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Caloric intake, stress, and menstrual function in athletes.

The cause of menstrual disturbance in athletes is still debated. Apart from the acute and chronic effects of exertion, other associated behavioral variables are suspected to play a key role. A longitudinal study with frequent blood sampling was undertaken to link information about nutrition and stress with a quantitative assessment of endocrine menstrual function in 18 endurance-trained athletes and 25 age-matched, nonathletic women. Four athletes did not show hormonal signs of follicular development. The 14 athletes with cyclic gonadal function did not differ from controls with regard to estradiol concentrations during the follicular phase and at midcycle. During the luteal phase, however, they showed significantly reduced areas under the estradiol and progesterone curves. Caloric intake, as assessed by nutritional diaries, correlated positively with the area under the progesterone curve during the luteal phase (rs = 0.70, P less than 0.01). Ratings of subjective stress in the area "partner, family, friends" correlated negatively with the luteal progesterone area (rs = 0.80; P less than 0.01). Data support the hypothesis that nutrition and stress may play a critical role in the genesis of menstrual disturbance in athletes.

Adult

A controlled trial of megestrol acetate on appetite, caloric intake, nutritional status, and other symptoms in patients with advanced cancer.

This double-blind, cross-over trial was designed to assess the effects of megestrol acetate (MA) on cancer-induced cachexia. Forty consecutive malnourished patients with advanced non-hormone-responsive tumors receiving no antineoplastic treatment were randomized to receive MA 480 mg/day versus placebo for 7 days. During day 8, a cross-over was made until day 15. Appetite, pain, nausea, depression, energy, and well-being were assessed with a visual analog scale (0 to 100 mm) at 9:00 AM and 4:00 PM during days 6, 7, 13, and 14. Weight (W;kg), tricep skinfold (TS; mm), arm circumference (AC; cm), and calf circumference (CC; cm) were measured at days 1, 8, and 15. Caloric intake (CI; Kcal/day) was determined during days 6, 7, 13, and 14. In 31 evaluable patients, the percentual difference in appetite at 9:00 AM, appetite at 4:00 PM, energy, and well-being after MA was +15.1, +14, +3.2, and +5.2, versus -12 (P = 0.03), -5.1 (P = 0.015), -10 (P = 0.024), and -8.3 (not significant) after placebo. Percentual difference in W, TS, AC, and CC after MA was +0.2, +1, -0.1, and +0.4 versus -0.8 (P = 0.03), -0.8 (P = 0.001), -0.3 (not significant), and -0.5 (P = 0.04) after placebo. CI during MA was 3480 +/- 1574 (48-hour intake), versus 2793 +/- 1542 (P less than 0.001) during placebo. Patients and investigators blindly chose MA in 20 (66%, P = 0.023) and 28 cases (92%, P less than 0.001), placebo in eight and two cases, and made no choice in three and one cases, respectively. Toxicity consisted of mild edema and nausea in three and two cases, respectively. After mean follow-up of 27 +/- 13 days, on an open basis, an average increase in W and AC of 4.8 +/- 1.7 kg and 2.8 +/- 1.7 cm was observed, respectively. The authors conclude that MA is a powerful appetite stimulant with subjective and objective effects on nutritional status.

Appetite

Regulation of bile acid pool size and plasma lipid levels in the SHR/N-corpulent rat: influence of the level of caloric intake.

In the obese progeny of the SHR/N-cp strain of the rat the bile acid pool was at least twice as large as that in their lean littermates even when only 6 weeks old. The composition of the pool remained unchanged in the obese females, but in their male counterparts the proportion of cholic acid was significantly increased. Cholestyramine feeding reduced the pool size by 26% in the obese rats, but a similar effect also occurred in the lean animals. The obese rats consumed about 60% more food per day than their lean littermates. When obese females were pair-fed to the intake of their lean controls from 6 to 11 weeks of age, the bile acid pool remained significantly enlarged, although not to the same extent as in the obese rats fed ad lib. Plasma cholesterol levels were reduced but remained significantly higher than the levels in the lean animals. The marked hypertriglyceridemia exhibited by the obese rats fed ad libitum did not develop in their pair-fed counterparts. In contrast, there was a comparatively smaller reduction in plasma cholesterol and triglyceride levels in the obese rats fed cholestyramine. Hepatic steatosis persisted in the pair-fed animals as well as in those given cholestyramine. Restricting caloric intake significantly reduced the body weight gain of the obese rats but had little effect on the extent of their corpulence. These studies show that at least some of the characteristics of this congenic strain, including hypertriglyceridemia and hepatic and intestinal hypertrophy, are due mainly to excess dietary intake.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals

Effect of palatable diet on growth, caloric intake and endocrine-metabolic profile in weanling rats with dorsomedial hypothalamic lesions.

Weanling male Sprague-Dawley rats received bilateral electrolytic lesions in the dorsomedial hypothalamic nuclei (DMNL rats); sham-operated rats served as controls. All animals were fed lab chow for 15 postoperative days. At that time they were subdivided into two groups each. One DMNL and one control group continued to be fed lab chow until the termination of the experiment on postoperative day 116. A second DMNL and control group were fed a high-fat diet and 32% sucrose solution (HF/SS diet). All DMNL rats showed reduced body weight and linear growth, but the HF/SS diet depressed these parameters further below the levels of the chow-fed groups. Both DMNL and control rats fed HF/SS had more carcass fat, heavier epididymal fat pads, more carcass fat per calories eaten, higher plasma levels of glucose, glycerol and free fatty acids but lower insulin levels than chow-fed DMNL rats and controls. This occurred in the face of lower body weights and caloric intake. Neither growth hormone nor insulin showed lesion effects. Rats with DMNL exhibited the same inverse relationship between plasma insulin and free fatty acids as controls. The data indicate that DMNL rats respond to the HF/SS diet essentially like sham-operated controls, i.e., they develop dietary obesity. Although they do show some small deficits, their lipogenic capacity is actually significantly greater than that of HF/SS-diet fed controls.

Animals

Protein, amino acid, and caloric intakes of selected pregnant women.

Toxemia of pregnancy is characterized by a combination of at least two of the following clinical symptoms: hypertension, edema, and proteinuria. In three successive trials over three consecutive years, the dietary intakes of a selected number of young pregnant women attending a Maternal and Infant Care Clinic at Tuskegee Institute were evaluated for protein, amino acids, and total calories. Women with toxemia were identified, and women without toxemia served as controls. The toxemic group generally consumed more protein than the controls, but values were statistically significant only in the first trial. However, all essential amino acids were consumed in significantly greater amounts by the toxemic group. Protein and essential amino acids were consumed in adequate amounts (at least two-thirds of the RDA) by both groups but in amounts smaller than the national average. Non-essential amino acids were also consumed in adequate amounts, with the toxemic group consuming larger quantities than the controls. Caloric intakes were adequate for young pregnant women. The relationships of glucosuria and of toxemia to protein and amino acid intake were similar and were opposite to the relationship of anemia to protein and amino acid intake. Meats and grains contributed the greatest quantity of protein and amino acids to the diet in all groups. Data seem to imply that any relationship of protein and amino acids with toxemia of pregnancy is a complex one involving several possibly interrelated nutritional parameters.

Adolescent

Rates of apoptosis and proliferation vary with caloric intake and may influence incidence of spontaneous hepatoma in C57BL/6 x C3H F1 mice.

Although the dysregulation of physiological signals and mechanisms controlling cell proliferation has been a major focus in cancer research, recent evidence suggests that explicit evaluation of apoptosis or physiological cell death may be equally important in understanding multistage carcinogenesis. Dietary restriction of rodents is well known to reproducibly retard development of spontaneous and chemically induced tumors. We reasoned that the decrease in metabolic and hormonal trophic factors induced with this intervention could promote selective cell deletion via apoptosis. To pursue this possibility, we quantified the spontaneous apoptotic rate in liver sections from diet-restricted (DR) and ad libitum-fed (AL) 12-month-old male C57BL/6 x C3H F1 mice, a murine strain known to develop a high incidence of spontaneous liver tumors by 18 months of age. The identification of hepatocyte apoptotic bodies was facilitated by in situ end-labeling immunohistochemistry. The basal rate of proliferation of hepatocytes was quantified utilizing proliferating cell nuclear antigen immunohistochemistry. The incidence of apoptotic bodies and total proliferating cell nuclear antigen-positive cells was enumerated in 14 mice/group by scoring 50,000 random hepatocytes/liver and expressed as the mean incidence/100 cells. When the comparison was made between diet groups, the apoptotic rate was significantly higher in the DR mice relative to the AL mice, while the proliferation rate was significantly lower (P < 0.01 and P < 0.05, respectively). The increase in spontaneous level of apoptosis and the decrease in proliferation rate in livers of DR mice were associated with a significantly lower rate of spontaneous hepatoma over a 36-month period. In summary, the results suggest that caloric intake may modulate the basal turnover rates of cell death and proliferation in a direction consistent with a cancer-protective effect in the DR mice and a cancer-promoting effect in AL mice.

Animals

Daily caloric intake of normal-weight adults: response to changes in dietary energy density of a luncheon meal.

The extent and time course of caloric compensation for surreptitious dilutions and supplements to the energy value of the diet were examined in free-living normal-weight adults. Ten subjects were provided lunches containing approximately 66% more or less calories than their customary midday meal for 2-wk periods which were interposed between 1-wk baseline or recovery periods. Diet records were kept throughout the study. Total energy intakes did not differ among the three control periods (weeks 1, 4, and 7) or between any of these periods and when subjects were provided the low-calorie meal. Total energy intake was significantly higher relative to all other periods when subjects ingested the high-calorie meal. To the extent that compensation occurred, it was apparent immediately and did not appear to change over the 2-wk study periods. The results suggest that humans compensate more readily for decreases than for increases in caloric intake.

Adult

Role of caloric intake in the weight loss after jejunoileal bypass for obesity.

Sixty-five patients were studied prospectively after jejunoileal bypass for obesity. Dietary intake pre- and postoperatively was measured either directly by weighing food or by a research dietary history. Of 65 measurements, 59 were made at least 6 months after operation, when over 75% of weight loss had been achieved. Fat absorption was measured in 42 of the patients. The entire group ate fewer calories (mean +/- SE = 2595 +/- 135) postoperatively than preoperatively (mean +/- SE = 3261 +/- 138). This difference was highly significant (P less than 0.001). Forty-eight patients ate less after their operation. The caloric deficit calculated from the observed weight loss could be accounted for entirely by the estimated decrease in intake in 22 of the 48 patients who ate less postoperatively. Moreover, measured fat malabsorption accounted for only 31% of the observed weight loss in those who ate more postoperatively and 21% in those who ate less. We conclude that a decrease in caloric intake, along with malabsorption, is an important factor in the long term postoperative weight loss (1-9 months) after jejunoileal bypass for obesity.

Body Weight

Fat, caloric intake, and obesity: lifestyle risk factors for breast cancer.

Dietary fat is a likely important determinant of postmenopausal breast cancer as part of an intricate and inseparable interaction of lifestyle cancer risk factors that include dietary fat, type of fat, energy intake and expenditure, and obesity. These factors possibly build upon individual susceptibilities derived from a complex array of polygenetic risk determinants. Epidemiologic studies have not provided conclusive evidence for a dietary fat-breast cancer association, partly because studies that focus on a single nutrient cannot always evaluate readily the interactive effects of other lifestyle factors. Further, persons generally underestimate their usual dietary intake, measured by either food frequency questionnaires (FFQs) or diet records. A dietary measurement model that accounts for this underreporting demonstrated that FFQs and diet records may not be able to detect a dietary fat-breast cancer association because of measurement error biases. Although meta-analysis of epidemiologic data across individual studies suggests only a week association between breast cancer and dietary fat, this result is compatible with the dietary measurement model and does not rule out a contributing role for dietary fat, either alone or with other causative factors. Research is needed that focuses on a comprehensive approach to dietary lifestyle choices and breast cancer risk and that emphasizes a fat-caloric intake-obesity linkage. The best hope for a definitive answer may rest with randomized, controlled clinical trials. Two such trials, the Women's Health Initiative and the Women's Intervention Nutrition Study, are under way.

Animals

Effect of restricted caloric intake on azoxymethane-induced colon tumor incidence in male F344 rats.

The effect of 30% caloric restriction on azoxymethane (AOM)-induced colon carcinogenesis was investigated in male F344 rats. Starting at 5 weeks of age, groups of animals were fed ad libitum a high-fat (23.5%) semipurified diet. At 7 weeks of age, all animals except the vehicle-treated groups were s.c. injected with AOM (15 mg/kg body wt, once weekly for 2 weeks). Four days after the second AOM injection, groups of animals were continued on high-fat diet and fed ad libitum (ad libitum group) whereas other groups were restricted to 70% of total calories (calorie-restricted group) consumed by the ad libitum group, but received same amounts of fiber, vitamins, and minerals. Thirty-two weeks after AOM injections, all animals were necropsied. The animals in the calorie-restricted group developed significantly fewer colon tumors and had a lower colon tumor incidence than did the rats in the ad libitum group. The size of colon tumors was also reduced in the calorie-restricted group.

Animals

Effect of restricted caloric intake on the development of the azoxymethane-induced glutathione S-transferase placental form positive hepatocellular foci in male F344 rats.

The modifying effect of 30% caloric restriction on the occurrence of azoxymethane (AOM)-induced glutathione S-transferase placental form (GST-P) positive hepatocellular foci was investigated in male F344 rats. Starting at 5 weeks of age, groups of animals were fed ad libitum a high-fat (23.5%) semipurified diet. At 7 weeks of age, all animals except the vehicle-treated groups were s.c. injected with AOM (15 mg/kg body wt., once weekly for 2 weeks). Four days after the second injection, groups of animals were continued on high-fat diet and fed ad libitum (ad libitum group) whereas other groups were restricted to 70% of total calories (calorie-restricted group) consumed by the ad libitum group, but received the same amounts of fiber, vitamins and minerals. Thirty-two weeks after AOM injections, all animals were necropsied and livers were sectioned and stained for GST-P by a immunohistochemical technique for quantitative analysis of enzyme altered foci of the liver. Comparing AOM treated groups. The density and the unit area of enzyme altered foci were significantly lower in the calorie-restricted group (3.84 +/- 1.55/cm2, 7.96 +/- 5.43%) than in the ad libitum group (10.14 +/- 3.62/cm2, 28.11 +/- 12.33%). The size of foci was also reduced in the calorie-restricted group (17.15 x 10(-3) mm2 vs. 32.36 x 10(-3) mm2). The incidence and density of hepatocellular foci in rats fed calorie restricted diet were significantly lower than those in rats fed ad libitum, comparing vehicle-treated groups. These results indicate that calorie restriction inhibited the occurrence of both of spontaneous and AOM induced GST-P positive foci in rats.

Animals

The relationships of transcephalic impedance, head growth and caloric intake to outcome in preterm infants.

Twenty-two preterm infants with birth weights less than 1 400 g were measured weekly with transcephalic impedance and occipital-frontal head circumference. Mean caloric intake/kg/day was calculated weekly. All infants were assessed at one year of age with Bayley Mental and Motor Scales and neurological assessment. Univariate and multivariate analyses were performed indicating that transcephalic impedance was the most powerful of the three measures as a predictor of sequelae.

Birth Weight

Caloric intake and Na+-K+-ATPase: differential regulation by alpha 1- and beta-noradrenergic receptors.

This study examined the effects of diet and treatment with noradrenergic receptor antagonists on weight gain and indices of Na+-K+-adenosine triphosphatase (ATPase) activity in the rat. When rats were fed a palatable cafeteria diet, their caloric consumption increased by about 80%, but they did not gain weight significantly. Ouabain binding and K+-p-nitrophenylphosphatase (NPPase) activity were increased in brown adipose tissue and soleus. These indices remained elevated after the rats were returned to a regular diet. When rats were fasted for 3 days, they lost weight, and the indices of Na+-K+-ATPase activity were markedly reduced in brown adipose tissue and soleus. After refeeding the fasted rats gained weight three times more rapidly than nonfasted rats with similar food intake. Indices of Na+-K+-ATPase activity remained as low as they had been when the rats were fasting. There was a consistent negative correlation between weight gain per calorie eaten and brown adipose tissue NPPase activity. Changes in Na+-K+-ATPase could therefore be involved in the effects of overfeeding and fasting on metabolic efficiency. Desmethylimipramine binding was increased by cafeteria diet and decreased by fasting, consistent with changes in sympathetic nervous system activity. Treatment with prazosin, an alpha 1-noradrenergic receptor antagonist, reduced Na+-K+-ATPase in either control or cafeteria diet-fed rats but did not alter the effect of cafeteria diet feeding. By contrast, treatment with propranolol, a beta-receptor antagonist, prevented the increase in Na+-K+-ATPase during cafeteria diet feeding.(ABSTRACT TRUNCATED AT 250 WORDS)

4-Nitrophenylphosphatase

Quantitative contribution of factors regulating rat colonic crypt epithelium: role of parenteral and enteral feeding, caloric intake, dietary cellulose level and the colon carcinogen DMH.

To elucidate the role and quantitative contribution of several exogenous factors which may regulate colon crypt mitotic activity, proliferative zone height (PZH) and crypt height, groups of rats were subjected to various feeding regimens both with and without treatment with the colon carcinogen, 1,2-dimethylhydrazine (DMH). The rats were divided into two major groups and one group was given eight weekly injections of DMH base at 9.5 mg kg-1 body weight. Throughout this period and for two additional weeks the rats were isocalorically fed either a defined nutritionally complete diet with different levels of dietary cellulose or they were parenterally (i.v.) fed a nutritionally complete liquid formula with different caloric levels. The rats were then injected with colchicine 3 h prior to sacrifice to arrest and to collect dividing cells at metaphase. The results of multiple regression analysis of all data were interpreted to indicate that parenteral feeding caused dramatic suppression of the colon crypt height (CH) and of the number of metaphase figures per crypt (MC). Increased cellulose intake stimulated CH but suppressed MC. The CH was also stimulated by DMH. CH was positively correlated to PZH and MC. The MC was suppressed by cellulose intake and negatively correlated to PZH but was positively correlated to CH. The PZH was positively correlated to CH. These findings were related to the role of luminal food, functional workload, kcal intake and treatment with DMH on the measured colon crypt parameters. A quantitative assessment of factors that regulate the measured colonic crypt parameters was accomplished.

1,2-Dimethylhydrazine

[Effects of various caloric intakes on nitrogen metabolism of the body, the muscles and the viscera during total parenteral nutrition with aminoacidic solution enriched with branched-chain amino acids].

Nitrogen metabolism was studied in ten injured/septic patients by means of a two compartment model, differentiating muscle from non muscle (central) tissue. During fasting muscle tissue loses a consistent amount of aminoacids which is retained in part by central tissue, giving rise to a positive nitrogen balance, whilst three methyl histidine and body nitrogen output are elevated. Total parenteral nutrition (glucose 15 kcal kg-1 day-1, nitrogen 0.30 g kg-1 die-1) improved body nitrogen balance and three methyl histidine excretion, but did not affect significantly either muscle or central nitrogen balance. Increasing caloric support to 30 kcal kg-1 day-1 did not showed any further effect on body nitrogen balance and three methyl histidine, while it improved significantly vs basal muscle nitrogen balance, but did not affect central nitrogen balance.

Amino Acids, Branched-Chain