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Biomedical subjects

I Ramirez

Publications and source records attributed to I Ramirez.

At least 73 records · Page 4Linked to original sources
PubMed1987

Diet texture, moisture and starch type in dietary obesity.

A series of experiments demonstrated that the texture of a diet has less effect on growth than does the water content. Rats fed diets containing 50-71% water become obese. On the other hand, diets containing as little as 30% or as much as 75% water failed to increase growth. Varying the concentration of the suspending agent (xanthan gum) from 0.5% to 2% greatly altered the viscosity of liquid diets but had no reliable effect on growth. Diets containing gelatinized starch became semi-solid when water was added but the rats still grew faster when fed the moist rather than the dry gelatinized starch diets. However, feeding a diet containing a very high level of gelatinized starch reduced growth independently of the moisture content. Rats fed a dry powdered diet gained weight at about the same rate as rats fed a pelleted diet. These results indicate that the moisture content of a diet has a major influence on its ability to induce obesity. The type of starch fed to the rats also seems to be an important determinant of growth rate.

Animals↗
PubMed1987

Practical liquid diets for rats: effects on growth.

Liquid diets based on the AIN-76 formula are described. The diets employ xanthan gum as a stabilizer. Information is provided on how these diets may be modified to meet the requirements of a particular experiment (e.g., variations in water content, type of protein or carbohydrate or fat, etc.). These diets are superior to widely used diets with regard to nutritional adequacy, cost, ease of preparation, versatility, stability, osmolality, and use of natural ingredients. An experiment is described which compares the effects of feeding rats a solid diet or a liquid diet prepared three different ways. The results confirm that a properly prepared liquid diet can produce overweight and obesity.

Animal Feed↗
PubMed1987

When does sucrose increase appetite and adiposity?

Two methods of sucrose feeding have been employed in studies with rodents. In the nutritional method, part or all of the starch in a diet is replaced with sucrose. In the solution method, animals maintained on a nutritionally complete diet are given a sucrose solution to drink. The solution method is generally a more effective and reliable method of producing obesity except for weanling rodents. These two methods yield different results with regard to interactions with the fat and protein content of the diet, efficiency of weight gain, disaccharide effects and effects of meal feeding. It is suggested that for the nutritional method, sucrose alters food intake and adiposity via its effects on fat oxidation. For the solution method, the critical factor may be presenting a wet source of calories rather than sucrose per se. Differences in the way sucrose is fed do not account for all divergent results. Different investigators conducting similar experiments have often obtained different results. For these and other reasons, animal studies do not support the idea that sucrose intake causes obesity in humans.

Animals↗
PubMed1987

Feeding a liquid diet increases energy intake, weight gain and body fat in rats.

Studies were undertaken to analyze the role of moisture content of foods in producing dietary obesity. Female CD rats consumed more energy when offered a sucrose solution and plain water to drink than when they were only given plain water, regardless of the sugar content of their diet (0-65%). This suggested that the overeating that commonly occurs when sucrose solutions are offered may not be due to sucrose per se. In subsequent experiments, rats were fed modified AIN-76 diets high in sucrose, starch or fat for 28-42 d. For some rats, the diet was liquefied by adding water to make a 32% suspension. Plain drinking water was always available. Rats fed high carbohydrate liquid diets, with or without solid diet, consumed 8-15% more energy than rats fed solid diet only. Rats fed liquid diets also gained 43-206% more weight than did rats fed solid diets. Analysis of carcass composition revealed that the liquid diets increased body fat. For high fat diets, the results were more complicated. Addition of water to a low cellulose, high fat diet did not increase adiposity, whereas addition of water to a high cellulose, high fat diet did increase adiposity. These results suggest that the obesity-inducing effects of feeding sugar solutions or cafeteria diets may be due, in part, to the high water content of these foods.

Adipose Tissue↗
PubMed1986

Second malignant neoplasm in treated Hodgkin's disease. Report of a patient and scope of the problem.

The condition of a 6-year-old boy was diagnosed as mixed-cellularity Hodgkin's disease that involved the right side of the neck. Five years after the completion of radiation therapy for the involved area, followed by six courses of chemotherapy with mechlorethamine hydrochloride (nitrogen mustard), vincristine sulfate, procarbazine hydrochloride, and prednisone, he developed cerebral gliosarcoma. Numerous second malignant neoplasms have been reported in adults following treatment for Hodgkin's disease; however, the sequence of events in our patient is a new finding that has not, to our knowledge, been reported previously. While the second malignant tumor may have been induced by prior treatment, direct evidence is lacking.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1986

Hypophagia following dietary obesity.

Two experiments examined the hypophagia that occurs when rats are switched from a high-fat to a low-fat diet. In the first experiment, rats fed a high-fat diet for eight weeks weighed 79 g more than rats fed a low-fat diet. Removal of the high-fat diet led to reduced food intake for at least four weeks. Reducing the body weight of the rats by a 24 hour fast did not alter the time course of the hypophagia. Plasma levels of free glycerol, free fatty acids and ketones were elevated during and after feeding the high-fat diet; suggesting that feeding a high-fat diet increases fat oxidation even after the high-fat diet is withdrawn. In the second experiment, feeding rats the high-fat diet for four weeks increased body weight and body fat. Starving the rats for two days after feeding the high-fat diet did not alter subsequent hypophagia and did not alter the percentage of body fat. This pattern of results is similar to that previously seen following termination of obesity-inducing insulin treatment. The results are consistent with the idea that a persistent increase in fat oxidation is responsible for the hypophagia.

Animals↗
PubMed1986

Intragastric feeding differentially affects apparent rate of gastric emptying of phenol red and carbohydrate.

The effects of intragastric feeding on subsequent gastric emptying of glucose and glucose polymer solutions were investigated in rats having chronic gastric catheters. Rats were tested by a modification of the serial test meal method of Hunt. Six ml of solution was fed by mouth or gastric catheter and stomach contents were drained 15 to 60 minutes later. Dilution of stomach contents by gastric secretions and the fluid used to rinse the stomach was assessed by measurement of phenol red and direct assay of the carbohydrate. These two indicators gave very different results. Intragastric feeding of severely food deprived rats appeared to accelerate gastric emptying 30 to 60 minutes after feeding when phenol red was used but not when carbohydrate was used as a marker. Intragastric feeding did not significantly affect the apparent rate of gastric emptying in this same 30-60 minute period in mildly food deprived rats. Even though phenol red and glucose usually give similar results, it is probably inappropriate to estimate the emptying of glucose solely on the basis of measurements of phenol red. When carbohydrate was used as a marker, the chief effect of intragastric feeding is to produce some dumping of gastric contents within 15 minutes after the beginning of intragastric infusion.

Animals↗
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↗