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

• Multivariate analysis conducted with triglycerides as dependent variable and shift work, BMI, smoking, age, leisure time physical activity level, energy intake, and alcohol intake as independent variables confirmed that shift work has a significant explanatory power for triglyceride levels (beta = 0.134, p = 0.0005) [6].
• To address this issue, we examined the relationship between serum ghrelin and resting metabolic rate (RMR), the thermic effect of food (TEF), fasting and postprandial respiratory quotient, physical activity level, peak aerobic capacity (VO(2 peak)), energy intake, and psychological measures of feeding behavior [7].
• Besides genetic determinants, dietary cholesterol, dietary fat, total caloric intake, alcohol consumption, cigarette smoking, and physical activity are known to influence concentrations of lipids in women [8].
• CONCLUSION: This study confirms that drug-induced changes in food preference can lead to an excessive energy intake largely as a result of a high intake of sucrose [9].
• 2. The absence of heterologous desensitization was specific to anorexia nervosa, because the women with amenorrhoea due to voluntary weight loss but with a normal energy intake showed a pattern similar to the controls (GH after hexarelin 60.3 +/- 9.5 and to GHRH 120 minutes later 6.2 +/- 1.0 (P < 0.05)) [10].

High impact information on Energy Intake

• Mutivariate analyses included age, smoking status, total energy intake, dietary cholesterol intake, percentages of energy obtained from protein and specific types of fat, and other risk factors [11].
• After control for pack-years of smoking, age, sex, race, height, weight, energy intake, and educational level, the combined intake of eicosapentaenoic acid and docosahexaenoic acid was inversely related to the risk of COPD in a quantity-dependent fashion [12].
• Ethanol can account for up to 10 percent of the energy intake of persons who consume moderate amounts of ethanol [13].
• We placed 34 women (mean age, 26 years) and 25 men (mean age, 25 years) on three mixed natural diets of identical nutrient composition, except that 10 percent of the daily energy intake was provided as oleic acid (which contains one cis double bond), trans isomers of oleic acid, or saturated fatty acids [14].
• In adults with less than 25 per cent intestinal absorption of the recommended caloric intake, the plasma taurine level was also significantly reduced and correlated inversely with the duration of parenteral nutrition [15].

Chemical compound and disease context of Energy Intake

• RESULTS: Most patients receiving megestrol acetate had increased caloric intake resulting in body weight gain (mainly fat mass) [16].
• These results are evidence that estrogen/ERalpha signaling is critical in female and male WAT; obesity in alphaERKO males involves a mechanism of reduced energy expenditure rather than increased energy intake [17].
• Chronic ethanol consumption for 12 weeks (mean daily ethanol intake 11.4 gm per body weight corresponding to 29% of total energy intake) did not cause histological changes but decreased GPT activity, increased glutamate dehydrogenase and pyruvate kinase activities and did not alter their pp/pv distribution [18].
• Dietary fat and fructose, which do not increase insulin secretion, lead to reduced leptin production, suggesting a mechanism for high-fat/high-sugar diets to increase energy intake and weight gain [19].
• This submaximal dose of insulin did not affect glucose or amino acid uptake or require a greater caloric intake to avoid hypoglycemia [20].

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

• Leptin regulates energy intake and expenditure partly by modulation of the melanocortin pathway in the hypothalamus [26].
• Our results show that relative to diabetic rats on the HC diet, the diabetic rats on the HF diet exhibited significantly reduced caloric intake (-40%), NPY expression in the arcuate nucleus (-27%), and elevated CRH expression in the paraventricular nucleus (+37%) [27].
• Leptin, the ob gene product, is produced by adipocytes, and it acts to decrease caloric intake and increase energy expenditure [28].
• In the 12 normal subjects, but not the obese, base-line urinary excretion of the norepinephrine metabolite, 3-methoxy-4-hydroxy phenylethyleneglycol was related to body fat whereas excretion of the norepinephrine metabolite vanilmandelic acid was related to fat-free mass and to total energy intake [29].
• Incretin hormones such as glucagon-like peptide-1 (GLP-1) and the longer lasting analog exendin-4 show clinical promise for the treatment of diabetes because of glucoregulatory activities that enhance beta-cell function and growth, and actions in the central nervous system that induce satiety and decrease caloric intake [30].

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].

References