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  • 1
    In: British Journal of Nutrition, Cambridge University Press (CUP), Vol. 103, No. 10 ( 2010-05-28), p. 1433-1441
    Abstract: The aim of these studies was to evaluate the potential of some nutritional approaches to prevent or reduce the body load of organochlorines (OC) in humans. Study 1 compared plasma OC concentrations between vegans and omnivores while study 2 verified if the dietary fat substitute olestra could prevent the increase in OC concentrations that is generally observed in response to a weight-reducing programme. In study 1, nine vegans and fifteen omnivores were recruited and the concentrations of twenty-six OC (β-hexachlorocyclohexane (β-HCH), p , p ′-dichlorodiphenyldichloroethane ( p , p ′-DDE), p , p ′-dichlorodiphenyltrichloroethane ( p , p ′-DDT), hexachlorobenzene, mirex, aldrin, α-chlordane, γ-chlordane, oxychlordane, cis -nonachlor, trans -nonachlor, polychlorinated biphenyl (PCB) nos. 28, 52, 99, 101, 105, 118, 128, 138, 153, 156, 170, 180, 183 and 187, and aroclor 1260) were determined. In study 2, the concentrations of these twenty-six OC were measured before and after weight loss over 3 months in thirty-seven obese men assigned to one of the following treatments: standard group (33 % fat diet; n 13), fat-reduced group (25 % fat diet; n 14) or fat-substituted group (1/3 of dietary lipids substituted by olestra; n 10). In study 1, plasma concentrations of five OC compounds (aroclor 1260 and PCB 99, PCB 138, PCB 153 and PCB 180) were significantly lower in vegans compared with omnivores. In study 2, β-HCH was the only OC which decreased in the fat-substituted group while increasing in the other two groups ( P  = 0·045). In conclusion, there was a trend toward lesser contamination in vegans than in omnivores, and olestra had a favourable influence on β-HCH but did not prevent plasma hyperconcentration of the other OC during ongoing weight loss.
    Type of Medium: Online Resource
    ISSN: 0007-1145 , 1475-2662
    Language: English
    Publisher: Cambridge University Press (CUP)
    Publication Date: 2010
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  • 2
    Online Resource
    Online Resource
    Cambridge University Press (CUP) ; 2013
    In:  Proceedings of the Nutrition Society Vol. 72, No. 3 ( 2013-08), p. 310-316
    In: Proceedings of the Nutrition Society, Cambridge University Press (CUP), Vol. 72, No. 3 ( 2013-08), p. 310-316
    Abstract: Diagnosis of metabolic syndrome includes a set of laboratory and physical findings, including central adiposity, elevated TAG, reduced HDL-cholesterol, hypertension and elevated fasting glucose or insulin resistance. While definitions have varied slightly, from a practical point of view, identifying dietary and lifestyle factors, including low levels of physical activity, are important in designing a diet and exercise programme that can help individuals with the metabolic syndrome to reduce the associated detrimental health consequences. Specific features of the metabolic syndrome require intervention, whether dietary or otherwise, to move towards normal ranges. It is important to remember that no one size or treatment fits all. While central obesity is perceived as the hallmark of the metabolic syndrome, other features need to be treated independently if they do not respond to lifestyle change. The future may hold treatments for the metabolic syndrome that involve modulation of inflammation.
    Type of Medium: Online Resource
    ISSN: 0029-6651 , 1475-2719
    Language: English
    Publisher: Cambridge University Press (CUP)
    Publication Date: 2013
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  • 3
    In: British Journal of Nutrition, Cambridge University Press (CUP), Vol. 105, No. 8 ( 2011-04-28), p. 1272-1276
    Abstract: The model developed by Forbes (1987) of how body fat mass (FM) and fat-free mass (FFM) change during periods of weight loss or gain (Δ body weight (BW)) assumed that they change in relationship to a constant C  = 10·4, where ΔFFM/ΔBW = 10·4/(10·4+FM). Forbes derived C based on aggregated, cross-sectional data from a small sample of women. The objective of the present study was to reanalyse the relationship described by Forbes and to explore whether this relationship is consistent across ethnicity and sex groups using cross-sectional data from a large sample of white and African-American men and women. Baseline data from white and African-American men and women aged 18–60 years, who participated in a clinical study at the Pennington Biomedical Research Center since 2001 and who underwent dual-energy X-ray absorptiometry scans, were available for analysis. To overcome differences in BMI distributions among the ethnicity-by-sex groups, a stratified random sample of participants was selected within each group such that numbers in each BMI category (  〈  25, 25–29·9, 30–34·9, 35–39·9, 40+ kg/m 2 ) were proportional to those within the group with the smallest sample size, yielding a sample of 1953 individuals. Linear regression models assessed the FM–FFM relationship across the four ethnicity-by-sex groups. The FM–FFM relationship varied little by ethnicity ( P  = 0·57) or by sex ( P  = 0·26). The constant describing the FM–FFM relationship was estimated to be 9·7 (95 % CI 9·0, 10·3). In conclusion, results from our large, biethnic sample of men and women found a FM–FFM relationship very close to that originally described by Forbes, absent of significant variability by ethnicity or sex.
    Type of Medium: Online Resource
    ISSN: 0007-1145 , 1475-2662
    Language: English
    Publisher: Cambridge University Press (CUP)
    Publication Date: 2011
    detail.hit.zdb_id: 2016047-1
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    SSG: 21
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  • 4
    Online Resource
    Online Resource
    Cambridge University Press (CUP) ; 1982
    In:  Proceedings of the Nutrition Society Vol. 41, No. 2 ( 1982-06), p. 95-108
    In: Proceedings of the Nutrition Society, Cambridge University Press (CUP), Vol. 41, No. 2 ( 1982-06), p. 95-108
    Type of Medium: Online Resource
    ISSN: 0029-6651 , 1475-2719
    Language: English
    Publisher: Cambridge University Press (CUP)
    Publication Date: 1982
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  • 5
    Online Resource
    Online Resource
    Cambridge University Press (CUP) ; 2000
    In:  Proceedings of the Nutrition Society Vol. 59, No. 3 ( 2000-08), p. 373-384
    In: Proceedings of the Nutrition Society, Cambridge University Press (CUP), Vol. 59, No. 3 ( 2000-08), p. 373-384
    Abstract: Food intake is a regulated system. Afferent signals provide information to the central nervous system, which is the centre for the control of satiety or food seeking. Such signals can begin even before food is ingested through visual, auditory and olfactory stimuli. One of the recent interesting findings is the demonstration that there are selective fatty acid taste receptors on the tongue of rodents. The suppression of food intake by essential fatty acids infused into the stomach and the suppression of electrical signals in taste buds reflect activation of a K rectifier channel (K 1.5). In animals that become fat eating a high-fat diet the suppression of this current by linoleic acid is less than that in animals that are resistant to obesity induced by dietary fat. Inhibition of fatty acid oxidation with either mercaptoacetate (which blocks acetyl-CoA dehydrogenase) or methyl­palmoxirate will increase food intake. When animals have a choice of food, mercaptoacetate stimulates the intake of protein and carbohydrate, but not fat. Afferent gut signals also signal satiety. The first of these gut signals to be identified was cholecystokinin (CCK). When CCK acts on CCK-A receptors in the gastrointestinal tract, food intake is suppressed. These signals are transmitted by the vagus nerve to the nucleus tractus solitarius and thence to higher centres including the lateral parabrachial nucleus, amygdala, and other sites. Rats that lack the CCK-A receptor become obese, but transgenic mice lacking CCK-A receptors do not become obese. CCK inhibits food intake in human subjects. Enterostatin, the pentapeptide produced when pancreatic colipase is cleaved in the gut, has been shown to reduce food intake. This peptide differs in its action from CCK by selectively reducing fat intake. Enterostatin reduces hunger ratings in human subjects. Bombesin and its human analogue, gastrin inhibitory peptide (also gastrin-insulin peptide), reduce food intake in obese and lean subjects. Animals lacking bombesin-3 receptor become obese, suggesting that this peptide may also be important. Circulating glucose concentrations show a dip before the onset of most meals in human subjects and rodents. When the glucose dip is prevented, the next meal is delayed. The dip in glucose is preceded by a rise in insulin, and stimulating insulin release will decrease circulating glucose and lead to food intake. Pyruvate and lactate inhibit food intake differently in animals that become obese compared with lean animals. Leptin released from fat cells is an important peripheral signal from fat stores which modulates food intake. Leptin deficiency or leptin receptor defects produce massive obesity. This peptide signals a variety of central mechanisms by acting on receptors in the arcuate nucleus and hypothalamus. Pancreatic hormones including glucagon, amylin and pancreatic polypeptide reduce food intake. Four pituitary peptides also modify food intake. Vasopressin decreases feeding. In contrast, injections of desacetyl melanocyte-stimulating hormone, growth hormone and prolactin are associated with increased food intake. Finally, there are a group of miscellaneous peptides that modulate feeding. β-Casomorphin, a heptapeptide produced during the hydrolysis of casein, stimulates food intake in experimental animals. In contrast, the other peptides in this group, including calcitonin, apolipoprotein A-IV, the cyclized form of histidyl-proline, several cytokines and thyrotropin-releasing hormone, all decrease food intake. Many of these peptides act on gastrointestinal or hepatic receptors that relay messages to the brain via the afferent vagus nerve. As a group they provide a number of leads for potential drug development.
    Type of Medium: Online Resource
    ISSN: 0029-6651 , 1475-2719
    Language: English
    Publisher: Cambridge University Press (CUP)
    Publication Date: 2000
    detail.hit.zdb_id: 2016335-6
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