European Journal of Nutrition (v.47, #8)
Body composition obtained from the body mass index by Daniele Martarelli; Benedetta Martarelli; Pierluigi Pompei (409-416).
Since obesity and related diseases are now considered epidemic, new and more accurate formulas for epidemiological studies are of interest to the scientific community. Several equations have been proposed to estimate the body composition simply from anthropometric measurements. However, with time, the body composition of the populations studied changes in relation to their food habits and lifestyle, and, therefore, the equations must be regularly updated and corrected.The aim of the study was to develop new equations to determine the body composition among the Italian population using the body mass index and independently by variables such as age and body structure.Bioelectrical impedance and anthropometric analysis of 764 Italian Caucasian subjects (342 females and 422 males), 11 to 80 years of age, were analysed. Females and males were analysed separately. Multiple regression analyses were performed in order to estimate the body composition of the subjects. The estimated masses were then compared with the measured masses using Bland and Altman plots. We also calculated the differences between the estimated and measured masses, reported as % of the body weight, for the 95, 85 and 75° percentile of the female and male groups. Finally we compared our formulas with the Watson equations, which are used to estimate the total body water.All body masses estimated were positively correlated to the measured values. Moreover, at any percentile analysed, our formulas resulted more precise than the Watson formula. Equations: Females: FM = 1.9337 BMI – 26.422; FFM = BW – FM; BCM = 0.3655 FFM + 4.865; TBW = 0.5863 FFM + 7.1732; Males: FM = 1.407 BMI – 21.389; FFM = BW – FM; BCM = 0.4485 FFM + 3.3534; TBW = 0.6997 + 1.4567.Although an inevitable inaccuracy must be expected in epidemiological studies, our equations are adequate to analyze the body composition state and changes occurring among the Italian population by simply considering weight and height.
Keywords: bioelectrical impedance; BMI; body composition; anthropometry
An explorative study of in vivo digestive starch characteristics and postprandial glucose kinetics of wholemeal wheat bread by Marion G. Priebe; Renate E. Wachters-Hagedoorn; Janneke A. J. Heimweg; Alexandra Small; Tom Preston; Henk Elzinga; Frans Stellaard; Roel J. Vonk (417-423).
Based on in vitro measurements, it is assumed that starch in wholemeal bread is rapidly digestible, which is considered to be less desirable for health.To evaluate the in vitro prediction, we characterized starch digestion of wholemeal wheat bread (WB) and postprandial glucose kinetics in healthy volunteers.In a crossover study 4 healthy men ingested either intrinsically 13C-enriched WB (133 g) or glucose (55 g) in water. Plasma glucose and insulin concentrations were monitored during 6 h postprandially. Using a primed continuous infusion of D-[6,6-2H2] glucose, the rate of systemic appearance of glucose was estimated (reflecting glucose influx) and the endogenous glucose production calculated.The glucose influx rate after WB was comparable with that after glucose in the early postprandial phase (0–2 h) (P = 0.396) and higher in the late postprandial phase (2–4 h) (P = 0.005). Despite the same initial glucose influx rate the 0–2 h incremental area under the curve (IAUC) of insulin after WB was 41% lower than after glucose (P = 0.037). Paradoxically endogenous glucose production after WB was significantly more suppressed than after glucose (0–2 h IAUC: P = 0.015, 2–4 h IAUC: P = 0.018).Starch in WB seems to be partly rapidly and partly slowly digestible. Postprandial insulin response and endogenous glucose production after WB ingestion might not solely be determined by the digestive characteristics of starch; other components of WB seem to affect glucose homeostasis. In vitro measurements might not always predict in vivo starch digestion precisely.
Keywords: bread; starch digestion; glucose kinetics; stable isotopes
Diet, obesity and obesogenic trends in two generations of Swedish women by Lauren Lissner; Agneta Sjöberg; Madlen Schütze; Leif Lapidus; Lena Hulthén; Cecilia Björkelund (424-431).
Secular trends in obesity and related lifestyle factors are reported in two generations of 38- and 50-year old Swedish women. Specifically, we describe changes in obesity and fat patterning, while examining concurrent shifts in factors that are proposed to be causally related to the modern obesity epidemic.A total of 1,270 women aged 38 or 50 were selected from population registries and examined in 1968/69 (born 1930 or 1918) or 2004/05 (born 1966 or 1954). Anthropometric methods and lifestyle questions were unchanged between earlier and later surveys. Dietary comparisons were based on 24-h recall, with additional questions about usual alcohol and salt consumption patterns. In subgroups, 24-h urinary sodium was determined.Weight, height, waist circumference, waist-hip ratio, triceps and subscapular skinfold measures were all significantly higher in later-born cohorts, although BMI and obesity were not significantly changed. Higher sodium excretion was observed among later-born sub-groups, consistent with reports of increasing salt preference. Lower proportions of energy as fat and sucrose, but higher carbohydrate, protein and fiber concentrations were reported by later-born cohorts. There were shifts towards increased frequency of wine and liquor consumption, but decreased beer. Leisure time physical activity and perceived stress levels both increased significantly over 36 years.A number of anthropometric and lifestyle differences between two generations of Swedish women were observed. Increases in subcutaneous and abdominal fatness were detected without significantly increasing BMI. While some aspects of diet showed improvement, increases in salt preference and sodium excretion are cause for concern.
Keywords: obesity; diet; salt; lifestyle; secular trends
Fucoxanthin restrains oxidative stress induced by retinol deficiency through modulation of Na+Ka+-ATPase and antioxidant enzyme activities in rats by Sangeetha Ravi Kumar; Bhaskar Narayan; Dr. Baskaran Vallikannan (432-441).
Retinol deficiency is a major public health problem world wide, affecting children and women, in particular. It causes a variety of disorders in the body affecting various cellular functions.To study the effect of fucoxanthin (FUCO), a non-provitamin-A carotenoid in comparison with retinol (ROH) on changes in antioxidant molecules, lipid peroxidation and membrane bound enzymes in tissue and microsomes, induced by ROH deficiency in rats.After induction of ROH deficiency by feeding a diet devoid of ROH for 8 weeks, rats were divided into two groups (n = 20/group) and administered orally a dose of either FUCO (0.83 µmol) or ROH (0.87 µmol). A group of ROH deficient rats (n = 5) and rats (n = 5) fed with ROH sufficient diet was considered as baseline and control groups respectively. Over a period of 8 h, activity of catalase (CAT), glutathione transferase (GST), level of lipid peroxidation (LPx), fatty acids in plasma, liver and liver microsomes and activity of Na+K+-ATPase in liver microsomes were evaluated.ROH restriction increased LPx (P < 0.05) in liver (~19%) and plasma (~34%) while the activities of CAT (90 ± 1%) and GST (17 ± 4%) decreased compared to control. Significant elevation (91%) was observed for Na+K+-ATPase activity in liver microsomes of ROH deficient when compared to control group and levels were lowered on administration of ROH (37–69%) and FUCO (51–57%), towards control over a period of 8 h. ROH and FUCO suppressed (P < 0.05) the LPx level (%) in plasma (34–62, 7–85), liver homogenate (9–71, 24–72) and liver microsomes (83–92, 61–87), while the activities of CAT in plasma (89–97%, 91–95%) and liver microsomes (84–93%, 85–93%) and GST in liver homogenate (43–53%, 44–51%) and liver microsomes (36–52%, 22–51%) were increased (P < 0.05) compared to ROH deficient group.Results show that FUCO, a non-provitamin-A carotenoid protects cell membrane by modulating Na+K+-ATPase (51–57% lowering) and the activities of CAT and GST at the tissue and microsomal level which are affected by ROH deficiency. This may be due to its antioxidant nature. These in turn reduce LPx caused by ROH deficiency.
Keywords: antioxidant enzyme; fucoxanthin; lipid peroxidation; retinol; retinol deficiency
Factors affecting the conversion of apple polyphenols to phenolic acids and fruit matrix to short-chain fatty acids by human faecal microbiota in vitro by Sarah Bazzocco; Ismo Mattila; Sylvain Guyot; Catherine M. G. C. Renard; Anna-Marja Aura (442-452).
Proanthocyanidins (PAs) in apples are condensed tannins comprised mostly of (−)-epicatechin units with some terminal (+)-catechins. PAs, especially those having a long chain-length, are absorbed in the upper intestine only to a small extent and are passed to the colon. In the colon they are subjected to microbial metabolism by colonic microbiota. In the present article, the ability of human microbiota to ferment apple PAs is studied. Freeze-dried fruit preparations (apple, enzymatically digested apple, isolated cell-walls, isolated PAs or ciders) from two varieties, Marie Ménard and Avrolles, containing PAs of different chain lengths, were compared. Fermentation studies were performed in an in vitro colon model using human faecal microbiota as an inoculum. The maximal extent of conversion to known microbial metabolites, was observed at late time point for Marie Ménard cider, having short PAs. In this case, the initial dose also contributed to the extent of conversion. Long-chain PAs were able to inhibit the in vitro microbial metabolism of PAs shown as low maxima at early time points. Presence of isolated PAs also suppressed SCFA formation from carbohydrates as compared with that from apple cell wall or faecal suspension without substrates. The low maximal extents at early time points suggest that there is a competition between the inhibitory effect of the PAs on microbial activity, and the ability to convert PAs by the microbiota.
Keywords: procyanidin; cell-wall; Malus domestica Borkh; in vitro fermentation; gut microbiota
Inulin-enriched pasta affects lipid profile and Lp(a) concentrations in Italian young healthy male volunteers by Francesco Russo; Guglielmina Chimienti; Giuseppe Riezzo; Gabriella Pepe; Giuseppe Petrosillo; Marisa Chiloiro; Emanuele Marconi (453-459).
Inulin has been suggested to have beneficial effects on lipids, especially on triglyceridemia. Few data are available about the effects of inulin on Lipoprotein(a), a low-density lipoprotein-like particle considered as an independent risk factor for atherosclerosis. Adding inulin to pasta could be a preventive strategy for delaying the onset of atherosclerosis.was to evaluate the effects of inulin-enriched pasta on lipid profile and on Lipoprotein(a) in young healthy subjects.Twenty-two young healthy male volunteers entered a randomized double blind cross-over study consisting of a 2-weeks run-in period, a baseline assessment, two 5-weeks study periods (11% inulin-enriched or control pasta), and an 8-weeks wash-out period in between. Serum lipid concentrations were evaluated by routine biochemical analyses and plasma Lipoprotein(a) concentrations by ELISA. The size of apolipoprotein(a) isoforms was determined by Western blot and immunodetection.Significant differences at baseline and in the treatment groups were found for HDL-cholesterol (P = 0.004), total cholesterol/HDL-cholesterol ratio (P = 0.006), triglycerides (P = 0.04), and Lipoprotein(a) (P = 0.02) concentrations (data analyzed by Friedman test). Dunn’s multiple comparison test was used to assess the significance of differences between inulin-enriched pasta diet vs. baseline. HDL-cholesterol concentrations increased by 35.9%; total cholesterol/HDL-cholesterol ratio, triglycerides, and Lipoprotein(a) concentrations decreased by 22.2, 23.4, and 16.5% respectively.Inulin-enriched pasta administration induced significant effects on lipid pattern parameters in young healthy volunteers, including a significant reduction in Lipoprotein(a) concentrations.
Keywords: atherosclerosis; blood lipids; diet; fiber; inulin; lipoprotein(a)
Dietary polyphenols identified as intracellular protein kinase A inhibitors by Jan Øivind Moskaug; Grethe I. Borge; Anne M. Fagervoll; Ingvild Paur; Harald Carlsen; Rune Blomhoff (460-469).
Dietary plants contain several thousands different polyphenols that can potentially influence normal and pathological cellular processes through modulation of intracellular signaling pathways. A few polyphenols have been shown to be potent inhibitors of protein kinases.To identify possible dietary protein kinase A (PKA) inhibitors we designed a method for screening of substances in crude mixtures of food items for modulation of intracellular PKA activity that enables high-throughput testing of a large number of compounds and extracts.Luciferase was mutated to render it sensitive to phosphorylation by PKA (luciferasePKA) and transfected into a human hepatoma cell line (HepG2). Cells were then treated with extracts from dietary plants, including berries, fruits and spices, and intracellular PKA-activity was assessed by change in bioluminescence in live cells by imaging.Several extracts were found to inhibit PKA activity in a 96-well platform high-throughput screen. Green tea, crowberry, clove and cinnamon extracts were found to reduce intracellular cAMP levels consistent with their ability to increase luminescence from luciferasePKA. Also pomegranate extract inhibited intracellular PKA and was used to estimate cellular association of polyphenols by HPLC and LC–MS. Pomegranate extract contains several anthocyanins, including delphinidin-3 glucoside. Delphinidin aglycone was found to inhibit cellular PKA activity in a concentration dependent manner. The inhibitory activity was found to be structure specific as a closely related compound to delphinidin had no activity.The current work identify phytochemicals in crude extracts which modulate cell signaling through PKA in a way that facilitate high through-put screening to help elucidate how plant based diet reduce risks of chronic diseases.
Keywords: polyphenols; protein kinase A; inhibitors; high-throughput screening; delphinidin
Does ascorbic acid supplementation affect iron bioavailability in rats fed micronized dispersible ferric pyrophosphate fortified fruit juice? by Juan Francisco Haro-Vicente; Darío Pérez-Conesa; Francisco Rincón; Gaspar Ros; Carmen Martínez-Graciá; Maria Luisa Vidal (470-478).
Food iron (Fe) fortification is an adequate approach for preventing Fe-deficiency anemia. Poorly water-soluble Fe compounds have good sensory attributes but low bioavailability. The reduction of the particle size of Fe fortificants and the addition of ascorbic acid might increase the bioavailability of low-soluble compounds. The present work aims to compare the Fe absorption and bioavailability of micronized dispersible ferric pyrophosphate (MDFP) (poorly soluble) to ferrous sufate (FS) (highly soluble) added to a fruit juice in presence or absence of ascorbic acid (AA) by using the hemoglobin repletion assay in rats.After a hemoglobin depletion period, four fruit juices comprised of (1) FS, (2) MDFP, (3) FS + AA, (4) MDFP + AA were produced and administered to a different group of rats (n = 18) over 21 days. During the repletion period, Fe balance, hemoglobin regeneration efficiency (HRE), relative bioavailability (RBV) and Fe tissue content were determined in the short, medium and long term.Fe absorption and bioavailability showed no significant differences between fortifying the fruit juice with FS or MDFP. The addition of AA to the juice enhanced Fe absorption during the long-term balance study within the same Fe source. HRE and Fe utilization increased after AA addition in both FS and MDFP groups in every period.Fe absorption and bioavailability from MDFP were comparable to FS added to a fruit juice in rats. Further, the addition of AA enhanced Fe absorption in the long term, as well as Fe bioavailability throughout the repletion period regardless of the Fe source employed.
Keywords: iron bioavailability; ascorbic acid; ferrous sulfate; micronized dispersible ferric pyrophosphate; rats
Dietary polyphenols protect against N-nitrosamines and benzo(a)pyrene-induced DNA damage (strand breaks and oxidized purines/pyrimidines) in HepG2 human hepatoma cells by Maria Eugenia Delgado; Ana Isabel Haza; Núria Arranz; Almudena García; Paloma Morales (479-490).
Dietary polyphenols have been reported to have a variety of biological actions, including anticarcinogenic and antioxidant activities.In the present study we investigated the protective effect of dietary polyphenols against N-nitrosodimethylamine (NDMA), N-nitrosopyrrolidine (NPYR) and benzo(a)pyrene (BaP)-induced DNA damage (strand breaks and oxidized purines/pyrimidines) in HepG2 cells.Human hepatocellular carcinoma (HepG2) cells, which retain many specialized liver functions and drug metabolizing enzyme activities, were used as in vitro model for human hepatocytes. NDMA, NPYR and BaP were employed to induce DNA damage. DNA damage (strand breaks, oxidized pyrimidines and oxidized purines) was evaluated by the alkaline single cell gel electrophoresis or comet assay.None of the polyphenols concentrations tested in presence or absence of Fpg (formamidopyrimidine-DNA glycosylase), or Endo III (Endonuclease III) caused DNA damage per se. Increasing concentrations of BaP (25–100 µM) induced a significant increase of DNA strand breaks, Fpg and Endo III sensitive sites in a dose dependent manner. Myricetin and quercetin decreased DNA strand breaks and oxidized pyrimidines induced by NDMA, but not oxidized purines. However, both flavonoids reduced oxidized pyrimidines and purines induced by NPYR. DNA strand breaks induced by NPYR were prevented by quercetin, but not by myricetin. BaP-induced DNA strand breaks and oxidized pyrimidines were strongly reduced by myricetin and quercetin, respectively. While oxidized purines induced by BaP were reduced by quercetin, myricetin had no protective effect. (+)-Catechin and (−)-epicatechin reduced DNA strand breaks, oxidized pyrimidines and oxidized purines induced by NDMA. DNA strand breaks, and oxidized purines induced by NPYR were also prevented by (+)-catechin and (−)-epicatechin, while the maximum reduction of oxidized pyrimidines was found by (+)-catechin and (−)-epicatechin at 10 µM. (+)-Catechin and (−)-epicatechin decreased also DNA strand breaks and oxidized pyrimidines but not oxidized purines induced by BaP.Our results clearly indicate that polyphenols protect human derived cells against DNA strand breaks and oxidative DNA damage effects of NDMA, NPYR or BaP, three carcinogenic compounds which occur in the environment.
Keywords: dietary polyphenols; N-nitrosamines; benzo(a)pyrene; DNA damage; comet assay
B-vitamins, homocysteine and gene polymorphism in adults with fasting or post-methionine loading hyperhomocysteinemia by Chien-Hsiung Cheng; Yi-Chia Huang; Feng-Pan Chen; Ming-Chih Chou; Tsung-Po Tsai (491-498).
Although fasting and post-methionine loading (PML) homocysteine concentrations are not necessarily related, a high percentage of hyperhomocysteinemia cases would be missed if methionine loading was not performed.The influences of B-vitamins and genetic polymorphism (methylenetetrahydrofolate reductase 677C → T, MTHFR 677C → T) on fasting and PML homocysteine concentrations and the relationship between fasting and PML homocysteine were studied.This study was a cross-sectional study. Healthy subjects were divided into either fasting hyper-homocysteinemia (≥12.2 µmol/l) (fasting hyper-hcy, n = 51), PML hyper-homocysteinemia (fasting homocysteine <12.2 µmol/l but PML homocysteine ≥25.6 µmol/l) (PML hyper-hcy, n = 29), or normo-homocysteinemia (fasting homocysteine <12.2 µmol/l and PML homocysteine <25.6 µmol/l) (normo-hcy, n = 118) group based on elevated fasting and PML homocysteine levels of the 75th percentile of the population. The concentrations of plasma fasting and PML homocysteine, serum folate, vitamin B-12, plasma pyridoxal 5′- phosphate (PLP) were measured. The genetic polymorphisms were determined.Fasting homocysteine, but not PML homocysteine and MTHFR 677C → T genotype, was significantly and inversely affected by serum folate concentration after adjusting for potential confounders (β = −0.062, P < 0.01). Fasting and PML homocysteine were highly associated in the fasting hyper-hcy and pooled groups (P < 0.01) but not in the PML hyper-hcy and normo-hcy groups. PML homocysteine did not interact with either serum folate (P = 0.302), vitamin B-12 (P = 0.465), plasma PLP (P = 0.996) or MTHFR 677C → T genotype (P = 0.136) to affect fasting homocysteine concentration.Approximately one-third (36.3%) of hyperhomocysteinemia cases would be missed if methionine loading were not performed. Even though subjects may have a normal fasting homocysteine concentration, they need further screening for their PML homocysteine.
Keywords: folate; vitamin B-12; vitamin B-6; gene polymorphism; post-methionine loading; hyperhomocysteinemia