Fructose consumption and its implications on public health are currently under study. This work reviewed the metabolic fate of dietary fructose based on isotope tracer studies in humans. The mean oxidation rate of dietary fructose was 45.0% ± 10.7 (mean ± SD) in non-exercising subjects within 3–6 hours and 45.8% ± 7.3 in exercising subjects within 2–3 hours. When fructose was ingested together with glucose, the mean oxidation rate of the mixed sugars increased to 66.0% ± 8.2 in exercising subjects. The mean conversion rate from fructose to glucose was 41% ± 10.5 (mean ± SD) in 3–6 hours after ingestion. The conversion amount from fructose to glycogen remains to be further clarified. A small percentage of ingested fructose (<1%) appears to be directly converted to plasma TG. However, hyperlipidemic effects of larger amounts of fructose consumption are observed in studies using infused labeled acetate to quantify longer term de novo lipogenesis. While the mechanisms for the hyperlipidemic effect remain controversial, energy source shifting and lipid sparing may play a role in the effect, in addition to de novo lipogenesis. Finally, approximately a quarter of ingested fructose can be converted into lactate within a few of hours. The reviewed data provides a profile of how dietary fructose is utilized in humans.

Lignans, derived from flaxseed, are phyto-oestrogens being increasingly studied for their health benefits. An 8-week, randomised, double-blind, placebo-controlled study was conducted in fifty-five hypercholesterolaemic subjects, using treatments of 0 (placebo), 300 or 600 mg/d of dietary secoisolariciresinol diglucoside (SDG) from flaxseed extract to determine the effect on plasma lipids and fasting glucose levels. Significant treatment effects were achieved (P,0·05 to ,0·001) for the decrease of total cholesterol (TC), LDL-cholesterol (LDL-C) and glucose concentrations, as well as their percentage decrease from baseline. At weeks 6 and 8 in the 600 mg SDG group, the decreases of TC and LDL-C concentrations were in the range from 22·0 to 24·38 % respectively (all P, 0·005 compared with placebo). For the 300 mg SDG group, only significant differences from baseline were observed for decreases of TC and LDL-C. A substantial effect on lowering concentrations of fasting plasma glucose was also noted in the 600 mg SDG group at weeks 6 and 8, especially in the subjects with baseline glucose concentrations $ 5·83 mmol/l (lowered 25·56 and 24·96 %; P¼ 0·015 and P¼ 0·012 compared with placebo, respectively). Plasma concentrations of secoisolariciresinol (SECO), enterodiol (ED) and enterolactone were all significantly raised in the groups supplemented with flaxseed lignan. The observed cholesterol-lowering values were correlated with the concentrations of plasma SECO and ED (r 0·128-0·302; P,0·05 to , 0·001). In conclusion, dietary flaxseed lignan extract decreased plasma cholesterol and glucose concentrations in a dose-dependent manner. Flax is one of the oldest domesticated crops (since 7000 BC) and flour from the seed was used in bread as early as 1000 BC (1) . Today, flaxseed is being increasingly used in the human diet because of its potential health benefits, particularly for cardiovascular protection (2 -4) . Flaxseed is the richest natural source of plant lignans, with secoisolariciresinol diglucoside (SDG) being the principal lignan compound. The concentrations of SDG in flaxseed vary with different cultivars. Eliasson et al. (5) reported that SDG concentrations in twenty-seven flaxseed species ranged from 1·19 to 2·59 % for (þ)-SDG and from 0·22 to 0·5 % (w/w) for its diastereoisomer, (2)-SDG. Westcott et al. (6) presented a range of SDG concentrations from 0·97 to 3·09 % (w/w) in eight varieties of defatted flaxseed meals. Flaxseed lignan along with soyabean isoflavones are phyto-oestrogens commonly consumed in the human diet (7) .To date, a number of clinical trials have been conducted using dietary flaxseed which suggested that SDG lignan may lower plasma cholesterol concentrations. However, the results did not show consistent benefit. In most of these studies, the concentration of lignans was not determined. Differences of study designs, subject characteristics and treatment conditions could confound the outcomes and interpretation of the results (2) . Nevertheless, multiple animal studies do indicate that d...

Sequence determinations in our laboratory have yielded the primary structures of ovomucoid third domains from 35 avian species. From that list, 12 sequences could be arranged into a contiguous set such that each sequence differs from a second by a single amino acid replacement. For this set of domains and for five additional domains of special interest, we report here the association equilibrium constants for their binding with bovine alpha-chymotrypsin, elastase I, and subtilisin Carlsberg. The results are interpreted with the aid of the three-dimensional structure of highly homologous Japanese quail ovomucoid third domain and of computer-generated models of the complexes of the inhibitor with the respective enzymes. The results show that (i) changes in inhibitor residues other than the primary recognition residue (P1) even sequentially far from the reactive site, may exert large effects on association equilibrium constant values provided these residues make contact with the enzyme, (ii) changes in residues other than P1 often exert large differential effects toward the different enzymes, i.e., the same change can make the inhibitor stronger for one enzyme and weaker for another, (iii) the sign and to some extent the magnitude of the changes can be rationalized from the known structures of the inhibitor and the enzyme, (iv) changes in surface residues which do not contact the enzyme in complex are virtually without effect, and (v) glycosylated and nonglycosylated inhibitors have the same constants. For confirmation of the validity of the equilibrium constant comparisons in a few cases, the rate constants kon and kd were determined and the resultant calculated equilibrium constant values compared to the directly determined numbers. An additional test of validity is provided by experiments where a glycosylated domain of one species is allowed to compete with an unglycosylated domain of another for the same enzyme.

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BackgroundHigh serum uric acid concentration (hyperuricemia) has been studied for its relationship with multiple adverse health outcomes, such as metabolic syndrome. Intervention studies have produced inconsistent outcomes for the relationship between fructose intake and serum uric acid concentration.MethodsThe association of dietary fructose intake with hyperuricemia risk in adults was examined using logistic regression and U.S. NHANES 1999-2004 databases. A total of 9,384 subjects, between the ages 20 and 80 years, without diabetes, cancer, or heart disease, were included.ResultsThe highest added or total fructose intake (quartiles by grams or % energy) was not associated with an increase of hyperuricemia risk compared to the lowest intake with or without adjustment (odds ratios = 0.515-0.992). The associations of alcohol and fiber intakes with the risk were also determined. Compared to the lowest intake, the highest alcohol intake was associated with increased mean serum uric acid concentration (up to 16%, P < 0.001) and hyperuricemia risk (odds ratios = 1.658-1.829, P = 0.057- < 0.001); the highest fiber intake was correlated with decreases of uric acid concentration (up to 7.5%, P < 0.002) and lower risk (odds ratios = 0.448-0.478, P = 0.001- < 0.001). Adults who were over 50 y old, male, or obese had significantly greater risk.ConclusionsThe data show that increased dietary fructose intake was not associated with increased hyperuricemia risk; while increased dietary alcohol intake was significantly associated with increased hyperuricemia risk; and increased fiber intake was significantly associated with decreased hyperuricemia risk. These data further suggest a potential effect of fructose consumption in an ordinary diet on serum uric acid differs from results found in some short-term studies using atypical exposure and/or levels of fructose administration.