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Biomedical subjects

I Ramirez

Publications and source records attributed to I Ramirez.

At least 55 records · Page 3Linked to original sources
PubMed1986

Integrated metabolic control of food intake.

Inhibition of glycolysis and fatty acid oxidation by combined treatment with 2-deoxyglucose (2DG) and methyl palmoxirate, or inhibition of glycolysis and lipolysis by combined treatment with 2DG and nicotonic acid synergistically increased food intake in rats. Methyl palmoxirate treatment alone increased food intake in rats fed a high-fat, but not low-fat diet. These results provide direct evidence for a mechanism in the control of food intake that integrates signals generated by the metabolism of glucose and fatty acids. In addition, they strongly indicate a role for fatty acid oxidation in the control of eating and raise the possibility that an interaction between glucose and fat metabolism underlies the link between regulation of body fat stores and short-term food intake.

Animals↗
PubMed1985

Immunologic evaluation in the nutritional assessment of children with cancer.

Eighty-one newly diagnosed untreated pediatric cancer patients (48 hematopoeitic malignancies, 17 solid tumors, 16 benign diseases) were evaluated with immunologic and nutritional parameters. The mean absolute lymphocyte count was adequate in the three groups. Reduced T-lymphocytes were seen in the solid tumors. Mitogenic response of hematopoietic and solid tumor patients' lymphocytes was low. Correlation of immunologic, dietary, and nutritional factors showed that for patients with solid tumors there was a positive significant correlation between weight/height percent and lymphocyte reactivity to phytohemagglutinin, concanavalin A, and pokeweed mitogen (p less than .05). Iron intake showed a significant positive correlation with in vitro mitogen reactivity for the solid tumor group (p less than .05) and benign diseases (p less than 0.01). Immune derangements found among patients with hematopoietic malignancies can be due to replacement of normal bone marrow with malignant cells. In solid tumor patients mitogen reactivity appears to be a reflection of nutritional state, and dietary iron is a possible factor.

Adolescent↗
PubMed1985

Relationship of fat metabolism to food intake.

A model for the role of body fat stores in the control of food intake is outlined. It is proposed that changes in the storage and mobilization of fuels into and from adipose tissue affect food intake indirectly by altering the supply of utilizable metabolic fuels. Experiments are reviewed in which this hypothesis is tested by an examination of the hypophagia that occurs following termination of obesity-producing injections of insulin. The results indicate that whereas excess mobilization of fat from adipose tissue does not entirely account for postinsulin hypophagia, changes in hepatic liquid metabolism may be a factor. It is proposed that the satiating effects of fat from either endogenous or exogenous sources may depend on the degree to which lipids are oxidized.

Adipose Tissue↗
PubMed1985

Oral stimulation alters digestion of intragastric oil meals in rats.

Rats were fed corn oil by gastric catheter, and plasma levels of triglycerides were measured 1-6 h later. In previous studies intragastric feeding of oil resulted in a more rapid rise in plasma triglycerides, followed by a more rapid fall, than oral feeding of the same amount of oil. In the present study administration of a small amount of oil or saccharin to the mouths of rats immediately before intragastric feeding prolonged the elevation in blood triglycerides 4 h later. This latter effect appeared only in rats having previous experience with oil paired with the taste. Oral stimulation with saccharin also increased the amount of fat remaining in the stomach 1 h after the intragastric meal. The amount of free fatty acids remaining in the stomach 1 h after intragastric feeding was not significantly influenced by oral stimulation, suggesting that lingual lipase is not responsible for the observed effects. These findings demonstrate that a taste which has been paired with fat intake can acquire the ability to influence the digestion of fat.

Animals↗
PubMed1985

Food intake in diabetic rats: isolation of primary metabolic effects of fat feeding.

The effects of varying dietary fat content on food intake and metabolism in streptozotocin-diabetic rats were examined. The metabolic consequences of fat feeding were separated from the marked adjustments in voluntary food consumption that occur when diabetic rats are fed diets containing different amounts of fat by feeding rats a fixed ration of food in which either fats or carbohydrates were reduced by equicaloric amounts, or in which only the concentration of fat, but not other dietary nutrients, was varied systematically. Resulting changes in metabolism and subsequent ad libitum food intake on refeeding were then measured. Rats did not increase their food intake after a prior reduction in carbohydrate consumption but did so after an equicaloric reduction in fat consumption. Urinary glucose excretion during rationing was a function of carbohydrate consumption and was not predictive of changes in food intake during refeeding. The more fat that rats consumed during rationing, the higher their levels of plasma triglycerides and ketone bodies were at the time of refeeding and the less they ate when allowed to eat ad libitum. The orderly changes in food consumption and in plasma triglycerides and ketones observed with variations in fat intake suggest that the effects of fat feeding on food intake in diabetic rats are mediated through the oxidation of ingested fat.

Animals↗
PubMed1985

Curability of Burkitt's lymphoma with high-dose cyclophosphamide-high-dose methotrexate therapy and intrathecal chemoprophylaxis.

Twenty-four children with Burkitt's lymphoma were treated beginning May 1976 with a regimen alternating high doses of cyclophosphamide and methotrexate in induction and consolidation; only high doses of methotrexate were used in the maintenance phase. Throughout therapy, which was planned for 54 weeks, intrathecal chemoprophylaxis using methotrexate, cytosine arabinoside, and hydrocortisone was coordinated with the high-dose methotrexate infusion therapy to provide CNS chemoprophylaxis that maintained therapeutic methotrexate spinal fluid levels (greater than 10(-6) mol/L) for approximately 60 hours. Twenty-two (92%) of the 24 children attained complete remission; two (8.3%) patients attained only partial remission, failing therapy. Two children died of infection while in complete remission; two children relapsed on therapy. Actual survival is 75%; the median follow-up time is 38+ months (range, 1 1/2+ to 84+ months). Relapses correlated with Murphy disease stage as follows: stage I--0/3, stage II--2/7, stage III--2/10, and stage IV--0/2. Serious side effects and toxicities of chemotherapy occurred in ten patients (metabolic disturbances after rapid tumor lysis, two; infectious and/or febrile episodes following cyclophosphamide therapy, three; methotrexate side effects, four; and complications of intrathecal therapy, one). Results of this therapy are similar to those of the best regimens that have been reported. Treatment has been adapted for use in Burkitt's lymphoma by the Pediatric Oncology Group; the responsiveness of other B cell lymphomas of childhood to this treatment is also being determined.

Adolescent↗
PubMed1984

Behavioral and physiological consequences of intragastric oil feeding in rats.

Four experiments were conducted to examine the appropriateness of intragastric feeding of vegetable oil. The first three experiments demonstrated that pairing intragastric feeding with a taste of saccharin, reduced subsequent saccharin preference slightly. A dose of lithium chloride which did not reduce food intake, produced a very strong conditioned aversion. It is therefore difficult to argue on the basis of taste aversions, that any reduction in food intake resulting from intragastric fat feeding is due to malaise. Intragastric fat feeding did not always reduce subsequent food intake; a large reduction in food intake was observed only when non-starved animals were given at least two previous spaced exposures to fat. The effects of oral and intragastric oil feeding on blood levels of triglycerides and free glycerol were examined. Blood triglycerides and glycerol rose sooner and fell sooner following intragastric than after oral oil feeding. Emulsifying the oil did not correct the abnormality; indeed it exaggerated the early rise in blood triglycerides and glycerol. These results indicate that interpretation of studies involving intragastric fat feeding is more complicated than generally recognized.

Animals↗
PubMed1983

Suppression of food intake by intragastric glucose in rats with impaired glucose tolerance.

Three experiments were performed to examine the relationship between impaired glucose tolerance and food intake. In the first experiment, normal rats that were given long-term insulin treatment, which was then withdrawn, ate less than controls when refed after food deprivation. Despite reduced intakes, rats previously treated with insulin became more hyperglycemic than controls during refeeding. In the second experiment, intragastric glucose injections reduced food intakes to a similar degree in control rats and in rats experiencing insulin withdrawal even though glucose loading produced a much greater increase in plasma glucose level in previously insulin-treated rats. In the third experiment, intragastric loads of a glucose polymer, Polycose, reduced food intake to the same degree in normal rats and in streptozotocin-diabetic rats both two and sixteen days after insulin withdrawal when diabetic rats were, respectively, hypo- and hyperphagic. The results show that impaired glucose tolerance does not appreciably alter the suppressive effects of glucose loading on food intake. Other effects of glucose administration, besides those on insulin-dependent glucose utilization, appear to reduce food intake after glucose loading.

Animals↗
PubMed1983

Food intake and blood fuels after oil consumption: differential effects in normal and diabetic rats.

The mechanisms by which fat feeding suppresses the hyperphagia of diabetic rats were examined. Rats that were allowed to consume a small amount (1.5 ml) of corn oil decreased subsequent food intake within 6 hr after ingesting. Diabetic rats decreased food intake much more than normal rats. Similar results were obtained when oil was given intragastrically. Analysis of blood samples revealed that diabetic rats showed greater increases in plasma ketones and triglycerides and smaller increases in plasma glycerol than normal rats following consumption of 1.5 ml corn oil. This difference between diabetic and normal rats appeared when rats were allowed to eat after oil ingestion as well as when they were fasted. Brief periods of food deprivation (2.5-4.5 hr) substantially increased plasma ketones and glycerol and decreased plasma triglycerides in both diabetic and normal rats. The results indicate that diabetic rats decrease food intake more than normal rats after fat feeding because they oxidize more of the ingested fat.

Animals↗
PubMed1983

Differential effects of medium- and long-chain triglycerides on food intake of normal and diabetic rats.

Three experiments were performed to examine the effect of ingestion of medium- (MCT) and long-chain (LCT) triglyceride oils at the beginning of the normal feeding period on subsequent food intake of normal and diabetic rats. In the first experiment, diabetic rats reduced food intake more than normal animals in the first 6 hr after ingestion of 2.0 ml of MCT or LCT oil. In the second experiment, diabetic rats reduced food intake to a similar extent by 6 hr after ingestion of 1.5 ml of MCT or LCT oil, but the time course of this effect depended on the oil ingested. Ingestion of MCT oil produced a decrease in food intake within 2 hr, whereas ingestion of LCT oil reduced food intake 2-4 hr later. In the third experiment, a direct comparison was made of the differential time course of food intake suppression by MCT or LCT oil in both normal and diabetic rats. Diabetic rats decreased food intake after ingestion of 1.5 ml MCT or LCT oil, whereas normal rats did not. Again, in diabetic rats, ingestion of MCT oil produced a more rapid reduction in food intake than ingestion of LCT oil. It is proposed that the more pronounced reduction in food intake of diabetic rats after oil ingestion is due to a greater degree of hepatic oxidation of ingested fat, whereas the differential effect of MCT and LCT oil ingestion in diabetic rats is due to a differential rate of delivery of the ingested lipid substrate to the liver.

Animals↗
PubMed1983

Metabolic concomitants of hypophagia during recovery from insulin-induced obesity in rats.

Rats were given daily injections of protamine-zinc insulin (PZI) that increased food intake and body weight. Termination of insulin treatment resulted in transient hypophagia and weight loss. Simultaneously with the weight loss, plasma levels of glycerol, free fatty acids, glucose, and ketones increased, whereas adipose tissue lipoprotein lipase activity and liver glycogen decreased. These changes in food intake and metabolism after termination of PZI treatment were accentuated in streptozotocin-diabetic rats. Two antilipolytic drugs (nicotinic acid and 3,5-dimethylpyrazole) blocked the elevation in plasma glycerol while having no effect on food intake. A 1-day fast after termination of insulin treatment equalized insulin-treated and control groups for plasma glycerol and ketones and reversed group differences in free fatty acids; the elevation in plasma glucose persisted despite starvation. Following starvation, previously PZI-treated rats ate less than controls on refeeding. The results show that enhanced lipolysis does not invariably accompany hypophagia during excess weight loss and suggest that a disturbance in carbohydrate metabolism or an increase in hepatic fatty acid oxidation may underlie this decrease in food intake.

Animals↗
PubMed1977

A factor analytic--genetic approach to the relation between obesity and behavior in mice.

Genetically heterogenous mice (N = 377) were reared on either high- or low-fat diets for the first 40 days of life. The mice were cross fostered to permit the separation of genetic and environmental effects in a sibling analysis. A total of 26 measures were taken on these mice, including oxygen consumption, activity, sucrose consumption, body weight changes when bitter or high-fat diets were given as the only food, and various morphological measures. A principal-factor analysis of these measures produced eight factors, most of which appeared to be "instrument" factors rather than general factors. Analyses of variance on the factor scores indicated that genetic influences contributed to five of the factors and sex contributed to three of the factors. However, none of the main effects of diet, gene by environment interactions, or sex by environment interactions were significant. Although obesity and behaviors were correlated, the magnitudes of the correlations were generally small.

Age Factors↗