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PubMed1993

The behavioral treatment of self-starvation and severe self-injury in a patient with borderline personality disorder.

The successful treatment by behavioral methods of self-starvation and self-injury in a 35-year-old psychiatric in-patient, with a diagnosis of borderline personality disorder, is described. An individualized program using positive and negative reinforcers to increase food and fluid intake was used, while a token economy therapeutic milieu with time out was used to decrease acts of self-injury and aggression. Progress in treatment generalized to a non-secure treatment environment, and was maintained at an 8-month follow-up. The study illustrates the differential response of active and passive self injurious behaviors to group-based and individual treatments, respectively.

Adult↗
PubMed1986

Regulation of carnitine palmitoyltransferase activity in the liver and brown adipose tissue in the newborn rat: effect of starvation and hypothermia.

The overt activity of hepatic carnitine palmitoyltransferase (CPT1) increased during the last day of gestation in the foetus and after prolonged starvation in the newborn kept at 37 degrees C. Its sensitivity to inhibition by malonyl-CoA decreased during the perinatal period studied. Brown fat CPT1 increased under the same experimental conditions. However, its sensitivity to malonyl-CoA remains unchanged. Hypothermia at 24 degrees C decreased in the liver and increased in brown adipose tissue CPT1 activity in response to fasting. Glucose injection at birth decreased CPT1 activity in the liver but did not have any effect in the presence of mannoheptulose. This effect of glucose was non-significant in brown adipose tissue.

Acyltransferases↗
PubMed1989

Effect of diabetes and starvation on the activity of rat liver epoxide hydrolases, glutathione S-transferases and peroxisomal beta-oxidation.

The activities of peroxisomal beta-oxidation, cytosolic and microsomal epoxide hydrolase as well as soluble glutathione S-transferases have been determined in the livers of alloxan- and streptozotocin-diabetic male Fischer-344 rats. Five, seven and ten days after initiation of diabetes serum glucose levels were elevated 3.6-, 5.7- to 6.2- and 6-fold, while the activities of peroxisomal beta-oxidation and cytosolic epoxide hydrolase were elevated 1.5- and 2.5-fold, 1.4- and 2.7-fold and 1.3- and 2.0-fold, respectively. The activities of microsomal epoxide hydrolase and glutathione S-transferases were reduced to about 71% and 80% of controls. Application of 10 I.U./kg depot insulin twice a day for 10 consecutive days to alloxan-diabetic individuals approximately restored the initial glucose levels and enzyme activities except for peroxisomal beta-oxidation. Starvation of Fischer-344 rats for 48 hours and 5 days similarly resulted in a 1.3-fold to 2.1-fold and 1.2- to 1.6-fold increase in peroxisomal beta-oxidation and cytosolic epoxide hydrolase activity, respectively. Microsomal epoxide hydrolase was significantly decreased to 57% and 61% of control activity whereas glutathione S-transferase was only marginally reduced to 91% and 92%. Except for glutathione S-transferases initial enzyme activities were restored upon refeeding within 10 days. These results are similar to those obtained upon feeding of hypolipidemic compounds with peroxisome proliferating activity, and may indicate that high levels of free fatty acids or their metabolites which are known to accumulate in liver in both metabolic states may act as endogenous peroxisome proliferators.

Animals↗
PubMed1988

Depression as a correlate of starvation in patients with eating disorders.

The relationship between depressive symptoms and starvation, reflected by body weight and biochemical parameters, was investigated in 64 patients fulfilling DSM-III criteria for anorexia nervosa or bulimia. Multiple regression analysis revealed significant effects of body weight and beta-hydroxybutyric acid, respectively, on such specific depressive symptoms as depressed or dysphoric mood when controlling for severity of psychopathology of the eating disorder.

3-Hydroxybutyric Acid↗
PubMed1988

Hypothalamus, frontal cortex and lymphocyte beta 2-adrenergic receptors in acute and chronic starvation in rat.

Hypothalamus and frontal cortex beta-adrenergic receptors, as measured by [125I]cyanopindolol binding, were investigated in male rats both after 4 days of acute starvation and after 2 weeks of semistarvation with dietary manipulation. Moreover, to test whether lymphocyte beta 2-adrenergic receptors can be used as a marker for brain beta-receptors, the parallel measurement of beta-adrenoceptors of lymphocyte, hypothalamus and frontal cortex was carried out in acutely starved rats. T3 and corticosterone in rat serum were also determined in this study. Our experiments showed that beta-adrenergic receptors in hypothalamus and frontal cortex, as well as those in lymphocytes remain unaltered in rats starved acutely for 4 days when compared with controls, despite reduced T3 and increased corticosterone levels. Chronic semistarvation on either a protein-rich or a carbohydrate-rich diet also resulted in decreased T3, increased corticosterone and no alterations of beta-adrenergic receptors in hypothalamus and frontal cortex.

Acute Disease↗
PubMed1987

Methionine is a regulator of starvation-induced proteolysis in Tetrahymena.

The ciliate Tetrahymena thermophila responds to starvation by drastically increasing the rate of proteolysis. The response was reversed by resuspending the cells in a defined growth medium. Among the components of this medium only amino acids were active in inhibiting proteolysis. One amino acid, methionine, accounted for at least 75% of the effect of the complete medium, strongly indicating that in Tetrahymena methionine is the main regulator of step-down proteolysis, a process generally connected with autophagy in eukaryotic cells. The fact that one amino acid has such a drastic effect should make the system well suited for further investigations of the regulation of this process.

Amino Acids↗
PubMed1985

Effects of cold adaptation and starvation on sciatic nerve fibers in the frog.

The conditions under which frogs are kept prior to experimentation were found to have a measurable effect on peripheral nerve structure. Frogs kept for 12 weeks at 4 degree C had markedly shrunken sciatic nerve fibers compared with frogs kept at 19 degrees C. Intermediate fiber shrinkage was found for frogs kept at 19 degrees C without feeding. Counts of neurofilaments and microtubules showed that fiber shrinkage was from a preferential loss of filaments, indicating cold- or starvation-induced atrophy of the axon's cyto-skeleton. This effect, however, was superimposed with additional osmotic axonal shrinkage, causing filament densities to increase per area. There were no changes in myelin sheath thickness due to cold adaptation or fasting.

Adaptation, Physiological↗
PubMed1983

Effect of starvation on the N-acetylglutamate system of rat liver.

Rats fasted for 3 and 6 days showed an increase in the activity, per g of liver but not per total liver, of the mitochondrial urea cycle enzymes, carbamylphosphate synthetase and ornithine transcarbamylase. The activity of N-acetylglutamate synthetase, both per g and per total liver, increased by the third day and then decreased on the sixth day of fasting. The cytosolic enzyme N-acetyldeacylase showed the same general pattern as the N-acetylglutamate synthetase except that the relative proportion of synthetase over deacylase was higher at the third day of starvation. The N-acetylglutamate level/g liver increases in relation to the number of days of fasting.

Acetyltransferases↗
PubMed1988

Starvation or diabetes decreases the content but not the mRNA of 6-phosphofructo-2-kinase in rat liver.

In rat liver, the activity of 6-phosphofructo-2-kinase (PFK-2) decreases upon starvation and in diabetes. Cyclic AMP-dependent phosphorylation of the enzyme is not sufficient to account for this decrease. PFK-2 content was therefore measured by immunotitration and relative PFK-2 mRNA levels were determined by hybridization with cDNA probes. The data are compatible with a posttranscriptional mechanism of regulation that involves decreased translational efficiency of PFK-2 mRNA and (or) increased turnover of the PFK-2 protein.

Animals↗
PubMed1992

Modulation of rat liver peroxisomal and microsomal fatty acid oxidation by starvation.

In this work the microsomal lauric acid omega-hydroxylation, fatty acid peroxisomal beta-oxidation, and the levels of cytochrome P-450 IVA1 were studied in liver tissue from starved rats. Starvation increased the peroxisomal beta-oxidation and the microsomal hydroxylation of fatty acids. The correlation between these activities would support the proposal that both processes are linked, contributing in part to catabolism of fatty acids in liver of starved rats.

Animals↗
PubMed1993

Starvation effect on rat kidney peroxisomal and microsomal fatty acid oxidation. A comparative study between liver and kidney.

Microsomal lauric acid 12-hydroxy lauric acid (omega)-hydroxylation and fatty acid peroxisomal beta-oxidation were studied in kidney tissue from starved rats. Starvation increased the microsomal omega-hydroxylation and peroxisomal beta-oxidation of fatty acids with a high correlation between both processes. Earlier, we reported similar results in liver. Our results support the hypothesis that the role of microsomal fatty acids omega-hydroxylation is the generation of substrate for peroxisomal beta-oxidation, with the final purpose of contributing to a catabolic or gluconeogenic pathway from fatty acids.

Animals↗
PubMed1996

Induction of glyoxylate cycle enzymes in rat liver upon food starvation.

The key enzymes of the glyoxylate cycle, isocitrate lyase and malate synthase, have been detected in liver of food-starved rats. Activities became measurable 3 days and peaked 5 days after the beginning of starvation. Both enzymes were found in the peroxisomal cell fraction after organelle fractionation by isopycnic centrifugation. Isocitrate lyase was purified 112-fold by ammonium sulfate precipitation, and chromotography on DEAE-cellulose and Toyopearl HW-65. The specific activity of the purified enzyme was 9.0 units per mg protein. The K(m)(isocitrate) was 68 microM and the pH optimum was at pH 7.4. Malate synthase was enriched 4-fold by ammonium sulfate precipitation. The enzyme had a K(m)(acetyl-CoA) of 0.2 microM, a K(m)(glyoxylate) of 3 mM and a pH optimum of 7.6.

Animals↗
PubMed1986

Thyroxine 5'-monodeiodinase activity in hepatocytes of rainbow trout, Salmo gairdneri: distribution, effects of starvation, and exogenous inhibitors.

L-Thyroxine (T4) 5'-monodeiodinase activity (MDA) of hepatocyte cell fractions of rainbow trout was evaluated by 125I- generation following incubation with [125I-3' or 125I-5']T4 at 12 degrees. Produced in approximately equal proportions, 3,5,[125I-3'] triiodo-L-thyronine and 125I- were the sole labeled products detected by gel permeation on G-25 Sephadex columns, confirming restriction of T4 deiodination in trout to removal of a single outer-ring iodine atom. T3 underwent no significant outer-ring deiodination. MDA activity, located mainly in the microsome fraction, was optimal at a pH of approximately 7.0 and was enhanced by dithiothreitol but not by reduced glutathione. Azide, thiocyanate, thiourea, and KCl exerted no significant influence on MDA, but MDA was inhibited by: 8-anilino-1-naphthalene sulfonic acid greater than N-ethyl maleimide greater than propylthiouracil greater than sodium salicylate greater than KI. Starvation for 2 weeks depressed MDA to 46% of the level of trout fed 1% of body wt once per day. This was due to a decreased Vmax of MDA. In conclusion, trout hepatic microsomal MDA is acutely and chronically susceptible to both exogenous and endogenous factors; as an enzyme responsible for extrathyroidal T3 generation, it may exert a key role in regulating peripheral thyroidal status under both natural and experimental conditions.

Animals↗
PubMed1984

Effects of anesthetics and starvation on in vivo gluconeogenesis in virgin and pregnant rats.

To study in vivo gluconeogenesis, female virgin rats were injected intravenously with 14C-alanine (ul) and the production of 14C-glucose was determined at two, five, or ten minutes thereafter. At ten minutes the appearance of 14C-glycogen in the liver was also determined. The intraperitoneal injection of sodium pentobarbital (Nembutal) (33 mg/kg body weight) 30 minutes prior the tracer did not affect the rate of gluconeogenesis in fed rats compared with unanesthetized animals, whereas in rats fasted 24 hours it produced a significant enhancement in all parameters studied. A similar effect in enhancing in vivo gluconeogenesis was observed with both pentobarbital or ether anesthesia when 3-14C-pyruvate was used as tracer in virgin rats fasted 24 hours. In contrast to the effect in virgin animals, pentobarbital anesthesia did not modify in vivo gluconeogenesis in either fed or 24-hour fasted 21-day pregnant rats. Ether anesthesia, however, caused an enhancement in 14C-glucose production from 3-14C-pyruvate in 24-hour fasted pregnant rats. On the basis of reported changes in sympathoadrenal activity produced by starvation and pregnancy, present results indicate that the enhancing effects of anesthetics on gluconeogenesis result from their capacity to stimulate adrenal medulla cathecholamine release or tissue sympathetic activity. Our findings also demonstrate that in an investigation of metabolic parameters it cannot be assumed that effects of anesthetics are always of the same degree and direction since they vary with the condition of the experimental subject.

Anesthetics↗
PubMed1984

Potentiation of 14C-glucose oxidation by priming glucose loads: effect of starvation.

The mechanism of the Staub-Traugott effect or facilitated glucose disposal after successive glucose loads has remained elusive. In earlier publications, we have shown it can be independent of circulating hormone and free fatty acid levels. We have also proposed that it might partially depend on the rapid induction of glycolytic pathways, which are known to be depressed by prolonged fast. Mature rats were given 1.75 gm/kg glucose doses intravenously at 60-minute intervals. Respiratory CO2 was collected at 15-minute intervals over a 120-minute period following administration of the carrier glucose plus 6 microCi/100 gm rat weight of 14C-D-glucose, given either as the first, second, or third challenge. In rats fasted 14 hours there was potentiation of labeled CO2 recovered after each successive load. After three days of starvation, both relative 14C-glucose oxidation to 14CO2 as well as absolute 14CO2 increments after each load were lower. The changes in relative oxidation of an intravenous glucose load might partly account for the facilitated disposal of blood glucose seen in the second and third hours in overnight-fasted rats (Staub-Traugott effect). However, although rats fasted for three days had suppressed the Staub effect, the increments in oxidation were attenuated but still present, suggesting that alterations of other pathways must participate in the disappearance of this effect after fasting.

Animals↗
PubMed1989

Protein and amino acid metabolism during early starvation as reflected by excretion of urea and methylhistidines.

Endogenous excretion of nitrogenous products was studied during early starvation in six healthy, nonobese subjects after six days on a well-defined diet, designed to achieve net protein balance and an adequate calorie supply. The diet contained 0.5 g myofibrillar-free protein and 35 kcal/kg body weight. The subjects then fasted for three days. Urine was collected for 24-hour periods and analyzed for urea, ammonia, 3-methylhistidine, and 1-methylhistidine. Blood glucose and serum urea levels were measured daily. In a second group of subjects, muscle biopsies for determination of free amino acid concentrations were taken in the overnight fasted state and after three days of fasting. During the period with a balanced diet, urea production fell initially and stabilized after two to three days at a level of 146 +/- 15 mmol/24 h. During the period of fasting, serum urea increased from 3.0 +/- 0.4 to a maximum value of 6.2 +/- 0.7 mmol/L and urea production rose markedly, to a peak of 293 +/- 16 mmol/24 h. Ammonia excretion was 24 +/- 2 mmol/24 h before and 71 +/- 13 mmol/24 h after three days of fasting. 3-Methylhistidine excretion was stable before fasting and then rose from 154 +/- 17 to 198 +/- 17 mumol/24 h. 1-Methylhistidine excretion was unchanged during fasting. Blood glucose levels were stable at 4.8 +/- 0.2 mmol/L before fasting and then fell to 3.7 +/- 0.3 mmol/L. Intracellular concentrations of amino acids in skeletal muscle decreased markedly during fasting; after three days of fasting the glutamine concentration had fallen by 34%.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Decreased glucose oxidation during short-term starvation.

Prolonged fasting (for days or weeks) decreases glucose production and oxidation. The effects of short-term starvation (ie, less than 24 hours) on glucose metabolism are not known. To evaluate this issue, glucose oxidation and glucose turnover were measured after 16-hour and subsequently after 22-hour fasting. Glucose oxidation was calculated by indirect calorimetry in 12 healthy men (age 22 to 44 years); glucose turnover was measured by primed, continuous infusion of 3-3H-glucose in eight of these 12 volunteers. After 16-hour fasting net glucose oxidation was 0.59 +/- 0.17 mg x kg-1 x min-1 and glucose tissue uptake 2.34 +/- 0.12 mg x kg-1 x min-1. No correlation was found between net glucose oxidation and glucose tissue uptake. Prolonging fasting with an additional 6 hours resulted in decreases of respiratory quotient (0.77 +/- 0.01 v 0.72 +/- 0.01) (P less than .005), plasma glucose concentration (4.7 +/- 0.1 v 4.6 +/- 0.1 mmol/L) (P less than .05), glucose tissue uptake (2.10 +/- 0.12 mg x kg-1 x min-1) (P less than .05), net glucose oxidation (0.09 +/- 0.04 mg x kg-1 x min-1) (P less than .005), and plasma insulin concentration (8 +/- 1 v6 +/- 1 mU/L) (P less than .005). Net glucose oxidation expressed as a percentage of glucose tissue uptake decreased from 22% +/- 8% to 2% +/- 1% (P less than .05). There was no net glucose oxidation in seven of 12 controls after 22-hour fasting.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Tissue-related changes in insulin receptor number and autophosphorylation induced by starvation and diabetes in rats.

Insulin action is subject to regulation at the level of the insulin receptor and at postreceptor levels. Starvation and diabetes are often associated with insulin resistance for glucose metabolism in various tissues. In muscle, fat, and liver, we examined whether changes in the functionality of the insulin receptor correlated with changes in insulin action in the starved and diabetic state. Insulin-stimulated receptor autophosphorylation reflects an early physiologic step in transmission of the insulin signal, and for that reason, changes in autophosphorylation activity of the insulin receptor were used as a marker to determine the functionality of the insulin receptor. Glycoprotein fractions prepared from skeletal muscle, diaphragm, epididymal fat, and liver of control, 3-day starved, short-term 3-day (S) diabetic (streptozotocin, 70 mg/kg intravenously), and long-term 6-month (L) diabetic (neonatal streptozotocin 100 micrograms/g intraperitoneally) rats were used in this study. Receptor activity was monitored by measuring insulin-stimulated [gamma-32P]adenosine triphosphate (ATP) receptor autophosphorylation. In addition, to obtain information about whether changes in receptor autophosphorylation are related to changes in receptor number, relative numbers of high-affinity insulin receptors were determined by affinity cross-linking of [125I]insulin to the receptor alpha-chain and quantitation of the yield of labeled receptor alpha-chain. Control, starved, S diabetic, and L diabetic rats had plasma insulin and glucose levels of 294 +/- 42, 90 +/- 24, 48 +/- 12, and 216 +/- 30 pmol/L and 6.7 +/- 0.2, 4.1 +/- 0.2, 23.3 +/- 0.7, and 21.6 +/- 2.9 mmol/L, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue↗