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MeSH Review

Energy Intake

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Disease relevance of Energy Intake

  • In analyses adjusted for age and dietary energy intake, vitamin E consumption appeared to be inversely associated with the risk of death from coronary heart disease [1].
  • However, despite increased leptin levels, animals fed a high-fat diet became obese without decreasing their caloric intake, suggesting that a high content of dietary fat changes the 'set point' for body weight, at least in part by limiting the action of leptin [2].
  • RESULTS: After adjustment for caloric intake, dietary folate had a significant protective association with the risk of recurrence of large-bowel adenoma (P for trend = .04) [3].
  • The associations between prostate cancer risk and insulin sensitivity or resistance were independent of total caloric intake and serum levels of insulin-like growth factors, sex hormones, and sex hormone-binding globulin [4].
  • Reduction in caloric intake was associated with a greater absolute rise in the serum bilirubin concentration in patients with Gilbert's syndrome and partial hepatic bilirubin uridine diphosphate glucuronyltransferase (UDPG-T) dysfunction compared to patients with hemolytic unconjugated hyperbilirubinemia and normal subjects [5].

Psychiatry related information on Energy Intake


High impact information on Energy Intake


Chemical compound and disease context of Energy Intake


Biological context of Energy Intake

  • In particular, syndecans have been implicated in modulation of the activity of the melanocortin system, which potently regulates energy intake, energy expenditure, and peripheral glucose metabolism [21].
  • Despite the identification of leptin as a key mediator of this process, the mechanism whereby changes of body adiposity are coupled to adaptive, short-term adjustments of energy intake remains poorly understood [22].
  • These findings associate prolactin influences with MMTV mRNA production in mice and help explain the link between chronic energy-intake restriction and reduced MMTV gene expression [23].
  • In both groups, 48 h of glucose infusion reduced food intake in proportion to caloric supply, resulting in virtually no change in total caloric intake as compared to before the infusion [24].
  • In normal animal tissue, triacylglycerol is maintained within a narrow range; even when the caloric intake is excessive, compensatory FA-induced upregulation of oxidation prevents overaccumulation [25].

Anatomical context of Energy Intake


Associations of Energy Intake with chemical compounds

  • Fenfluramine and fluoxetine spare protein consumption while suppressing caloric intake by rats [31].
  • Fluoxetine, a drug that blocks reuptake of serotonin, similarly spared protein consumption while reducing caloric intake [31].
  • In these experiments, animals were pair-fed mixtures of laboratory chow and refined preparations of casein, sucrose, and lard to permit comparisons among nutrients with total energy intake held constant or with additional energy provided in the form of a single nutrient [32].
  • Intraperitoneal doses of 15 micrograms triiodothyronine (T3)/100 g body wt per d caused an increase in caloric intake from 26.5 +/- 1.7 (mean +/- SEM) kcal/100 g per d to 38.1 +/- 1.5 kcal/100 g per d [33].
  • Fat increased pancreatic NE turnover when added in amounts sufficient to double the caloric intake [34].

Gene context of Energy Intake

  • Provision of a 45% fat diet increased energy intake and body weight in both Pomc(-/-) and Pomc(+/-) mice [35].
  • Sustained i.c.v. treatment with histamine thus makes it possible to partially restore the distorted energy intake and expenditure in leptin-resistant mice [36].
  • Administration of GH, which is known to cause a major decrease in plasma IGFBP-1 and in IGFBP-2 in hypophysectomized animals, did not result in a change in calorically restricted normal adult subjects, suggesting that a normal caloric intake is required for GH to suppress IGFBP-2 [37].
  • These results demonstrate that intake of an LF diet was associated with slower LAPC-4 prostate tumor growth relative to mice fed an HF diet, independent of total caloric intake, and this effect may be mediated through modulation of the insulin/IGF axis [38].
  • Although there was no significant pattern of interaction between either BMI or energy intake and polymorphisms assessed, specific sources of energy did appear to be more related to colon cancer risk in the presence of specific IRS2 and IGF1 genotypes [39].

Analytical, diagnostic and therapeutic context of Energy Intake

  • RESULTS: The Pearson correlation coefficients for various carotenoids as measured by the questionnaire, with the corresponding measurements in plasma specimens, ranged from 0.33 to 0.44 (all P < .001), adjusted for total energy intake, body mass index, age, sex, smoking status, and total plasma cholesterol [40].
  • Hydrazine sulfate compared with placebo addition to chemotherapy resulted in significantly greater caloric intake and albumin maintenance (P less than .05) [41].
  • Oral glucose tolerance even in those patients in whom fasting plasma glucose levels normalized was still grossly diabetic at the end of the hospital stay, deteriorating further after three days of liberalized caloric intake [42].
  • Cross-sectional analyses were adjusted for age, smoking, energy intake, and concentration or intake of folate and vitamin B-6, where appropriate [43].
  • Either a prospective randomized or a prospective randomized crossover design was used to examine the effects of two isocaloric, high-carbohydrate diets on the whole-blood glucose and insulin responses to mixed caloric intake and exercise in healthy nonpregnant (n = 14) and pregnant (n = 12) women [44].


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  15. Nutritional requirement for taurine in patients receiving long-term parenteral nutrition. Geggel, H.S., Ament, M.E., Heckenlively, J.R., Martin, D.A., Kopple, J.D. N. Engl. J. Med. (1985) [Pubmed]
  16. Megestrol acetate in patients with AIDS and cachexia. Oster, M.H., Enders, S.R., Samuels, S.J., Cone, L.A., Hooton, T.M., Browder, H.P., Flynn, N.M. Ann. Intern. Med. (1994) [Pubmed]
  17. Increased adipose tissue in male and female estrogen receptor-alpha knockout mice. Heine, P.A., Taylor, J.A., Iwamoto, G.A., Lubahn, D.B., Cooke, P.S. Proc. Natl. Acad. Sci. U.S.A. (2000) [Pubmed]
  18. The effect of chronic ethanol ingestion on ethanol metabolizing enzymes in isolated periportal and perivenous rat hepatocytes. Väänänen, H., Salaspuro, M., Lindros, K. Hepatology (1984) [Pubmed]
  19. Update on adipocyte hormones: regulation of energy balance and carbohydrate/lipid metabolism. Havel, P.J. Diabetes (2004) [Pubmed]
  20. A submaximal dose of insulin promotes net skeletal muscle protein synthesis in patients with severe burns. Ferrando, A.A., Chinkes, D.L., Wolf, S.E., Matin, S., Herndon, D.N., Wolfe, R.R. Ann. Surg. (1999) [Pubmed]
  21. Mice lacking the syndecan-3 gene are resistant to diet-induced obesity. Strader, A.D., Reizes, O., Woods, S.C., Benoit, S.C., Seeley, R.J. J. Clin. Invest. (2004) [Pubmed]
  22. Leptin action in the forebrain regulates the hindbrain response to satiety signals. Morton, G.J., Blevins, J.E., Williams, D.L., Niswender, K.D., Gelling, R.W., Rhodes, C.J., Baskin, D.G., Schwartz, M.W. J. Clin. Invest. (2005) [Pubmed]
  23. Prolactin effects on the dietary regulation of mouse mammary tumor virus proviral DNA expression. Hamada, N., Engelman, R.W., Tomita, Y., Chen, R.F., Iwai, H., Good, R.A., Day, N.K. Proc. Natl. Acad. Sci. U.S.A. (1990) [Pubmed]
  24. Leptin receptor-deficient obese Zucker rats reduce their food intake in response to a systemic supply of calories from glucose. Gilbert, M., Magnan, C., Turban, S., André, J., Guerre-Millo, M. Diabetes (2003) [Pubmed]
  25. Lipotoxicity of beta-cells in obesity and in other causes of fatty acid spillover. Unger, R.H., Zhou, Y.T. Diabetes (2001) [Pubmed]
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  31. Fenfluramine and fluoxetine spare protein consumption while suppressing caloric intake by rats. Wurtman, J.J., Wurtman, R.J. Science (1977) [Pubmed]
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  33. Functional relationship of thyroid hormone-induced lipogenesis, lipolysis, and thermogenesis in the rat. Oppenheimer, J.H., Schwartz, H.L., Lane, J.T., Thompson, M.P. J. Clin. Invest. (1991) [Pubmed]
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