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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
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 In the first experiment, normal rats that were given long-term insulin treatment, which was then withdrawn, ate less than controls when refed after food deprivation.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↗
PubMed1983

Energy and nutrient intake of children with cancer.

Two hundred seventy-seven pediatric cancer patients received a nutritional assessment. Initial dietary intakes of patients with no prior treatment indicated a diet similar to that of the general population. The caloric intake was 75% of the RDA in a group of patients with non-malignant diseases and 80% of the RDA in the groups of patients with solid tumors and hematopoietic malignancies. Protein intake was greater than 100% of the RDA for all groups. Dietary iron was the nutrient lowest in intake, with a range of 70% to 78% of the RDA. At six-month evaluations, no significant changes occurred except for an increase in iron, niacin, riboflavin, and protein intakes in the group with solid tumors.

Adolescent↗
PubMed1982

Metabolic and physiologic effects of a hunger-inducing injection of insulin.

Rats injected subcutaneously with 5 U/kg of regular insulin increased food intake above control levels in a 2 hr test and showed a median latency to eat of 59 min. One week later, rats were injected again with saline or insulin (5 U/kg), deprived of food and killed 60 +/- 10 min later. Insulin treatment produced a marked reduction in plasma glucose, plasma ketone bodies and liver glycogen, as well as a marked acceleration of gastric emptying. The results indicate that a variety of changes in peripheral metabolism and physiology may underlie the increase in food intake observed after insulin injection and that it is premature to ascribe the hunger-inducing effect of insulin treatment solely to a decline in blood glucose.

Animals↗
PubMed1982

Glycerol is not a physiologic signal in the control of food intake in rats.

Rats were given two daily subcutaneous injections of either 40, 80 or 160 mg/kg of glycerol or control injections of glucose. Glycerol injections did not reliably affect body weight gain at any dose tested whether animals were maintained in constant light or a 12 hr light/dark cycle. Only injections of 160 mg/kg of glycerol given twice daily significantly reduced daily food intake; however, this dose also raised plasma glycerol concentrations briefly to an unphysiologic level. Continuous intravenous infusions of 390 or 780 mg/rat/day of glycerol had no effect on food intake, even though plasma glycerol levels increased markedly within the normal range. These findings indicate that reductions of food intake and body weight after administration of glycerol are probably responses to a treatment which is not physiologic.

Animals↗
PubMed1981

Estradiol-induced changes in lipoprotein lipase, eating, and body weight in rats.

Daily injections of 5 micrograms estradiol benzoate (EB) for 1, 2, 3, and 12 days decreased parametrial and retroperitoneal adipose tissue lipoprotein lipase activity in ovariectomized rats. Nearly all of this decrease occurred within the 1st day. In contrast, EB-induced body weight loss and hypophagia were very slight during the 1st day after EB administration and increased substantially over the next 2 days. EB did not affect gastrocnemius muscle lipoprotein lipase activity over the first 3 days, but did decrease muscle lipoprotein lipase activity after 12 days. These changes in adipose and muscle lipoprotein lipase activity suggested that EB-induced redistribution of fuel would be greater after 3 days of treatment than after 12 days of treatment. Tests with two different in vivo triglyceride uptake methods confirmed this suggestion. EB-treated rats were hypertriglyceridemic after 12 days of treatment, but not after 3 days of treatment. Elevated plasma triglycerides were associated with an increased rate of triglyceride entry. These findings are consistent with the hypothesis that EB administration temporarily results in redistribution of triglyceride fuel from adipose tissue to muscle, resulting in a transient decrease in rate of weight gain.

Adipose Tissue↗
PubMed1981

Deficits in pituitary and brain cell nuclear retention of (3H)Estradiol in diabetic rats deprived of insulin: time course and metabolic correlates.

Withdrawal of exogenous insulin for 24 h in ovariectomized, streptozotocin-diabetic rats significantly impairs estradiol uptake in whole homogenate fractions of hypothalamus-preoptic area and pituitary gland. Significant reductions in cell nuclear fractions from the same tissues are seen after 36 h of insulin deprivation. Subsequent reinstatement of insulin treatment does not yield full recovery of estradiol uptake after 24 h of insulin replacement. Fat content of the diet has no effect on brain or pituitary estradiol uptake in diabetic animals deprived of insulin for 36 h. Circulating levels of triglycerides, ketones, glucose, glycerol and free fatty acids were found to predict uptake levels to a significant extent, but no single metabolite is reliably predictive across tissues. These data demonstrate that insulin-dependent changes in brain and pituitary uptake of estradiol in rats are slow to develop, and they support the hypothesis that at least some of the reproductive dysfunctions observed in diabetic rats may be the result of impaired cell nuclear estradiol binding in hypothalamus and pituitary.

Animals↗
PubMed1981

Estrous behavior and pituitary and brain cell nuclear retention of [3H]estradiol in chronically insulin-deficient female rats.

Chronic insulin deficiency, produced by administration of 60 mg/kg streptozotocin, leads to reduced estrous behavior and lower estradiol uptake in both whole homogenate and cell nuclear fractions of hypothalamus-preoptic area and pituitary gland in ovariectomized rats. High dietary fat intake produces an ameliorative effect on both lordosis behavior and estradiol uptake, relative to animals fed a standard, carbohydrate-rich diet. Plasma glucose levels are significantly correlated with estradiol uptake levels in brain and pituitary, and with plasma radioactivity levels. The data support the hypothesis that some of the reproductive dysfunctions manifest in female diabetic rats are the result of alterations in nuclear binding of estradiol by central nervous tissue, and that chronic fuel deprivation may represent an important correlate of disruptions in normal steroid action among diabetics.

Animals↗
PubMed1980

Effect of ascorbic acid in vitro on lymphocyte reactivity to mitogens.

The direct effects of ascorbic acid and dehydroascorbic acid in vitro on human lymphocyte proliferation to phytohemagglutinin (PHA) and concanavalin A (Con A) stimulation were determined. Cells exposed to physiologic and high concentrations of ascorbic acid and dehydroascorbic acid showed poorer tritiated thymidine ([3H]TdR) incorporation than controls without the vitamin. The inhibitory effect was dose-dependent, with the greatest inhibition occurring as the concentration of ascorbic acid and dehydroascorbic acid was increased. At supraoptimal concentrations of PHA and Con A, there was no recovery of the mitogen response, indicating that ascorbic acid did not inhibit the response by competition. Viability studies of cells in culture showed that concentrations of ascorbic acid and dehydroascorbic acid, which consistently inhibited mitogenic stimulation of lymphocytes, were noncytotoxic throughout the culture period. Timed addition of ascorbic acid to PHA-stimulated lymphocytes in culture demonstrated inhibition of [3H]TdR incorporation when ascorbic acid was added as late as 96 hours after initiation of culture. However, the greatest inhibitory effect was observed when ascorbic acid was added at initiation or early in culture. Inhibition was also evident when RNA and protein synthesis were determined. The results suggest that physiologic and high concentrations of ascorbic and dehydroascorbic acid affect early metabolic events in the process of mitogen-stimulated lymphocyte activation.

Ascorbic Acid↗
PubMed1980

T lymphocytes in colostrum and peripheral blood differ in their capacity to form thermostable E-rosettes.

The cellular population of human breast milk collected within 5 days postpartum consists primarily of lipid laden polymorphonuclear leukocytes and macrophages, whereas lymphocytes comprise < 10% of the total cells. A discontinuous density gradient technique was developed to obtain highly enriched (75 +/- 6%) fractions of milk lymphocytes. The majority of milk lymphocytes are T cells as determined by their capacity to form rosettes at 4 degrees C with sheep erythrocytes (E). The lymphocytic origin of the rosetted cells was confirmed by morphologic evaluation of Wright-Giemsa-stained cytocentrifuge slides. A novel finding is that a large proportion of milk T lymphocytes form E-rosettes at 37 degrees C as well as at 4 degrees C. The capacity to form thermostable E-rosettes is not a general property of T lymphocytes in the postpartum period, since peripheral blood T lymphocytes from milk donors form few thermostable E-rosettes. In addition, peripheral blood lymphocytes did not acquire the capacity to form thermostable E-rosettes after density gradient centrifugation nor after incubation with autologous milk. The finding that T lymphocytes in milk form thermostable E-rosettes suggests that milk T lymphocytes may be activated or immature. In either case, these data support the concept that lymphocytes that home to the mammary gland are a select subset of the total lymphocyte population.

Cell Separation↗