Effect of dietary fructose on triglyceride transport and glucoregulatory hormones in hypertriglyceridemic men.

Effects of dietary fructose on triglyceride metabolism and on basal levels and meal responses of glucose, insulin, and glucagon were studied in six hypertriglyceridemic men, two of whom were also diabetic. Constant composition, weight-maintaining formula diets were used with substitution of fructose for 20% of the carbohydrate calories in both fat-containing (45% carbohydrate) and fat-free (85% carbohydrate) periods; each of the four dietary periods was at least 2 weeks long in every subject. No effect of fructose on fasting levels of triglycerides could be seen in any of the diets. No alterations of triglyceride transport occurred with fructose substitution in the fat-containing diets, but significant reductions of triglyceride transport rates were seen with fructose substitution in the 85% carbohydrate diets using both the heparin infusion lipolytic rate method and the 3H-glycerol methods of assessment of tryglyceride turnover (- 16 and - 21%, respectively). Dietary fructose induced no significant changes in either basal levels or responses during a "formula tolerance test" of glucose, insulin, or glucagon. Thus, dietary fructose given for several weeks does not appear to cause further elevations of plasma triglyceride levels in hypertriglyceridemic men.     

Effects of dietary fructose on plasma glucose and hormone responses in normal and hyperinsulinemic men

Twelve men with abnormally high insulin responses to a sucrose load and 12 normal men were fed diets containing 0, 7.5, or 15% of the calories as fructose for 5 weeks each. The diets contained approximately 43% of the calories as total carbohydrate, 42% as fat and 15% as protein. Mean insulin responses of the hyperinsulinemic men were initially 235% of control responses. Plasma glucose concentrations 1 hour after the sucrose load were significantly higher in hyperinsulinemic men than in controls. There were no initial differences between the two groups in glucagon or gastric inhibitory polypeptide (GIP) responses. Consumption of 7.5 and 15% Fructose diets increased fasting plasma glucose and GIP responses in both groups. Consumption of the 15% fructose diet resulted in significantly higher insulin and glucose responses than consumption of the other two diets. These results indicate that moderate levels of dietary fructose can produce undesirable changes in glucose metabolism of both normal and hyperinsulinemic men.     

Seminal fructose in normal and infertile men

Fructose levels and fructolysis index in human semen were analysed to assess a correlation, if any, between the levels of this glycolysable sugar and sperm concentration. Semen was collected from normospermic men and men with azoospermia or oligospermia. Seminal fructose levels were elevated in men with obstructive azoospermia and in men who remained azoospermic following vasoepididy mostomy done to correct epididymal blockage. Men with sperm concentration of less than 20 million/ml pre-operatively or following vasoepididy mostomy, showed significantly high levels of fructose and lower fructolysis index. Fructose levels in normospermic infertile men, as well as in men with normal sperm counts (more than 20 million/ml), were similar to that in men of proven fertility.     

Association between dietary factors and plasma adiponectin concentrations in men

BACKGROUND: Adiponectin, an adipocyte-derived peptide, improves insulin sensitivity, has antiinflammatory and antiatherogenic effects, and is associated with a lower risk of ischemic heart disease (IHD) and type 2 diabetes. However, little is known about dietary predictors of plasma adiponectin concentrations in humans. OBJECTIVE: Our objective was to examine cross-sectionally the association between dietary factors and plasma adiponectin in men. DESIGN: Our study included 532 male participants of the Health Professionals Follow-Up Study who were selected as control subjects for an investigation of biological predictors of IHD. Diet, lifestyle, and anthropometric data were assessed by questionnaires. RESULTS: After multivariable adjustment, adiponectin was significantly inversely related to glycemic load (-1.3 mg/L per 1-SD increase; P = 0.02) and tended to be positively associated with total fat intake (0.7 mg/L per 0.5% of energy from fat instead of carbohydrates; P = 0.06). We also found a significant nonlinear association between plasma adiponectin concentrations and alcohol intake (P for quadratic trend = 0.01). Thus, whereas nondrinkers had mean plasma adiponectin concentrations of 16.48 mg/L, those who consumed 0.1-4.9, 5.0-14.9, 15.0-29.9, or >/=30 g alcohol/d had mean concentrations of 16.79 (P = 0.77 compared with nondrinkers), 18.97 (P = 0.02), 19.11 (P = 0.01), and 18.39 (P = 0.10) mg/L, respectively. CONCLUSIONS: Moderate alcohol intake is associated with higher adiponectin concentrations, whereas a carbohydrate-rich diet with a high glycemic load is associated with lower adiponectin concentrations in men with no history of cardiovascular disease. Although the strength of these associations was modest, our observations highlight the hypothesis that dietary factors may modulate plasma adiponectin concentrations-a potential mediator related to a reduced IHD risk.     

Compromised zinc status in rats adversely affects calcium metabolism in platelets

The effect of zinc status on external calcium uptake by rat platelets and the relation of uptake to aggregation malfunction were studied. For 11 d, immature male rats were fed either a low zinc diet (0.3 mg/kg) ad libitum, a zinc-adequate diet (100 mg/kg) ad libitum, or the adequate diet pair-fed. Washed platelets were loaded with fura-2 acetoxymethyl ester for measurement of cytosolic free calcium. The resting calcium concentration was higher in platelets from rats of low zinc status than in those from controls. When platelets were stimulated with a minimal level (0.12 mumol/L) of ADP, the free cytosolic calcium concentration increased to a greater extent when calcium was present in the external medium than in its absence. The difference was considered to be external uptake. Zinc status had no effect on internal release, but platelets from zinc-deficient rats took up significantly less external calcium. In conclusion, low zinc status in rats adversely affects calcium metabolism in platelets. Decreased uptake of external calcium by ADP-stimulated platelets is associated with defective aggregation.     

Prenatal zinc supplementation of zinc-adequate rats adversely affects immunity in offspring

We previously showed that zinc (Zn) supplementation of Zn-adequate dams induced immunosuppressive effects that persist in the offspring after weaning. We investigated whether the immunosuppressive effects were due to in utero exposure and/or mediated via milk using a cross-fostering design. Pregnant rats with adequate Zn nutriture were supplemented with either Zn (1.5 mg Zn in 10% sucrose) or placebo (10% sucrose) during pregnancy (3 times/wk). At postnatal d 3, 4 pups of Zn-supplemented dams (Zn-P) were exchanged with 4 of placebo-supplemented dams (P-Zn). The remaining pups continued with their biological mothers (Zn-Zn and P-P). Pups were orally immunized with dinitrophenol ovalbumin-BSA and/or cholera toxin B subunit (CTB), and serum Zn concentrations and cellular and humoral responses were assessed. Pups of Zn-supplemented dams had higher serum Zn when fostered either by placebo- or Zn-supplemented dams compared to pups of placebo-supplemented dams (P < 0.01). Postnatal Zn exposure reduced the number of Peyer's patches in both the Zn-Zn and P-Zn groups (P < 0.01). Prenatal Zn exposure suppressed CTB- (P = 0.05) and BSA-specific proliferation response of Peyer's Patch lymphocytes (P = 0.07). Prenatal Zn exposure effects on the splenocyte cytokine response were differently influenced by fostering mothers' Zn status. Antigen presenting cell (APC) activity of splenocytes was lower in the Zn-Zn group than in the P-P group (P < 0.08). In conclusion, prenatal Zn exposure increases serum Zn levels in pups and suppresses antigen-specific proliferation and antibody responses and APC function, whereas postnatal exposure may suppress the mucosal immune reservoir.     

Low vitamin D status adversely affects bone health parameters in adolescents

BACKGROUND: The effects of subclinical vitamin D deficiency on bone mineral density (BMD) and bone turnover in adolescents, especially in boys, are unclear. OBJECTIVE: We aimed to investigate the relations of different stages of vitamin D status and BMD and bone turnover in a representative sample of adolescent boys and girls. DESIGN: BMD was measured by dual-energy X-ray absorptiometry at the nondominant forearm and dominant heel in a random sample of 12- (n = 260) and 15-y-old (n = 239) boys and 12- (n = 266) and 15-y-old (n = 250) girls. Serum 25-hydroxyvitamin D, parathyroid hormone, osteocalcin, and type I collagen cross-linked C-telopeptide were assessed by using enzyme-linked immunoassays. Relations between vitamin D status and bone health indexes were assessed by using regression modeling. RESULTS: Using multivariate regression to adjust for potential physical, lifestyle, and dietary confounding factors, we observed that 12- and 15-y-old girls with high vitamin D status (>/=74.1 nmol/L) had significantly greater forearm (but not heel) BMD (beta = 0.018; SE = 0.008; P < 0.05 for each age group) and lower serum parathyroid hormone concentrations and bone turnover markers than did those with low vitamin D status. These associations were evident in subjects sampled throughout the year and in winter only. There was no significant relation between vitamin D status and BMD in boys. CONCLUSIONS: Maintaining serum 25-hydroxyvitamin D concentrations above approximately 50 nmol/L throughout the year may be a cost-effective means of improving bone health. Increased emphasis on exploring strategies for improving vitamin D status in adolescents is needed.     

Association between dietary phyto-oestrogens and bone density in men and postmenopausal women

Phyto-oestrogens have been associated with a decreased risk for osteoporosis, but results from intervention and observational studies in Western countries have been inconsistent. In the present study, we investigated the association between habitual phyto-oestrogen intake and broadband ultrasound attenuation (BUA) of the calcanaeum as a marker of bone density. We collected 7?d records of diet, medical history and demographic and anthropometric data from participants (aged 45-75 years) in the European Prospective Investigation into Cancer-Norfolk study. Phyto-oestrogen (biochanin A, daidzein, formononetin; genistein, glycitein; matairesinol; secoisolariciresinol; enterolactone; equol) intake was determined using a newly developed food composition database. Bone density was assessed using BUA of the calcanaeum. Associations between bone density and phyto-oestrogen intake were investigated in 2580 postmenopausal women who were not on hormone replacement therapy and 4973 men. Median intake of total phyto-oestrogens was 876 (interquartile range 412)?μg/d in postmenopausal women and 1212 (interquartile range 604)?μg/d in men. The non-soya isoflavones formononetin and biochanin A were marginally significant or significantly associated with BUA in postmenopausal women (β?=?1·2; P?相似文献   

Association between dietary pattern and serum C-reactive protein in Japanese men and women

Background

Dietary pattern may influence the risks of cardiovascular disease, atherosclerosis, type 2 diabetes, and metabolic syndrome through its effects on inflammation. We evaluated the association between dietary pattern and serum high-sensitivity C-reactive protein (hs-CRP) in a Japanese population.

Methods

In this cross-sectional analysis, we used baseline data from 3905 men and 5640 women (age 40–69 years) who participated in a population-based cohort study between November 2005 and December 2007. Participants with possible inflammation-related diseases, current analgesic use, high hs-CRP levels (≥3000 ng/mL) or extreme dietary energy intake were excluded. We used 46 items from a validated short food frequency questionnaire and examined major dietary patterns by factor analysis.

Results

We identified 5 dietary patterns: healthy (high in vegetables and fruit), Western (high in meat and fried foods), seafood (high in shellfish, squid, fish, etc.), bread (high in bread and low in rice), and dessert (high in confections and fruit). After adjustment for age, alcohol use, smoking, physical activity, and body mass index, hs-CRP levels in men were inversely associated with the healthy, bread, and dessert patterns (P-trend: 0.01, 0.06, and <0.01, respectively) and positively associated with the seafood pattern (P-trend = 0.02). In women, hs-CRP levels were inversely associated with the healthy pattern (P-trend = 0.06) and positively associated with the Western pattern (P-trend = 0.06).

Conclusions

The healthy dietary pattern may be associated with suppressed inflammation in Japanese men and women, independently of body mass index and other factors. The sex-specific associations of hs-CRP with other dietary patterns (eg, the seafood pattern) require further study.Key words: dietary pattern, C-reactive protein, inflammation, factor analysis     

Response of plasma glucose, fructose and insulin to dietary glucose and fructose in the lactating sow

Twenty-two Hampshire-Yorkshire X Large White sows of second and third parity were allotted randomly to one of three dietary treatments. Five sows were fed 6.0 kg/day of a corn-soybean meal lactation diet (control diet). Twelve sows were fed the control diet in which 24% of the composition was supplied by corn syrup containing 72% fructose on a dry matter basis (fructose diet) and five sows were fed the control diet in which 24% of the composition was supplied by powdered dextrose (glucose diet). All diets were fed from days 1 through 21 of lactation. Blood was collected from all sows immediately prior to feeding and hourly for 6 hours postprandial via jugular vein cannulae following a single feeding on seven separate but nonconsecutive days during the 21-day period. Fructose was absorbed from the digestive tract of sows as evidenced by elevated (P less than 0.01) conventions of fructose in plasma. Sows fed the fructose diet also had higher (P less than 0.01) plasma glucose concentrations than did those fed the glucose and control diets. The concomitant elevated glucose concentration following ingestion of the fructose diet was not associated (P greater than 0.10) with increased insulin concentration. Fructose in plasma was associated with a slight but significant increase in insulin although the mean concentration of insulin in plasma was only one-third that measured in sows fed the glucose and control diets. These data suggest that fructose in vivo has a glucose-sparing effect presumably mediated through a physiological mechanism that lowers insulin concentration.     

Rapid income growth adversely affects diet quality in China--particularly for the poor!

To study the impact of income change--specifically rapid income growth--on diet behavior over time and by socioeconomic level, we used data from a prospective study of China begun in 1989 (followed up in 1991, 1993 and 1997). The subpopulation used in this study included 5783 subjects aged 20-45 years old from 3129 households. Dietary intakes were measured using a combination of the weighing method and three consecutive 24-h recalls. Detailed income and price data were collected, and predicted household per capita income was used in multivariate longitudinal random-effects models that described the consumption of several food groups and nutrients. Income elasticity was used to measure the changes for the effects of income over time on (a) the probability of consuming any food and (b) the quantity of food consumed. The structure of the Chinese diet is shifting away from high-carbohydrate foods toward high-fat, high-energy density foods. The variation in the income effects that we uncovered indicated that important changes in income effects took place between 1989 and 1997, with the changes varying considerably by socioeconomic status. These shifts in income effects indicate that increased income might have affected diets and body composition in a detrimental manner to health, with those in low-income groups having the largest increase in detrimental effects due to increased income. Extrapolating from our estimates, higher income levels in the future could lead to the reversal of the health improvements achieved in the last two decades, if diet-related noncommunicable diseases cannot be controlled.     

The effect of inactivity on dietary intake and energy homeostasis.

Reduced physical activity commonly occurs in patients with disease or chronic disabilities, in the elderly, and in certain patients with obesity. Surprisingly, information on the effect of inactivity on energy homeostasis is scarce and often difficult to interpret. In models of reduced physical activity, such as space flights, bed-rest and confinement, subjects frequently lose weight (< 5%), predominantly in the form of fat-free mass. In some cases this is compensated by an increase in fat mass, which means that changes in weight are poor indicators of energy balance. The extent to which spontaneous reduction in energy intake (in most studies energy intake is fixed) compensates or overcompensates for the reduction in energy expenditure (mainly physical activity and to a small extent in BMR, typically < 6%) is largely underexamined. Preliminary observations suggesting that there is a preferential selection of low-energy-dense foods (low in fat) require confirmation under carefully controlled experimental conditions. It is concluded that a comprehensive and systematic evaluation is needed to address the effects and relevance of various degrees of physical inactivity to energy homeostasis, in relation to disease and space medicine.     

Plasma fructose, uric acid, and inorganic phosphorus responses of hyperinsulinemic men fed fructose

We fed 12 men with abnormally high insulin responses to a sucrose load and 12 controls normal diets containing 0, 7.5, or 15% of the calories as pure fructose for 5 weeks each in a crossover design. Purified wheat starch replaced the fructose in the 0 and 7.5% diets. The two groups were matched for age, height, and weight. At the beginning of the study and at the end of each of the three 5-week periods, plasma responses to a sucrose load (2 gm/kg body weight) were measured. Initially there were no significant differences in the plasma fructose, uric acid, or inorganic phosphorus responses of the two groups. Plasma fructose responses to a sucrose load were significantly higher after the men consumed the 7.5 and 15% fructose diets than after the 0% diet. Uric acid responses tended to be greater in the hyperinsulinemic men than in controls and increased as the levels of fructose in the diet increased. The inorganic phosphorus levels after a sucrose load were higher in the hyperinsulinemic men than in controls when they consumed the 7.5 and 15% fructose diets. These results indicate that moderate levels of dietary fructose can affect plasma fructose, uric acid, and inorganic phosphorus levels, especially in hyperinsulinemic men.     

Metabolic effects of dietary fructose in healthy subjects.

To determine if dietary fructose causes adverse metabolic effects, we used a crossover design to compare a diet containing 20% of energy from fructose with an isoenergic high-starch diet that contained less than 3% fructose. Fourteen healthy subjects consumed each diet for 28 d. There were no significant differences between the diets in the mean values of hemoglobin A1C, serum glycosylated albumin, fasting plasma glucose, peak postprandial plasma glucose, integrated plasma glucose, fasting serum lactate, or fasting serum triglycerides. Peak postprandial serum lactate was significantly higher during the fructose diet at days 1, 7, and 14 but not at days 21 or 28. Peak postprandial serum triglycerides were significantly higher only at day 1 of the fructose diet. Day-28 fasting serum total and LDL cholesterol for the fructose diet were 9.0% and 11.0% higher, respectively, than the corresponding values for the starch diet. A high-fructose diet compared with a high-starch diet resulted in significantly higher fasting serum total and LDL cholesterol and also caused transient changes in postprandial serum lactate and triglycerides.     

Dietary heme adversely affects experimental colitis in rats, despite heat-shock protein induction

Objective

Research on dietary modulation of inflammatory bowel disease is in its infancy. Dietary heme, mimicking red meat, is cytotoxic to colonic epithelium and thus may aggravate colitis. Alternatively, heme-induced colonic stress might also result in potential protective heat-shock proteins (HSPs). Therefore, we investigated the effect of dietary heme on trinitrobenzene sulfonic acid (TNBS)-induced colitis in rats.

Methods

Rats were fed a high-fat control diet or a similar diet supplemented with heme. After dietary adaptation, rats were rectally infused with TNBS for colitis induction or saline for sham treatment. Colitis severity was evaluated and several markers were quantified in colonic mucosa isolated 1 wk after colitis induction. Furthermore, cytotoxicity of fecal water and serum α-1-acid glycoprotein were measured.

Results

Dietary heme increased cytotoxicity of the fecal water. Heme-fed sham-treated rats had higher colonic HSP-25 and heme-oxygenase-1 mRNA levels, which was confirmed by immunohistochemistry. HSP induction by heme was associated with decreased protein levels of myeloperoxidase and interleukin-1β after subsequent TNBS infusion. However, no dietary effects were observed on histologic colitis score. Furthermore, body weight gain, colon length, and food intake were lower and α-1-acid glycoprotein concentrations were higher in heme-fed colitic rats. In addition, somatostatin, involved in mucosal repair, was not changed with TNBS infusion in heme-fed rats.

Conclusion

Dietary heme adversely affects colitis, despite HSP induction. We speculate that the irritating influence of dietary heme, being continuously present in the colon, impairs recovery after colitis induction. A diet high in red meat might be a risk factor for inflammatory bowel disease development.     

Food neophobia in childhood affects dietary variety

Objective To determine whether children with food neophobia (unwillingness to try new foods) have more restrictive diets than children without neophobia.

Subjects Seventy children were classified into 3 groups based on scores obtained on the Food Neophobia Scale: neophobic group, score greater than 41; neophilic group, score less than 27; and average group, score of 28 to 40.

Design Dietary data were collected and analyzed for 3 days selected randomly. The dependent variables measured were energy and nutrient intakes, servings of each Food Guide Pyramid group, and Health Eating Index (HEI) scores.

Statistical analyses χ², 1-way analysis of covariance, and Scheffe multiple comparisons tests were conducted.

Results The 3 groups were similar with respect to the number of children meeting two thirds of the RDA/DRI for energy and most nutrients. The exception was vitamin E: fewer neophobic children met two thirds of the recommended value for this nutrient than average and neophilic children. The overall HEI score was significantly lower for the neophobic group compared with the average and neophilic groups. The HEI index showed that children with neophobia had a higher intake of saturated fat and less food variety than children without food neophobia.

Applications Dietitians should emphasize increased food variety for children within the context of a healthful diet. Research should be conducted to determine the effects of dietary variety on quality of diet and health of children. J Am Diet Assoc. 2000;100:1474-1478,1481.     

Dyslipidemic high-fat diet affects adversely bone metabolism in mice associated with impaired antioxidant capacity

Objective

The present study examined impacts of dyslipidemic high-fat diet on the bone antioxidant system and bone metabolism in growing mice. Furthermore, the relationship was studied between them.

Methods

Male C57BL/6 mice (4 wk old) were fed with normal diet, high-fat diet (HFD), or HFD supplemented with 0.1% antioxidant lipoic acid (LA). After 13-wk feeding, the markers of plasma lipids status, bone metabolism in plasma and in urine, and femora oxidative stress were measured. To provide molecular evidence for abnormal bone metabolism affected by HFD, bone cell-specific mRNA levels were tested by real-time quantitative polymerase chain reaction. Moreover, insulin-like growth factor I and tumor necrosis factor-alpha in plasma and their mRNA levels in femur were measured.

Results

The feeding dyslipidemic HFD induced both inhibitory bone formation reactions and enhancement of bone resorption reactions, accompanied by impaired bone antioxidant system, low levels of insulin-like growth factor I in plasma and in bone, and high levels of tumor necrosis factor-alpha in plasma but not in bone. In contrast, these alternatives were prevented completely or partially in mice fed LA supplement. Further, plasma propeptide of ? collagen C-propeptide as a marker of bone formation was positively correlated with both total antioxidant capacity (r = 0.683, P < 0.001) and reduced glutathione/oxidized glutathione ratio (r = 0.565, P < 0.003) of bone. Cross-linked N-telopeptides of bone type ? collagen as a marker of bone resorption was negatively correlated with both total antioxidant capacity (r = −0.753, P < 0.001) and glutathione/oxidized glutathione ratio (r = −0.786, P < 0.001).

Conclusion

Dyslipidemia induces impaired bone antioxidant system. Oxidative stress could be an important mediator of hyperlipidemia-induced bone loss.