Nutrition Research - Articles in Press

Tomato paste supplementation improves endothelial dynamics and reduces plasma total oxidative status in healthy subjects - Corrected Proof

2012-05-17

Abstract: Consumption of tomato products is linked to beneficial outcomes through antioxidant and anti-inflammatory mechanisms. The aim of this study was to determine whether a 14-day period of tomato paste supplementation would improve endothelial function. Nineteen volunteers (mean age, 39 ± 13 years; 8 men/11 women) were studied in a randomized (exposure sequence), single-blind (operator), crossover design. The study consisted of a supplementation arm (70 g tomato paste containing 33.3 mg of lycopene) and a control arm, during which no tomato paste was added to their regular diet. Volunteers maintained their regular diet during study arms. Two-week washout periods preceded each arm. Flow-mediated dilatation (FMD) measured by brachial artery ultrasonography was used as an estimate of endothelial function at day 1 (acute response) and day 15 (midterm response). Plasma lipid peroxides were measured with a photometric enzyme-linked immunosorbent assay as an index of total oxidative status. Tomato supplementation led to an overall FMD increase compared with the control period (P = .047 for repeated-measures 3 × 2 analysis of variance). At day 1, FMD was not significantly increased (P = .329). By day 15, tomato supplementation resulted in an increase in FMD by 3.3% ± 1.4%, whereas at the control arm, FMD declined by −0.5% ± 0.6% (P = .03); magnitudes of change are absolute FMD values. Total oxidative status decreased at the end of the supplementation period compared with baseline values (P = .038). Daily tomato paste consumption exerts a beneficial midterm but not short-term effect on endothelial function. Further studies are warranted to explore the effects of tomato paste on endothelial dilation in different age groups and comorbidities.

Renoprotective effects of (+)-catechin in streptozotocin-induced diabetic rat model - Corrected Proof

2012-05-17

Abstract: Diabetic nephropathy is a complication of diabetes mellitus leading to end-stage renal disease. Oxidative stress and inflammation play a major role in the pathogenesis of diabetic nephropathy. Green tea, known for its antioxidant and anti-inflammatory properties, has been shown to be renoprotective. We hypothesized that (+)-catechin (CTN), a component of green tea, is responsible for the renoprotection. Our investigation of the therapeutic potential of CTN in streptozotocin-induced diabetic rats demonstrated for the first time that the effects of CTN treatment were comparable with the effects of an angiotensin-converting enzyme inhibitor (ACEi) enalapril for the treatment of albumin excretion. After 12 weeks of CTN treatment with 35 mg/d in the drinking water, urinary albumin excretion and plasma creatinine concentrations in all the diabetic treatment groups were reduced, compared with the diabetic group with no treatment. Urine creatinine and creatinine clearance were higher in diabetic groups treated with CTN and ACEi compared with the diabetic group with no treatment. Endothelin 1, lipid peroxidation, concentration of alanine transferase enzyme, and expression of fibronectin were lower in all the treatment groups compared with the diabetic group with no treatment. Concentrations of free thiols were higher in the CTN-treated group compared with the diabetic rats with no treatment. Our findings suggest that CTN has renoprotective properties comparable with ACEi, and coadministration of CTN and enalapril might be useful in reducing albumin excretion as well as improving endothelial function. (+)-Catechin might be successfully used in the future for clinical situations where ACEi is poorly tolerated or contraindicated.

Food intake in women two years or more after bariatric surgery meets adequate intake requirements - Corrected Proof

2012-05-14

Abstract: Restricted food intake after bariatric surgery can be an important factor both in the long-term control of body weight and in the onset of nutritional deficiencies. The objective of this study was to assess the adequacy of food intake in women two or more years after bariatric surgery according to the excess weight lost. A group of 141 women who underwent banded Roux-en-Y gastric bypass (RYGB) was divided according to the percentage of excess weight they lost (%EWL)<50; 50┤75; = 75. The habitual energy and nutrient intakes were determined by a 24-hour recall over two days and the probability of adequate intake was based on the Dietary Reference Intake. The mean total estimated energy requirement (EER) as well as energy, macronutrient and cholesterol intakes did not differ among the groups. Only the %EWL<50 group had an intake equal to their EER, but they presented a higher number of inadequacies, such as low levels of magnesium, folic acid and vitamins C and E. Calcium and dietary fiber intakes were extremely low in all three groups. In conclusion, weight loss after surgery is associated with food habits that favor energy intake over micronutrient intake.

Sulforaphane retards the growth of UM-UC-3 xenographs, induces apoptosis, and reduces survivin in athymic mice - Corrected Proof

Fengqian Wang, Yujuan Shan — 2012-05-07

Abstract: Sulforaphane (SFN), an isothiocyanate that exists exclusively in cruciferous vegetables, may be the most promising preventive agent for bladder cancer (BC) to date. We previously observed that SFN dramatically inhibits human BC T24 cells in vitro. Our hypothesis is that SFN may attenuate BC growth. To test our hypothesis, we investigated the effect of SFN on human BC UM-UC-3 cell xenografts implanted into athymic mice. Sulforaphane extract was routinely prepared in our laboratory, and its content was measured with high-performance liquid chromatography. Athymic mice were injected subcutaneously with a UM-UC-3 cell suspension (2.0×106 cells/200 μL per mouse) and randomly divided into 2 groups. The positive control group was orally gavaged with water, and the treatment group was orally administered SFN from broccoli sprout (12 mg/kg body weight) for 5 weeks. At the end of the experiment, tumor tissues were harvested and processed for hematoxylin and eosin staining and immunohistochemistry. The average tumor volume decreased from 4.1±1.67 cm3 in the positive control mice to 1.5±0.72 cm3 in the SFN-treated mice, evidencing an inhibitory rate of 63%. The SFN extract also reduced the appearance of tumors, including karyopyknosis and angiogenesis. Sulforaphane extract induced caspase 3 and cytochrome c expression but reduced the expression of survivin. Sulforaphane extract retards the growth of UM-UC-3 xenografts in vivo, confirming its future potential in BC therapy.

Delphinidin-3-O-galactoside protects mouse hepatocytes from (−)-epigallocatechin-3-gallate–induced cytotoxicity via up-regulation of heme oxygenase-1 and heat shock protein 70 - Corrected Proof

Hirofumi Inoue, Mari Maeda-Yamamoto, Atsushi Nesumi, Akira Murakami — 2012-05-07

Abstract: Delphinidin-3-O-galactoside (D3G) is a water-soluble anthocyanin with antioxidant activity. (−)-Epigallocatechin-3-gallate (EGCG) is also known as a powerful antioxidant but concomitantly possesses a prooxidative property. We hypothesized that D3G is capable of protecting the EGCG-induced cytotoxicity and endoplasmic reticulum (ER) stress via inducing self-protective proteins and antioxidant enzymes. (−)-Epigallocatechin-3-gallate (200-500 μM) dose dependently decreased the viability of hepa1c1c-7 mouse hepatocytes, whereas D3G (50-500 μM) did not change it. Pretreatment with D3G significantly suppressed EGCG-induced cytotoxicity in a time-dependent manner (0, 6, and 24 hours). (−)-Epigallocatechin-3-gallate drastically decreased heme oxygenase-1 and heat shock protein 70 messenger RNA (mRNA) levels, whereas, pretreatment with D3G markedly attenuated their down-regulations. Delphinidin-3-O-galactoside remarkably decreased EGCG-induced ER stress responses such as C/EBP-homologus protein mRNA expression and X-box–binding protein-1 mRNA splicing. Taken together, our data suggest that D3G is capable of masking the EGCG-induced cytotoxicity and ER stress, presumably through up-regulation of antioxidant enzymes and heat shock proteins.

Vitamin E supplementation protects erythrocyte membranes from oxidative stress in healthy Chinese middle-aged and elderly people - Corrected Proof

Yongye Sun, Aiguo Ma, Yong Li, Xiuxia Han, Qiuzhen Wang, Hui Liang — 2012-04-30

Abstract: Elderly people are subject to higher levels of oxidative stress than are young people. Vitamin E, as a powerful antioxidant residing mainly in biomembranes, may provide effective protection against oxidative membrane damage and resultant age-related deterioration, especially in the elderly. We hypothesized that appropriate levels of vitamin E supplementation would protect erythrocyte membranes from oxidative stress and thus improve membrane fluidity in healthy middle-aged and elderly people. To test this, we conducted a 4-month double-blind, randomized trial in which 180 healthy subjects (55-70 years old) were randomly divided into 4 groups: group C (control), and 3 treatment groups in which daily doses of 100 mg (VE1), 200 mg (VE2), and 300 mg (VE3) dl-α-tocopheryl acetate were administered. We measured plasma α-tocopherol concentration, malondialdehyde, and superoxide dismutase levels, erythrocyte hemolysis, and erythrocyte membrane fluidity at the beginning and end of the trial. After 4 months supplementation, plasma α-tocopherol concentrations in the 3 treatment groups had increased by 71%, 78%, and 95%, respectively (all P < .01), and significant decreases in plasma malondialdehyde concentrations were observed in these groups (all P < .05). Erythrocyte hemolysis was decreased by 20% to 38% after vitamin E supplementation (all P < .05), and in addition, groups VE2 and VE3 showed dramatic improvements in erythrocyte membrane fluidity (P < .01). Surprisingly, superoxide dismutase activity also decreased significantly in the treatment groups (all P < .05). In summary, vitamin E supplementation apparently alleviates oxidative stress in healthy middle-aged to elderly people, at least in part by improving erythrocyte membrane fluidity and reducing erythrocyte hemolysis.

Association between endothelial nitric oxide gene intron 4a4b VNTR polymorphism and plasma homocysteine concentrations in Tunisian male patients with myocardial infarction - Corrected Proof

2012-04-30

Abstract: Many studies have shown that hyperhomocysteinemia may be an independent risk factor for coronary artery disease. However, not all prospective studies support an association between elevated plasma homocysteine levels and coronary artery disease. Nitric oxide (NO) plays a relevant role in various events during atherogenesis, and in vitro data suggest that NO may modulate total homocysteine (tHcy) concentrations, whereas polymorphisms of the endothelial nitric oxide (NOS3) gene have been reported to be related to an increased risk of myocardial infarction (MI) and hyperhomocysteinemia, but the results have been controversial. We hypothesized that the NOS3 synthase 4a4b VNTR polymorphism is a determinant of tHcy concentrations and tested this in 310 patients with MI and 250 controls. The NOS3 gene intron 4a4b VNTR polymorphism was analyzed by polymerase chain reaction analysis. There was no significant difference in the homocysteine levels between patients with MI and controls. The frequencies of the NOS34b4b, 4b4a, and 4a4a genotypes in the MI group were significantly different from those in the control group. In patients with MI, plasma tHcy concentrations were significantly different among the NOS3 genotypes (13.5±4.5, 18.5±3.9, and 20.4±2.1 μmol/L for 4b4b, 4a4b, and 4a4a genotypes, respectively; P<.001). However, no significant difference was observed for tHcy concentrations in the control group. In conclusion, the NOS34a4b gene polymorphism (presence of 4a allele) is associated with MI and influences plasma tHcy concentrations in patients with MI in the Tunisian male population.

Fish oil supplementation maintains adequate plasma arachidonate in cats, but similar amounts of vegetable oils lead to dietary arachidonate deficiency from nutrient dilution - Corrected Proof

Rebecca J. Angell, Melena K. McClure, Karen E. Bigley, John E. Bauer — 2012-04-27

Abstract: Because fatty acid (FA) metabolism of cats is unique, effects of dietary fish and vegetable oil supplementation on plasma lipids, lipoproteins, lecithin/cholesterol acyl transferase activities, and plasma phospholipid and esterified cholesterol (EC) FAs were investigated. Cats were fed a commercial diet supplemented with 8 g oil/100 g diet for 4 weeks using either high-oleic-acid sunflower oil (diet H), Menhaden fish oil (diet M), or safflower oil (diet S). When supplemented, diet M contained sufficient arachidonate (AA), but diets H and S were deficient. We hypothesized that diet M would modify plasma lipid metabolism, increase FA long-chain n-3 (LCn-3) FA content but not deplete AA levels. Also, diet S would show linoleic acid (LA) accumulation without conversion to AA, and both vegetable oil supplements would dilute dietary AA content when fed to meet cats' energy needs. Plasma samples on weeks 0, 2, and 4 showed no alterations in total cholesterol or nonesterified FA concentrations. Unesterified cholesterol decreased and EC increased in all groups, whereas lecithin/cholesterol acyl transferase activities were unchanged. Diet M showed significant triacylglycerol lowering and decreased pre–β-lipoprotein cholesterol. Plasma phospholipid FA profiles revealed significant enrichment of 18:1n-9 with diet H, LA and 20:2n-6 with diet S, and FA LCn-3FA with diet M. Depletion of AA was observed with diets H and S but not with diet M. Diet M EC FA profiles revealed specificities for LA and 20:5n-3 but not 22:5n-3 or 22:6n-3. Oversupplementation of some commercial diets with vegetable oils causes AA depletion in young cats due to dietary dilution. Findings are consistent with the current recommendations for at least 0.2 g AA/kg diet and that fish oil supplements provide both preformed LCn-3 polyunsaturated FA and AA.

Diet promotes sleep duration and quality - Corrected Proof

Katri Peuhkuri, Nora Sihvola, Riitta Korpela — 2012-04-27

Abstract: Sleep, much like eating, is an essential part of life. The mechanisms of sleep are only partially clear and are the subject of intense research. There is increasing evidence showing that sleep has an influence on dietary choices. Both cross-sectional and epidemiologic studies have demonstrated that those who sleep less are more likely to consume energy-rich foods (such as fats or refined carbohydrates), to consume fewer portions of vegetables, and to have more irregular meal patterns. In this narrative review, we pose the opposite question: can ingested food affect sleep? The purpose of this review is to discuss the evidence linking diet and sleep and to determine whether what we eat and what kind of nutrients we obtain from the food consumed before bedtime matter. In addition, scientific evidence behind traditional sleep-promoting foods such as milk and some herbal products is briefly described. These are reviewed using data from clinical trials, mostly in healthy subjects. In addition, we discuss the possible mechanisms behind these observations. Lastly, we summarize our findings that emerging evidence confirms a link between diet and sleep. Overall, foods impacting the availability of tryptophan, as well as the synthesis of serotonin and melatonin, may be the most helpful in promoting sleep. Although there are clear physiological connections behind these effects, the clinical relevance needs to be studied further.

High l-carnitine concentrations do not prevent late diabetic complications in type 1 and 2 diabetic patients - Corrected Proof

2012-04-27

Abstract: Increased intake of l-carnitine, a cofactor in cellular energy metabolism, is recommended for diabetic patients with late complications. However, its clinical benefits remain controversial. We hypothesized that patients with low l-carnitine levels would have an increased rate of diabetic complications. To test this hypothesis, we evaluated the relationship of l-carnitine concentrations in blood with the prevalence and severity of late diabetic complications in type 1 and 2 diabetic patients. Human blood samples were collected from 93 and 87 patients diagnosed as having type 1 or type 2 diabetes, respectively, and 122 nondiabetic individuals. The determination of free l-carnitine concentrations in whole blood lysates was performed using ultra-performance liquid chromatography with tandem mass spectrometry. In diabetic patients, diabetic complications such as neuropathy, retinopathy, nephropathy, or hypertension were recorded. The average l-carnitine concentration in the blood of control subjects was 33 ± 8 nmol/mL, which was not significantly different from subgroups of patients with type 1 (32 ± 10 nmol/mL) or type 2 diabetes (36 ± 11 nmol/mL). Patients with low (<20 nmol/mL) l-carnitine levels did not have increased occurrences of late diabetic complications. In addition, patient subgroups with higher l-carnitine concentrations did not have decreased prevalence of late diabetic complications. Our results provide evidence that higher l-carnitine concentrations do not prevent late diabetic complications in type 1 and 2 diabetic patients.

Platycodon grandiflorum root attenuates vascular endothelial cell injury by oxidized low-density lipoprotein and prevents high-fat diet–induced dyslipidemia in mice by up-regulating antioxidant proteins - Corrected Proof

Mi Ja Chung, Soo-Hyun Kim, Jeong-Won Park, Young Jin Lee, Seung-Shi Ham — 2012-04-20

Abstract: We hypothesized that a Platycodon grandiflorum root (PG) ethyl acetate extract (PGEA) would help reduce the vascular cell injury caused by oxidized low-density lipoprotein (oxLDL) and prevent high-fat (HF) diet–induced dyslipidemia and oxidative stress by up-regulating antioxidant proteins. We investigated the protective effects of PGEA against vascular endothelial cell injury induced by oxLDL and dyslipidemia induced by an HF diet, and the mechanisms underlying these effects were studied. The protective effects of PGEA were investigated with respect to calf pulmonary arterial endothelial (CPAE) cell viability and the lactate dehydrogenase release during oxLDL treatment. The in vivo effects of PGEA were examined using C57BL/6 mice, which were fed an HF diet for 9 weeks. The HF diet was supplemented with 0, 25, or 75 mg/kg PGEA during the last 4 weeks of the experimental period. Histologic analyses of hepatic lipid accumulation were performed. The changes in antioxidant protein levels induced by PGEA, which protects against HF diet–induced oxidative stress, were measured using a proteomics approach. We found that PGEA exhibited antioxidant activity. In CPAE cells, PGEA inhibited both oxLDL-induced cell death and lactate dehydrogenase release. In the HF diet–induced obese mice that received PGEA, we observed significantly reduced plasma and hepatic lipid levels, demonstrating that PGEA has beneficial effects on hyperlipidemia. In addition, we found that PGEA caused the up-regulation of antioxidant proteins. These findings suggest that the antioxidant effects of PGEA may protect against oxidative stress-related diseases.