Apparent ileal and total-tract nutrient digestion by pigs as affected by dietary nondigestible oligosaccharides.
(9/6589)
The effects of two types of nondigestible oligosaccharides (NDO), fructooligosaccharides (FOS), and transgalactooligosaccharides (TOS) were studied on growing and weanling pigs' nutrient digestion. Dietary NDO were included at the expense of purified cellulose. Twenty-five 57-d-old growing pigs, averaging 15.9+/-.6 kg on d 0 of the experiment, were fed a corn-based control diet or the control with 6.8 or 13.5 g of FOS/kg or 4.0 or 8.0 g of TOS/kg (five pigs per diet). Feces were collected on d 28 to 32, and small-intestinal digesta were collected (slaughter technique) on d 42 to 47 of the experiment. Feeds, feces, and digesta were analyzed for DM, inorganic matter, CP, ether extract, and crude fiber. Dietary NDO did not significantly affect apparent fecal and small intestinal digestion of nutrients in growing pigs. After being fed a NDO-free diet through d 10 after weaning, 38-d-old weanling pigs (n = 20), averaging 10.4+/-.8 kg on d 0 of the experiment, were fed a control diet (based on cornstarch, casein, and oat husk meal) or the control with 10 or 40 g of FOS or TOS/kg (four pigs per diet). Feces and urine were collected on d 13 to 17, and ileal digesta were collected via a postvalve T-cecum cannula on d 33 to 37 of the experiment. Feeds, feces, and digesta were analyzed for DM, inorganic matter, CP, ether extract, starch, NDF, ADF, ADL, Ca, P, Mg, Fe, Cu, and Zn. Nonstarch neutral-detergent soluble carbohydrates (NNSC) completed the mass balance for the carbohydrates. Urine was analyzed for N and minerals. The apparent fecal digestion of NNSC increased in the NDO-supplemented diets. The TOS-fed pigs tended (P<.10) to have a higher apparent fecal digestion of CP than the FOS-fed and control pigs but excreted more N via the urine (P<.01). Nitrogen and mineral balances were not affected. The FOS was nearly completely degraded prececally. Mean fiber digestion was lower at the fecal compared with the ileal level, as was the extent of NDO effects. This indicates that fiber digestion requires more than 2 wk to adapt to dietary NDO. Apparent ileal digestion of hemicellulose increased for the NDO-supplemented diets (P<.05), but that of NNSC decreased (P<.001). Thus, under the well-controlled conditions of this experiment, dietary NDO hardly affected nutrient digestion in well-kept growing and weanling pigs. However, digestion of dietary nonstarch carbohydrates may be affected. (+info)
Glucocorticoid mediation of dietary energy restriction inhibition of mouse skin carcinogenesis.
(10/6589)
Dietary energy restriction (DER) inhibits carcinogenesis in numerous animal models. DER is a potent and reproducible inhibitor of two-stage mouse skin carcinogenesis when administered during the promotion phase. Previous research demonstrated that adrenalectomy abolished cancer prevention by food restriction. Several lines of evidence suggest that glucocorticoid elevation in the DER mouse mediates the prevention of skin cancer. Our research tested the hypothesis that elevated glucocorticoid hormone activates the glucocorticoid receptor (GR) and that this activated receptor interferes with the activator protein-1 (AP-1) transcription factor. Induction of AP-1 by the phorbol ester tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA) is essential to tumor promotion. We have been unable to demonstrate elevated activated GR in the epidermis of the DER mouse, perhaps because only indirect strategies have been possible with the use of epidermis from DER mice. However, DER blocked the induction of AP-1 and c-jun, a constituent protein of AP-1, in the epidermis of mice. Current studies are focused on the inhibition of signaling down the MAP-1/Raf-1 kinase pathway that leads to induction of constituent proteins of AP-1, including c-Jun. Although several pathways lead to the induction of AP-1 transcriptional activity, the MAP-1/Raf-1 pathway can be activated by protein kinase C (PKC); previous studies from our laboratory demonstrated an inhibition of PKC activity and a reduction in selected isoforms of PKC in the epidermis of the DER mouse. Our current working hypothesis is that elevated glucocorticoid hormone in the DER mouse reduces the amount and activity of PKC isoforms important in the activation of MAP-1/Raf-1 kinase pathway. We propose that this results in attenuation in the induction of the AP-1 transcription factor by TPA. Because AP-1 induction by TPA is obligatory for mouse skin promotion, we propose this as an essential component of the mechanism of DER prevention of mouse skin carcinogenesis. (+info)
Modulation of estrogen action in the rat pituitary and mammary glands by dietary energy consumption.
(11/6589)
We are investigating the mechanisms through which estrogens induce development of prolactin (PRL)-producing pituitary tumors and mammary carcinomas in rats and how these mechanisms are affected by dietary energy consumption. The hypothesis under examination is that dietary energy restriction inhibits tumorigenesis in estrogen-responsive tissues by altering cellular responsiveness to estrogenic hormones. In the Fischer 344 (F344) rat strain, a 40% restriction of energy consumption virtually abolishes development of estrogen-induced pituitary tumors. Inhibition of pituitary tumorigenesis in the F344 strain by energy restriction results from modulation of estrogen regulation of cell survival, not cell proliferation. In contrast, energy restriction has no inhibitory effect on estrogen-induced pituitary tumor development in the ACI rat strain. However, energy restriction markedly inhibits induction of mammary carcinomas in female ACI rats treated with 17beta-estradiol. Data presented herein indicate that dietary energy restriction modulates the responsiveness of specific cell populations to estrogenic hormones and thereby inhibits estrogen-induced tumorigenesis in a manner specific to both rat strain and tissue. (+info)
Caloric restriction leads to regional specialisation of adipocyte function in the rat.
(12/6589)
The study analysed the responses of three metabolic parameters in five distinct adipose tissue depots to caloric restriction (4 weeks) in the rat. The aims were to evaluate whether specific adipose tissue depots were recruited for triacylglycerol (TAG) storage and/or mobilisation, and to determine to what extent specific adipose tissue depots exhibited preferences for the source of fatty acid (FA) for TAG storage. Caloric restriction led to a general enhancement of the response of lipoprotein lipase (LPL), FA synthesis and glucose utilisation to a meal. Effects were particularly marked in the parametrial, perirenal and interscapular depots compared with mesenteric and subcutaneous depots. There was no evidence that individual depots selectively expressed a preference for the pathways concerned with the generation of FA for storage (the exogenous (LPL) and the endogenous (synthesis) pathway). However, the temporal sequence of activation of these pathways differed in a manner consistent with a switch from preponderant use of FA produced via de novo synthesis during the very early phase of feeding towards later use of FA derived from circulating TAG. The overall excursions in insulin levels observed in the calorie-restricted rats were comparable to those found in free-feeding rats, but the magnitude and the rapidity of the individual metabolic responses of the adipocyte were augmented. The data are consistent with a general enhancement of insulin sensitivity and responsiveness in adipose tissue of calorie-restricted rats, together with adaptive regional specialisation of adipocyte function. These adaptations would be predicted to facilitate the immediate conservation of dietary nutrients by promoting their storage as the FA or glycerol moieties of adipose tissue TAG and thereby to ensure the regulated release of FA and glycerol from adipose tissue in accordance with the requirement for glucose conservation and/or production. (+info)
Macronutrient intake and change in mammographic density at menopause: results from a randomized trial.
(13/6589)
To examine the effects of dietary fat intake on breast cancer risk, we are conducting a randomized trial of dietary intervention in women with extensive areas of radiologically dense breast tissue on mammography, a risk factor for breast cancer. Early results show that after 2 years on a low-fat, high-carbohydrate diet there is a significant reduction in area of density, particularly in women going through menopause. In women who went through menopause during the 2-year follow-up, the mean decreases in area of density and percentage of density in the intervention group were 11.0 cm2 and 11.0%, respectively, whereas the control group decreased 4.5 cm2 and 5.2%. The purpose of this analysis was to determine whether changes in intake of specific macronutrients could account for the observed reduction in breast density in these women. Differences between 2-year and baseline values of macronutrients (averaged over 3 nonconsecutive days of food intake) were calculated. We examined the effect of dietary variables, adjusted for changes in total calorie intake and weight and for family history of breast cancer, on changes in area of density and percentage of density using linear regression. Reduction in total or saturated fat intake or cholesterol intake was significantly associated with decreased dense area (p < or = .004). The most significant dietary variable associated with reduction in percentage of density was reduction in dietary cholesterol intake (P = 0.001), although reducing saturated fat intake was of borderline significance (P = 0.05). The effect of the membership in the intervention and control groups on change in area of density or percentage of density was reduced by models that included changes in intake of any fat, or cholesterol, or carbohydrates. The observation of an effect of diet at menopause on breast density, a marker of increased risk of breast cancer, may be an indication that exposures at this time have an enhanced effect on subsequent risk. (+info)
Insulin resistance of muscle glucose transport in male and female rats fed a high-sucrose diet.
(14/6589)
It has been reported that, unlike high-fat diets, high-sucrose diets cause insulin resistance in the absence of an increase in visceral fat and that the insulin resistance develops only in male rats. This study was done to 1) determine if isolated muscles of rats fed a high-sucrose diet are resistant to stimulation of glucose transport when studied in vitro and 2) obtain information regarding how the effects of high-sucrose and high-fat diets on muscle insulin resistance differ. We found that, compared with rat chow, semipurified high-sucrose and high-starch diets both caused increased visceral fat accumulation and insulin resistance of skeletal muscle glucose transport. Insulin responsiveness of 2-deoxyglucose (2-DG) transport measured in epitrochlearis and soleus muscles in vitro was decreased approximately 40% (P < 0.01) in both male and female rats fed a high-sucrose compared with a chow diet. The high-sucrose diet also caused resistance of muscle glucose transport to stimulation by contractions. There was a highly significant negative correlation between stimulated muscle 2-DG transport and visceral fat mass. In view of these results, the differences in insulin action in vivo observed by others in rats fed isocaloric high-sucrose and high-starch diets must be due to additional, specific effects of sucrose that do not carry over in muscles studied in vitro. We conclude that, compared with rat chow, semipurified high-sucrose and high-cornstarch diets, like high-fat diets, cause increased visceral fat accumulation and severe resistance of skeletal muscle glucose transport to stimulation by insulin and contractions. (+info)
Validity and reproducibility of a quantitative food frequency questionnaire for a cohort study in Japan.
(15/6589)
BACKGROUND: A self-administered quantitative food frequency questionnaire (Qx) was developed for a population-based cohort study on cancer in Takayama, Japan. METHODS: The Qx was tested among 58 male and 59 female volunteers. Average daily nutrient intakes for the previous year calculated from the Qx were compared with those from 3-day food records and four 24-h recalls. The Qx was also validated among 37 volunteers by comparing the nutrient intakes calculated from the Qx with 12 1-day food records during a year. We also calculated the intra-class correlation coefficients for various nutrients between the Qx and the second Qx administered by the same volunteers 1 year after the first survey. RESULTS: Pearson correlation coefficients between total energy from the Qx and 3-day records were 0.38 for men and 0.25 for women and those between the Qx and 24-h recalls were 0.19 and -0.02 for men and women, respectively. Correlations between the several nutrients from the Qx and 3-day records ranged from 0.2 to 0.5 for both men and women. These correlations after energy adjustment ranged from 0.2 to 0.6 for men and from 0.1 to 0.7 for women. In general, the correlations for various nutrients between the Qx and 12 1-day records were higher than those described above. The intra-class correlation coefficients ranged from 0.46 to 0.78 in men and from 0.36 to 0.67, except for vitamin C in women. When the information on portion size was excluded, almost all of the above indices showed somewhat lower figures. CONCLUSION: These results suggest that our food frequency questionnaire with portion size information can be used to estimate nutrient intakes of each individual. (+info)
Dietary variety within food groups: association with energy intake and body fatness in men and women.
(16/6589)
BACKGROUND: Short-term experimental studies suggest that dietary variety may influence body fatness but no long-term human studies have been reported. OBJECTIVE: The purpose of this study was to determine whether dietary variety within food groups influences energy intake and body fatness. DESIGN: Seventy-one healthy men and women (aged 20-80 y), who provided accurate reports of dietary intake and completed a body-composition assessment, were studied. RESULTS: Dietary variety was positively associated with energy intake within each of 10 food groups (r = 0.27-0.56, P < 0.05). In multiple regression analysis with age and sex controlled for, dietary variety of sweets, snacks, condiments, entrees, and carbohydrates (as a group) was positively associated with body fatness (partial r = 0.38, P = 0.001) whereas variety from vegetables was negatively associated (partial r = -0.31, P = 0.01) (R2 = 0.46, P < 0.0001). In separate models, both a variety ratio (variety of vegetables/variety of sweets, snacks, condiments, entrees, and carbohydrates) and percentage dietary fat were significant predictors of body fatness (controlled for age and sex, partial r = -0.39 and 0.31, respectively, P < 0.01). However, dietary fat was no longer significantly associated with body fatness when the variety ratio and dietary fat were included in the same model. CONCLUSIONS: Our data, coupled with those of previous short-term studies, suggest that a high variety of sweets, snacks, condiments, entrees, and carbohydrates coupled with a low variety of vegetables promotes long-term increases in energy intake and body fatness. These findings may help explain the rising prevalence of obesity. (+info)