Relation between plasma antioxidant vitamin levels, adiposity and cardio-metabolic profile in adolescents: Effects of a multidisciplinary obesity programme

Objective: Essential hypertensive patients (EH) are characterized by endothelial dysfunction caused by a reduced nitric oxide (NO) availability due to reactive oxygen species excess and low-grade inflammatory condition. Ghrelin is a recently identified growth hormone-releasing peptide, with recognized cardiovascular actions. Possible effects on endothelial dysfunction have been never investigated in EH. In this study we evaluated whether exogenous ghrelin can improve endothelial dysfunction in the forearm microcirculation of untreated mild-moderate EH. Methods: In 9 EH (51.8±8.1 yrs) and 9 normotensive subjects (NS, 50.5±3.5 yrs), we studied the forearm blood flow (FBF, strain-gauge plethysmography) response to intrabrachial acetylcholine (ACh, 0.15-15 mg/100 ml/min) with and without NO synthase blockade by L-NMMA (100 μg/100 ml/min), or the antioxidant vitamin (Vit) C (8 mg/100 ml/min). The protocol was repeated under exogenous ghrelin intra-arterial infusion (200 ng/min, 30’ pre-infusion). Results: In NS, maximal vasodilation (VD) to ACh (480±20%) was inhibited by L-NMMA (292±22, -39±7%; P<0.001) and unchanged by Vit C (482±34%). Ghrelin failed to modify these vascular responses. In EH, VD to ACh was blunted vs NS (337±45%; P<0.001) and resistant to L-NMMA (313±32, -7±3%). Vit C increased the response to ACh (509±57%; P<0.01 vs ACh alone) and restored the inhibiting effect of L-NMMA (332±42, -34±8%; P<0.001). Ghrelin, while not modifying the basal FBF, it increased (P<0.001) the VD to ACh (448±55%) and restored the inhibitory effect of L-NMMA on ACh (355±43, -20±6%; P<0.001). Vit C only slightly improved VD to ACh under ghrelin infusion (486±45%). In EH ghrelin significantly (P<0.05) decreased plasma venous malodialdehyde (from 6.9±1.5 to 5.2±1.0 μmol/L), lipoperoxides (from 9.1±1.9 to 6.6±2.3 μmol/L) and IL-6 (from 11.1±0.6 to 9.3±1.0 pg/mL) and increased plasma antioxidant capacity (from 407±109 to 630±97 mmol/L). Response to sodium nitroprusside was similar between EH and NS and not affected by ghrelin. Conclusions: Exogenous ghrelin is able to ameliorate endothelial dysfunction by restoring NO availability in the forearm microcirculation of EH, an effect probably determined by antioxidant and/or anti-inflammatory activities.

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Plasma antioxidant vitamin status of periparturient cows supplemented with α-tocopherol and β-carotene

Animal Feed Science and Technology ◽

10.1016/j.anifeedsci.2003.11.002 ◽

2004 ◽

Vol 114 (1-4) ◽

pp. 279-285 ◽

Cited By ~ 23

Author(s):

Rajiv Chawla ◽

Harjit Kaur

Keyword(s):

Antioxidant Vitamin ◽

Vitamin Status ◽

Periparturient Cows ◽

Plasma Antioxidant ◽

Β Carotene

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Effect of glutathione S‐transferase M1 and Tl polymorphism on the level of plasma antioxidant vitamin in Korean subclinical hypertensive patients after kale juice supplementation (1035.9)

The FASEB Journal ◽

10.1096/fasebj.28.1_supplement.1035.9 ◽

2014 ◽

Vol 28 (S1) ◽

Author(s):

Myung‐Hee Kang ◽

Jeong‐Hwa Han ◽

Hye‐Jin Lee ◽

Tae Seok Kim

Keyword(s):

Antioxidant Vitamin ◽

Glutathione S Transferase ◽

Hypertensive Patients ◽

Plasma Antioxidant

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Nonalcoholic Red Wine Extract and Quercetin Inhibit LDL Oxidation without Affecting Plasma Antioxidant Vitamin and Carotenoid Concentrations

Clinical Chemistry ◽

10.1093/clinchem/46.8.1162 ◽

2000 ◽

Vol 46 (8) ◽

pp. 1162-1170 ◽

Cited By ~ 82

Author(s):

Mridula Chopra ◽

Patricia E E Fitzsimons ◽

John J Strain ◽

David I Thurnham ◽

Alan N Howard

Keyword(s):

Red Wine ◽

Plasma Lipids ◽

Ex Vivo ◽

Hdl Cholesterol ◽

Ldl Oxidation ◽

Lag Phase ◽

Antioxidant Vitamin ◽

Plasma Vitamin ◽

Plasma Antioxidant

Abstract Background: Antioxidant enrichment of LDL can increase its resistance to oxidation and hence reduce its atherogenicity. The objective of the present study was to investigate whether in vivo supplementation with nonalcoholic red wine extract and quercetin can increase the oxidative resistance of LDL, and also whether the supplementation has any effect on other antioxidative micronutrients present in the blood. Methods: Twenty-one male subjects were supplemented with a placebo drink for 2 weeks and randomized into two groups. One group (n = 11) received the red wine extract (1 g/day, equivalent to 375 mL of red wine) and the other group (n = 10) quercetin (30 mg/day) for 2 weeks, followed by a 5-week washout period. Results: In the red wine extract-supplemented group, ex vivo copper-initiated oxidation of LDL (lag phase, mean ± SD) was 40 ± 11 min at the baseline, and increased significantly to 47 ± 6 min [P <0.05 compared with placebo (38 ± 4 min) and the washout values (40 ± 5 min)]. In the quercetin-supplemented group, the lag phase was 44 ± 11 and 40 ± 5 min for the baseline and placebo, respectively, and increased significantly to 51 ± 7 min [P <0.05 compared with placebo and washout (41 ± 9 min)] after supplementation. Plasma lipids (triglycerides, total cholesterol, LDL- and HDL-cholesterol) did not change during the study period. Supplementation with red wine extract or quercetin had no effect on plasma vitamin C and E, retinol, and carotenoid concentrations. Conclusions: Alcohol-free red wine extract and one of its components, quercetin, can inhibit LDL oxidation after in vivo supplementation; such “inhibition” is unrelated to changes in antioxidant vitamin and carotenoid concentrations.

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