS) and thiobarbituric acid reactive substances (TBARS) were measured at baseline, and at 60, 120, 180 and 240 min after fructose absorption. RESULTS: Baseline plasma 15-F2t isoPs concentrations were significantly increased in T2DM patients compared with controls (310+/-47 versus 237+/-20 pg/mL, respectively; P<0.01) and rose significantly (P<0.01) to 414+/-45 pg/mL in diabetic patients. No change in TAS or TBARS was observed in either group. CONCLUSION: Plasma 15-F2t isoPs are increased during acute fructose loading in T2DM. Knowing the potentially deleterious effect of plasma 15-F2t isoPs-in particular, vascular lesions-and in light of our results, it is necessary to reconsider fructose consumption in T2DM patients, as we can now show, for the first time, a possible association between acute fructose loading and deleterious effects in such patients. FAU - Faure, P AU - Faure P AD - Inserm, ERI17, laboratoire d'etude de la physiopatologie de l'hypoxie (HP2), departement de biologie integree, hopital Albert-Michallon, CHU de Grenoble, 38042 Grenoble, France. pfaure@chu-grenoble.fr FAU - Polge, C AU - Polge C FAU - Monneret, D AU - Monneret D FAU - Favier, A AU - Favier A FAU - Halimi, S AU - Halimi S LA - eng PT - Journal Article DEP - 20080307 PL - France TA - Diabetes Metab JT - Diabetes & metabolism JID - 9607599 RN - 0 (Blood Glucose) RN - 0 (Lactates) RN - 0 (Lipoproteins) RN - 0 (Triglycerides) RN - 27415-26-5 (8-epi-prostaglandin F2alpha) RN - 30237-26-4 (Fructose) RN - 97C5T2UQ7J (Cholesterol) RN - B7IN85G1HY (Dinoprost) SB - IM EIN - Diabetes Metab. 2008 Jun;34(3):297 MH - Adult MH - Blood Glucose/analysis MH - Body Mass Index MH - Cholesterol/blood MH - Diabetes Mellitus, Type 2/*blood MH - Dinoprost/*analogs & derivatives/blood MH - Fasting MH - Female MH - Fructose/*pharmacology MH - Humans MH - Lactates/blood MH - Lipoproteins/blood MH - Male MH - Middle Aged MH - Reference Values MH - Triglycerides/blood EDAT- 2008/03/11 09:00 MHDA- 2008/08/07 09:00 CRDT- 2008/03/11 09:00 PHST- 2007/09/17 00:00 [received] PHST- 2007/11/08 00:00 [revised] PHST- 2007/11/19 00:00 [accepted] PHST- 2008/03/11 09:00 [pubmed] PHST- 2008/08/07 09:00 [medline] PHST- 2008/03/11 09:00 [entrez] AID - S1262-3636(08)00032-3 [pii] AID - 10.1016/j.diabet.2007.11.003 [doi] PST - ppublish SO - Diabetes Metab. 2008 Apr;34(2):148-54. doi: 10.1016/j.diabet.2007.11.003. Epub 2008 Mar 7.