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PubMed1996

In vivo amino acid metabolism of gut and liver during short and prolonged starvation.

During starvation, splanchnic organs are proportionally more affected by protein loss than other organs. Amino acid membrane transport is one of the regulating mechanisms of protein turnover, but until now in vivo data were lacking. To study in vivo phenylalanine and tyrosine membrane transport and protein turnover in splanchnic organs, a primed continuous infusion of L-[2,6-3H]phenylalanine was given to control rats (postabsorptive) and after short (40 h) and prolonged (112 h) starvation. Data were analyzed using a three-compartment model previously used in muscle membrane transport studies. Inward and outward amino acid plasma-tissue membrane transport rates in both the liver and gut were upregulated after prolonged starvation. Metabolic shunting of phenylalanine and tyrosine increased in the gut but decreased to zero in the liver after prolonged starvation. In conjunction with this, gut and liver protein turnover increased after prolonged starvation. In the liver the net uptake of gluconeogenic precursors also increased, indicative for increased gluconeogenesis. The observed changes in amino acid metabolism in both splanchnic organs after prolonged starvation may reflect an adaptation of the gut and liver to nutritional deprivation and could be of benefit during refeeding.

Acute Disease↗
PubMed1984

The actions of prostaglandin E2, naloxone and testosterone on starvation-induced suppression of luteinizing hormone-releasing hormone and luteinizing-hormone secretion. In vitro and in vivo studies.

In man and other mammals, starvation is accompanied by a severe suppression of luteinizing hormone-releasing hormone (LHRH) and luteinizing-hormone (LH) secretion, which is caused by unknown alterations in hypothalamic functions. Prostaglandin E2 (PGE2), endorphins and testosterone (T) are know to be strongly involved in the regulation of LHRH release. The present study examined whether the influence of these substances on LHRH and LH secretion was affected by starvation. In vitro experiments checked the release of PGE2 and LHRH from median eminences (ME) of fed male rats and ones starved for 5 days. Stimulation with potassium (80 mM) induced an equally strong release of PGE2 and LHRH from the MEs of both fed and starved rats. When PGE2 (10(4) M) was added to the superfusion medium, the potassium-stimulated release of LHRH was significantly enhanced in both groups of animals. The results clearly showed that in the terminal region of the hypothalamic LHRH system the release of this hormone and the action of PGE2 were not altered by starvation. In vivo experiments tested whether the effects of LHRH, PGE2, naloxone (NAL), or T on LH secretion were different in intact or castrated male rats fed or starved for 3 and 5 days. LHRH (250 ng/kg) stimulated the same amount of LH secretion in fed and starved rats. The starvation-induced LH suppression was not due to a dysfunction at the pituitary level. The stimulatory action of PGE2 (1 mg/kg) on LH was gradually reduced throughout the starvation period. NAL (5 mg/kg) had little, respectively, no effect on LH release on the 3rd or 5th day of starvation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1969

Amino acid metabolism during prolonged starvation.

Plasma concentration, splanchnic and renal exchange, and urinary excretion of 20 amino acids were studied in obese subjects during prolonged (5-6 wk) starvation. Splanchnic amino acid uptake was also investigated in postabsorptive and briefly (36-48 hr) fasted subjects.A transient increase in plasma valine, leucine, isoleucine, methionine, and alpha-aminobutyrate was noted during the 1st wk of starvation. A delayed, progressive increase in glycine, threonine, and serine occurred after the 1st 5 days. 13 of the amino acids ultimately decreased in starvation, but the magnitude of this diminution was greatest for alanine which decreased most rapidly during the 1st week of fasting. In all subjects alanine was extracted by the splanchnic circulation to a greater extent than all other amino acids combined. Brief fasting resulted in an increased arterio-hepatic venous difference for alanine due to increased fractional extraction. After 5-6 wk of starvation, a marked falloff in splanchnic alanine uptake was attributable to the decreased arterial concentration. Prolonged fasting resulted in increased glycine utilization by the kidney and in net renal uptake of alanine. It is concluded that the marked decrease in plasma alanine is due to augmented and preferential splanchnic utilization of this amino acid in early starvation resulting in substrate depletion. Maintenance of the hypoalaninemia ultimately serves to diminish splanchnic uptake of this key glycogenic amino acid and is thus an important component of the regulatory mechanism whereby hepatic gluconeogenesis is diminished and protein catabolism is minimized in prolonged fasting. The altered renal extraction of glycine and alanine is not due to increased urinary excretion but may be secondary to the increased rate of renal gluconeogenesis observed in prolonged starvation.

Adolescent↗
PubMed2006

Sequence of Atlantic cod (Gadus morhua) GLUT4, GLUT2 and GPDH: Developmental stage expression, tissue expression and relationship to starvation-induced changes in blood glucose.

cDNAs of putative glucose transporters, GLUT4 and GLUT2, were cloned from Atlantic cod (Gadus morhua). The GLUT4 cDNA encodes a 503 amino acid and the GLUT2 cDNA a 506 amino acid protein. Phylogenetic analysis, amino acid sequence alignment, and tissue distribution support categorizing them as homologues of mammalian GLUT4 and 2. GLUT4 clusters with GLUT4s from fish and other vertebrates. It shows 84% amino acid identity to GLUT4 from coho salmon and brown trout and 65% identity with other vertebrates. It is most highly expressed in heart, strongly expressed in red and white skeletal muscle and present at lower levels in gill, gonad, intestine, and kidney. GLUT2 clusters with GLUT2 from rainbow trout and other vertebrates. It shows 75% amino acid identity with rainbow trout and 62% identity with chicken GLUT2. In Atlantic cod, GLUT2 is most highly expressed in liver with lower levels noted in intestine and kidney. Food deprivation for 2 months was used as a vehicle to monitor GLUT expression at different blood glucose levels. Starvation resulted in a decrease in blood glucose and liver glycogen that recovered following 20 days of re-feeding. GLUT4 expression in heart was decreased with starvation and increased with re-feeding. GLUT4 mRNA level in heart correlated with blood glucose. It is suggested that this relationship is related to insulin responsiveness. GLUT4 expression in white muscle increased with starvation and decreased with re-feeding. It is proposed that this is due to the necessity to maintain high levels of the glucose transporter protein in the face of starvation-associated proteolysis. GLUT2 expression in liver correlated with blood glucose, consistent with higher rates of glucose transport from liver to blood in the fed state than in the food-deprived state. Glycerol-3-phosphate dehydrogenase (GPDH) cDNA was also cloned. It encodes a 351 amino acid protein, which is 73-90% identical to GPDH from numerous other fish species. GPDH is ubiquitously expressed. Expression in heart decreased with starvation and increased with refeeding, whereas expression in liver did not change with starvation. In other studies, gene expression was monitored at nine time points from fertilization of eggs to larval development. GLUT4 is detectable in fertilized eggs and is fully expressed by the halfway to hatching point. GLUT2 is not evident at fertilization, is detectable at halfway to hatching, and fully expressed at hatching. GPDH expression was evident from fertilization.

Amino Acid Sequence↗
PubMed2002

Effects of starvation on gonadotropin and thyrotropin subunit mRNA levels and plasma hormone levels in the male Japanese quail (Coturnix coturnix japonica).

Contents of mRNAs encoding LHbeta-, FSHbeta-, TSHbeta- and common a-subunit precursor molecules were measured in male Japanese quail deprived of food for three days. Plasma LH, FSH, thyroxine and triiodothyronine levels were also measured in the same birds. Plasma LH levels declined during the period of food deprivation. Levels in starved birds were not different from those in control birds after one day of starvation but were significantly lower after three days. Plasma FSH levels showed a similar decline, although the changes were not significant. Plasma thyroxine levels did not decrease during starvation, whilst plasma triiodothyronine levels decreased drastically and significantly soon after the start of starvation. All the hormone subunit mRNA contents in starved birds also decreased, with differences from control birds significant 3 days after the start of starvation. Plasma FSH levels showed a strong positive correlation with pituitary FSHbeta mRNA levels, while plasma LH levels had a strong positive correlation with common a mRNA levels and practically no correlation or even a negative correlation with LHbeta mRNA levels. These results suggest that starvation suppresses not only gonadotropin and thyrotropin secretion but also their synthesis in the pituitary gland. Furthermore, these results showed that FSH and LH have different synthesis and secretion dynamics in the Japanese quail. Contradicting results with TSHbeta mRNA and thyroid hormones lead us to assume that starvation affects thyroid hormone metabolism in peripheral tissue, presumably in the liver.

Animals↗
PubMed2002

Effects of starvation and refeeding on gonadotropin and thyrotropin subunit mRNAs in male Japanese quail.

The contents of mRNAs encoding LH beta-, FSH beta-, TSH beta- and common alpha-subunit precursor molecules were measured in food-deprived and subsequently re-fed male Japanese quail. Pituitary LH beta, FSH beta and common alpha mRNA levels were decreased by starvation, and increased to the control levels by re-feeding. The rates of decreases of LH beta and common alpha mRNA levels were greater the corresponding rate for FSH beta levels. Pituitary TSH beta mRNA levels were not decreased by starvation, but increased transitorily by re-feeding. Plasma LH and triiodothyronine levels were decreased by starvation, and then increased to control levels by re-feeding, while plasma FSH and thyroxine levels did not show significant changes. Plasma LH and FSH levels showed positive correlations with pituitary common alpha and FSH beta mRNA levels, respectively, while plasma thyroxine levels showed a negative correlation with TSH beta mRNA levels. Hepatic weight was decreased slightly but significantly by starvation, and then showed a remarkable rebound after re-feeding was started. These results suggest that LH synthesis and secretion are more sensitive to starvation than FSH synthesis and secretion in Japanese quail, and that LH production recovered to initial levels within several days when birds were fully fed. Also, there is a possibility that the synthesis of TSH is accelerated transitorily by re-feeding. Furthermore, these results showed that there are different relationships between the plasma levels of LH, FSH, and TSH and the various hormone subunit mRNA levels. The remarkable change in hepatic weight leads us to assume that hepatic thyroid hormone metabolism is affected by starvation and re-feeding.

Animals↗
PubMed2004

Muscle-type specific intramyocellular and hepatic lipid metabolism during starvation in wistar rats.

The physiological dynamics of intramyocellular lipids (IMCLs) in different muscle types and of hepatocellular lipids (HepCLs) are still uncertain. The dynamics of IMCLs in the soleus, tibialis anterior, and extensor digitorum longus (EDL) muscles and HepCL during fed, 12- to 72-h starved, and refed conditions were measured in vivo by (1)H-magnetic resonance spectroscopy (MRS) in Wistar rats. Despite significant elevations of free fatty acids (FFAs) during starvation, HepCLs and IMCLs in soleus remained constant. In tibialis anterior and EDL, however, IMCLs increased significantly by 170 and 450% after 72 h of starvation, respectively. After refeeding, elevated IMCLs dropped immediately in both muscles. Total muscle long-chain acyl-CoAs (LCACoAs) remained constant during the study period. Hepatic palmitoleoyl-CoA (C16:1) decreased significantly during starvation while total hepatic LCACoAs increased significantly. Consistent with constant values for FFAs, HepCLs, IMCLs, and muscle LCACoAs from 12-72 h of starvation, insulin sensitivity did not change. We conclude that during starvation-induced adipocytic lipolysis, oxidative muscles dispose elevated FFAs by oxidation, while nonoxidative ones neutralize FFAs by reesterification. Both mechanisms might prevent impairment of insulin signaling by maintaining low levels of LCACoAs. Hepatic palmitoleoyl-CoA might have a special role in lipid metabolism due to its unique dynamic profile during starvation.

Animals↗
PubMed1991

Effects of refeeding subsequent to starvation on the plasma cell population in the villous lamina propria of the rat small intestine.

The effects of refeeding subsequent to starvation on the plasma cell population in the lamina propria of the small intestinal villi were studied in adult rats utilizing the immunohistochemical method to detect IgA, IgM and IgG. Under normal conditions of stimulation, intestinal plasma cells (IPC) occur only as a sparse population. However, the present study demonstrated that extensive hyperplasia of IPC could be induced by refeeding after starvation. Starvation for a period of 4 to 6 days alone produced only a small change in the IPC population. In contrast, refeeding subsequent to starvation (for 4 to 6 days) was accompanied by a large increase in the population of IPC: the proportions of these cells among the lamina propria cells often rose to more than 50% within 3 or 6 days. The large majority of the proliferating IPC were found to express IgA, whereas cells bearing IgM or IgG occurred in extremely small numbers in the lamina propria. The mechanism whereby extensive IPC hyperplasia can occur in response to refeeding after starvation is discussed in relation to the possible promotion of transmission of antigenic macromolecules across the mucosal barrier induced by this procedure. It is also suggested that the origin of the proliferating IPC may be correlated with the B cell precursors in the germinal centers of the Peyer's, patches, which are more resistant to starvation than other lymphoid cells.

Animals↗
PubMed1989

Mobilization of copper among tissues in the estuarine crab Scylla serrata (Forskal) under imposed starvation.

The quantitative changes in copper free and bound to proteins in haemolymph and different forms of copper in muscle and hepatopancreas under imposed starvation were studied in the estuarine mud crab Scylla serrata. During the course of starvation, both haemolymph copper free and bound to proteins significantly declined and the regression analyses of these data further revealed that the haemolymph copper-free proteins were more affected than copper-bound proteins. The multiple stress condition namely injury and exsanguination along with starvation resulted in an earlier release and/or degradation of both these proteins. Hepatopancreas periodically accumulates and releases copper during starvation. The copper levels in haemolymph and hepatopancreas during different days of starvation showed a close inverse relationship between these two tissues. These changes in hepatopancreas were predominantly reflected in the copper that exists in association with low molecular weight substances. It is found that the copper thus accumulated was partly released back into haemolymph and a fraction may be excreted. This study also indicates the major role played by the low molecular weight substances in accommodation, detoxification and mobilization of copper in the decapod hepatopancreas during imposed starvation.

Animals↗
PubMed1986

Age and thyroid hormone as factors in the responses of BHE rats to starvation-refeeding.

The interacting effects of thyroid hormone, age, and duration of starvation on the enzyme and liver lipid responses of BHE rats to starvation-refeeding were studied. Rats were starved for 2, 4, or 7 days and refed a 65% glucose diet for 2 days. The rats were either 150 or 420 days of age and injected daily with either saline or 10 micrograms thyroxine/100 g body weight. Neither age nor duration of starvation affected the glucose-6-phosphate dehydrogenase or malic enzyme activity or liver lipid response to starvation-refeeding. However, thyroxine treatment potentiated the response to starvation-refeeding in the 420-day-old rats when the duration of starvation increased from 2 to 7 days.

Age Factors↗
PubMed1999

Effects of pyridostigmine and naloxone on the abnormal TSH response to TRH during starvation in humans.

BACKGROUND: Starvation is associated with a blunted TSH response to thyrotropin-releasing hormone (TRH) (peak minus baseline < 5 mIU/L), despite basal TSH and thyroid hormone levels within the normal range. In light of the inhibitory effect of somatostatin on TSH secretion, we examined whether this condition is caused by an increased hypothalamic somatostatinergic tone in starving subjects. The possible involvement of endogenous opioids in the mechanism underlying the abnormal TSH response to TRH was also evaluated. METHODS: The TSH response to TRH (25 micrograms in an intravenous bolus), serum total and free T4 and T3 levels, and 24-hour urinary-free cortisol levels were measured in 28 normal men (age 27-35 years) within 10% of their ideal body weight. They were randomly divided into 4 groups of 7. In 21 subjects (groups 1, 2, and 3), TRH tests were performed after an overnight (8 hours) fast, placebo administrations (control test), and after prolonged (56 hours) starvation. TRH tests after prolonged starvation were performed either after placebos (in all subjects) or the administration of pyridostigmine (180 mg orally) (in 7 subjects, group 1); naloxone (0.8 mg in an i.v. bolus injection) (in 7 subjects, group 2); or the combination of pyridostigmine and naloxone (in 7 subjects, group 3). The remaining 7 subjects (group 4) were tested at weekly intervals with TRH plus placebo, TRH plus naloxone, TRH plus pyridostigmine, and TRH plus naloxone plus pyridostigmine after a fasting period of 8 hours. RESULTS: In all subjects of groups 1, 2, and 3, TRH-induced TSH rise was significantly lower after prolonged starvation than after overnight fast. Neither pyridostigmine nor naloxone, given alone, changed the basal levels of TSH and the TSH response to TRH after prolonged starvation. In contrast, the concomitant administration of naloxone and pyridostigmine significantly enhanced the TRH-induced TSH rise. After overnight fasting, naloxone administration in group 4 subjects did not change the TSH response to TRH, whereas pyridostigmine significantly enhanced the TSH response to TRH. When naloxone was given together with pyridostigmine and TRH the TSH response was similar to that observed in the TRH plus pyridostigmine test. CONCLUSIONS: These data indicate that naloxone-sensitive endogenous opioids exert an inhibitory effect on the cholinergic stimulatory control of TSH secretion during prolonged starvation. This suggests that an enhanced hypothalamic somatostatinergic activity is involved in the mechanism underlying the reduced TSH response to TRH.

Adult↗
PubMed2001

Lack of cytochrome P450 2E1 (CYP2E1) induction in the rat liver by starvation without coprophagy.

Starvation potentiates the hepatotoxicity of a variety of small molecules, including chlorinated hydrocarbons and nitrosamines, through the induction of CYP2E1. A change in CYP2E1 expression during starvation may also alter the pharmacokinetic profiles of xenobiotics. Northern blot and Western blot analyses revealed that hepatic CYP2E1 was not induced during starvation in rats placed in metabolic or wire-bottom cages in contrast to the induction of CYP2E1 in animals housed in solid-bottom cages. We studied the effect of coprophagy on the expression of hepatic CYP2E1 during starvation. The extent of coprophagy was 24% in fed rats. Fecal matter of starving rats was reduced to 14% of control and starving rats re-ingested ~1.6 g of feces per day. The effect of fecal matter on CYP2E1 expression (i.e., 1.6 g/kg/day for 3 days) was assessed in fed or starving rats. Starving rats gavaged with fecal matter for 3 days resulted in a 3.5-fold increase in the level of CYP2E1 mRNA, while fed rats gavaged with feces failed to show an increase in the mRNA. The increase in the CYP2E1 mRNA level accompanied the induction of CYP2E1. Starving rats gavaged with methanol extract of feces (500 mg/kg/day for 3 days) showed a 3.3-fold increase in CYP2E1 mRNA level in the liver. These results provide evidence that CYP2E1 is not induced by starvation without coprophagy, raising the contention that the mechanistic basis for CYP2E1 induction by starvation should be reevaluated.

Animals↗
PubMed1979

The gastro-entero-pancreatic hormone secretion after a mixed meal in normal subjects before and after a 72 hour period of starvation.

The responses of plasma gastro-entero-pancreatic (GEP) hormones and free fatty acids (FFA) to a standard mixed meal before and after starvation have been measured. Raised insulin, glucose and FFA levels were found following refeeding after starvation and levels of secretin and C-terminal glucagon-like-immunoreactivity (C-GLI), raised by starvation, were rapidly suppressed on refeeding. The responses of gastrin and N-terminal glucagon-like-immunoreactivity (N-GLI) to a standard mixed meal were not altered by starvation. Although this study does not directly support that secretin and glucagon are responsible for the hyperglycaemia or hyperinsulinaemia of starvation diabetes, a role for both hormones in the raised FFA levels is proposed, as well as a role for glucagon in the initial hyperglycaemic response to a meal after starvation.

Adult↗
PubMed1984

Ketone body kinetics in humans: the effects of insulin-dependent diabetes, obesity, and starvation.

The kinetics of acetoacetate (A) and beta-hydroxybutyrate (B) have been studied following the injection as a pulse or continued infusion of [3-14C]acetoacetate (A*) or [14C]beta-hydroxybutyrate (B*) into six newly diagnosed, untreated, ketotic diabetic patients, ten obese subjects in the postabsorptive state, and the ten obese subjects after 1-2 weeks starvation (50 cal per day). Employing a compartmental model of acetoacetate and beta-hydroxybutyrate kinetics developed using CONSAM for normal subjects, the rate coefficients (Lij), rates of release of newly synthesized acetoacetate and beta-hydroxybutyrate into the blood (UA, UB), and fractional removal of each compound (FCRA and FCRB) were calculated. Ketone body release into blood (UA + UB) in diabetic subjects was threefold higher than normal (mean +/- SD, 208 +/- 118 versus 81 +/- 66 mumol min-1 m-2) and in obese subjects the rate increased on starvation from 171 +/- 70 to 569 +/- 286 mumol min-1 m-2. In each case most of the increase was in beta-hydroxybutyrate. The major change in diabetes and on starvation of the obese subjects was in the rate coefficient for removal of ketone bodies. Normally 0.168 +/- 0.109 min-1, it was 0.055 +/- 0.040 min-1 in the diabetic patients and fell from 0.066 +/- 0.040 to 0.027 +/- 0.019 min-1 in the obese subjects on starvation. In normal subjects, FCRA was similar to FCRB (0.226 +/- 0.142 versus 0.188 +/- 0.124 min-1). However, in diabetics, FCRA was 0.074 +/- 0.044 and FCRB was 0.050 +/- 0.034 min-1 and both were lower than normal. On starvation of obese subjects, FCRA fell from 0.199 +/- 0.047 to 0.089 +/- 0.035 min-1, whereas FCRB fell from 0.141 +/- 0.040 to 0.033 +/- 0.012 min-1. Therefore, the removal of beta-hydroxybutyrate was impaired more than that of acetoacetate in all patients. Our results confirm previous observations that ketosis is associated with high rates of ketogenesis and a decrease in fractional clearance. In addition, we found that in diabetes, obesity, and in obese subjects following starvation, most of the increased synthesis was in beta-hydroxybutyrate and that the clearance of beta-hydroxybutyrate decreased more than that of acetoacetate.

3-Hydroxybutyric Acid↗
PubMedDate not supplied

[Effect of various periods of starvation on the character of exhibited changes of energy metabolism in the rat liver during the administration of phenobarbitol and corn oil].

Alterations in content of long-chain acyl-CoA and value of phosphate potential (PP) were studied in liver tissue after administration of phenobarbital and corn oil into rats, starved within 4 hrs and 12 hrs before the experiment. As compared with the 4 hrs period, starvation within 12 hrs caused an accumulation of acyl-CoA and a decrease in PP (ATP/ADP X Pi) in liver tissue. The same alterations in the patterns studied were found after administration of corn oil. However, the 12 hrs starvation amplified distinctly the effect of oil administration on the content of acyl-CoA and on the PP value. Phenobarbital, administered simultaneously with the oil, removed completely the effect of corn oil on the patterns studied during the both periods of starvation, but it caused only slight influence on the starvation induced alterations in acyl-CoA and PP. The data obtained suggest that within the two periods of starvation studied it has been possible to differentiate the unspecific effects of starvation and the alterations induced by specific agents.

Acyl Coenzyme A↗
PubMed1996

[Specificity and time of the appearance of His+ reversions induced by histidine starvation in Salmonella typhimurium].

It was previously established that reversion of the hisG46 allele of Salmonella typhimurium to prototrophy occurred upon histidine starvation. In this paper, it was shown that histidine starvation does not affect the appearance of mutants resistant to L-arabinose and rifampicin. Threonine starvation did not change the frequency of His+ revertants. Analysis of His+ revertant clones did not reveal additional L-arabinose resistance mutations. Thus, these experiments allowed the conclusion that amino acid starvation does not lead to a nonspecific increase in the mutation rate. In addition, it was shown that spontaneous His+ revertants start to arise after two to three hours of histidine starvation, this process lasting for four days. Nevertheless, original His+ cells did not grow in a culture generating His+ revertants. Traces of histidine and novobiocin added to a minimal medium retarded reversion realization. However, the occurrence of revertants was not markedly inhibited by chloramphenicol. Based on the results, it is assumed that adaptive His+ reversions occurred due to a special mode of replication induced upon histidine starvation and requiring no de novo protein synthesis.

Adaptation, Physiological↗
PubMed1998

Effect of starvation on organ blood flow in the senescent rat.

To investigate the amino acid requirements of the senescent rat, as part of a study directed toward nutritional support in the aged, it was necessary to determine amino acid levels in plasma and tissue, but also regional blood flow of the animals subjected to fast. Only this latter allows the determination of the amounts of each amino acid present in the tissue before starvation by extrapolation of values measured during starvation. As plasma and tissue amino acid had been previously determined, the aim of this study had been to measure regional blood flow in the liver, kidney, testis, spleen, stomach, small intestine and large intestine in senescent rats submitted to 1, 5, 9 and 15 days of starvation. Twenty-four-month-old male Wistar rats (n = 16) were divided into four groups (n = 4), and submitted to starvation for 1, 5, 9 and 15 days. Blood flow in the liver, kidney, testis, spleen, stomach, and small and large intestine was measured by injecting 0.5 ml of a microsphere solution (15 microns diameter) labelled with 57Co, 0.25 microCi/ml. Over the 15-day period studied, the response to starvation showed two distinct phases: an early effect (from day 1 to day 9) in which there were decreases in the weight of the organs and in organ blood flow, and a second phase (from day 9 to day 15) in which blood flow and organ weight were maintained. However, organ blood flow related to mass was not substantially affected by starvation. This implies that measurement of substrate plasma concentration alone can reliably reflect organ substrate flow.

Aging↗
PubMed2004

Latent membrane protein 1 of Epstein-Barr virus plays an important role in the serum starvation resistance of Epstein-Barr virus-immortalized B lymphocytes.

We have previously shown that SNU-1103, which is a latency type III Epstein-Barr virus (EBV)-transformed lymphoblastoid cell line (LCL) that was developed from a Korean cancer patient, resists serum starvation-induced G(1) arrest. In this study, we examined the role of latent membrane protein-1 (LMP-1) in serum starvation resistance, since LMP-1 is known to be essential for EBV-mediated immortalization of human B lymphocytes. The LMP-1 gene from SNU-1103 was introduced into the EBV-negative BJAB cell line, and shown to be associated with resistance to G(1) arrest during serum starvation. Western blot analyses of the LMP-1-transfected cells revealed several protein alterations as compared to vector-transfected control cells. The expression of key cell-cycle regulatory proteins was affected in the G(1) phase: the expression of cyclin D3, CDK2, p27, and E2F-4 was up-regulated, and the expression of cyclin D2, CDK6, p21, and p103 was down-regulated during serum starvation. These results imply that of the several EBV viral genes expressed in EBV-negative B lymphoma cells, LMP-1 mediates resistance to serum starvation-induced G(1) arrest. However, we cannot rule out the possibility that other EBV genes are also involved in the cell-cycle progression of the EBV-transformed LCL during serum starvation, since the altered protein expression profile of the LMP-1 transfectants was distinct from that of the SNU-1103 cells that expressed all of the EBV viral proteins.

B-Lymphocytes↗