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PubMed2006

Unphosphorylated H1 is enriched in a specific region of the promoter when CDC2 is down-regulated during starvation.

Tetrahymena thermophila macronuclear histone H1 is phosphorylated by a cdc2 kinase, and H1 phosphorylation regulates CDC2 expression by a positive feedback mechanism. In starved wild-type cells, decreased expression of the CDC2 gene is correlated with a global reduction in the phosphorylation of H1 and reduced phosphorylation of H1 in the region upstream of the CDC2 gene. To determine whether the reduced H1 phosphorylation upstream of the CDC2 gene is merely a reflection of global dephosphorylation or is due to specific targeting of dephosphorylation of H1 to the CDC2 promoter during starvation, the CDC2 promoter was mapped, and the distributions of phosphorylated and unphosphorylated H1 across the CDC2 gene were determined using chromatin immunoprecipitation. Unphosphorylated H1 is specifically enriched in a region of the CDC2 promoter when the gene's expression is reduced during starvation but not when CDC2 is highly active in growing cells. The region of unphosphorylated H1 coincides with a region that is essential for CDC2 expression. These studies are the first in vivo demonstration that the phosphorylation of H1 is being regulated at a fine level and that unphosphorylated H1 can be specifically targeted to a promoter, where it likely regulates transcription in a gene-specific manner.

Animals↗
PubMed2002

The immunosuppressant rapamycin mimics a starvation-like signal distinct from amino acid and glucose deprivation.

RAFT1/FRAP/mTOR is a key regulator of cell growth and division and the mammalian target of rapamycin, an immunosuppressive and anticancer drug. Rapamycin deprivation and nutrient deprivation have similar effects on the activity of S6 kinase 1 (S6K1) and 4E-BP1, two downstream effectors of RAFT1, but the relationship between nutrient- and rapamycin-sensitive pathways is unknown. Using transcriptional profiling, we show that, in human BJAB B-lymphoma cells and murine CTLL-2 T lymphocytes, rapamycin treatment affects the expression of many genes involved in nutrient and protein metabolism. The rapamycin-induced transcriptional profile is distinct from those induced by glucose, glutamine, or leucine deprivation but is most similar to that induced by amino acid deprivation. In particular, rapamycin treatment and amino acid deprivation up-regulate genes involved in nutrient catabolism and energy production and down-regulate genes participating in lipid and nucleotide synthesis and in protein synthesis, turnover, and folding. Surprisingly, however, rapamycin had effects opposite from those of amino acid starvation on the expression of a large group of genes involved in the synthesis, transport, and use of amino acids. Supported by measurements of nutrient use, the data suggest that RAFT1 is an energy and nutrient sensor and that rapamycin mimics a signal generated by the starvation of amino acids but that the signal is unlikely to be the absence of amino acids themselves. These observations underscore the importance of metabolism in controlling lymphocyte proliferation and offer a novel explanation for immunosuppression by rapamycin.

Amino Acids↗
PubMed2005

The H1 phosphorylation state regulates expression of CDC2 and other genes in response to starvation in Tetrahymena thermophila.

In Tetrahymena thermophila, highly phosphorylated histone H1 of growing cells becomes partially dephosphorylated when cells are starved in preparation for conjugation. To determine the effects of H1 phosphorylation on gene expression, PCR-based subtractive hybridization was used to clone cDNAs that were differentially expressed during starvation in two otherwise-isogenic strains differing only in their H1s. H1 in A5 mutant cells lacked phosphorylation, and H1 in E5 cells mimicked constitutive H1 phosphorylation. Sequences enriched in A5 cells included genes encoding proteases. Sequences enriched in E5 cells included genes encoding cdc2 kinase and a Ser/Thr kinase. These results indicate that H1 phosphorylation plays an important role in regulating the pattern of gene expression during the starvation response and that its role in transcription regulation can be either positive or negative. Treatment of starved cells with a phosphatase inhibitor caused CDC2 gene overexpression. Expression of the E5 version of H1 in starved cells containing endogenous, wild-type H1 caused the wild-type H1 to remain highly phosphorylated. These results argue that Cdc2p is the kinase that phosphorylates Tetrahymena H1, establish a positive feedback mechanism between H1 phosphorylation and CDC2 expression, and indicate that CDC2 gene expression is regulated by an H1 phosphatase.

Animals↗
PubMed1974

Energy provision, tissue utilization, and weight loss in prolonged starvation.

Daily weight loss measurements in 76 fasting, obese patients (58 females, 18 males) have shown a characteristic pattern of rapid loss initially (up to day 14) followed by a slower but uniform reduction in weight. There were significant sex differences. Measurements of tissue breakdown showed that the initial rapid weight loss was due to the continuing utilization by the nervous system of glucose derived from lean tissue. This requirement fell noticeably from the second week of starvation. Irreversible fluid elimination also contributed to the initial phase of rapid weight loss. Fat remained the primary source of energy throughout starvation and in established fasting (more than 14 days) contributed 96% of that requirement.

Adipose Tissue↗
PubMed1974

Long-term follow-up of therapeutic starvation.

A total of 75 grossly obese patients were admitted to hospital for 80 episodes of prolonged starvation. Five took their own discharge within two weeks of admission and 12 defaulted from follow-up within 12 months of discharge. The others were all followed up for periods of 12 to 64 months. Altogether 39 episodes in 34 patients were classified as failures, eight as modified successes, and 16 as successes, though five of the latter patients subsequently defaulted. Success was associated with regular follow-up attendance but could not be otherwise predicted. A number of patients obtained tangible benefit from starvation despite a subsequent gain in weight.

Adolescent↗
PubMed2003

Long term mortality after severe starvation during the siege of Leningrad: prospective cohort study.

OBJECTIVES: To determine whether starvation during periods of increased growth after birth have long term health consequences. DESIGN: Analysis of cardiovascular risk factors and mortality in a longitudinal follow up after the 1941-4 siege of Leningrad. Mortality measured from 1975 up to the end of 1999. SETTING: St Petersburg, Russia (formerly Leningrad). PARTICIPANTS: 5000 men born 1916-35 who lived in Leningrad, randomly selected to take part in health examinations in 1975-7. Of the 3905 men who participated, a third had experienced the siege. MAIN OUTCOME MEASURES: Relative risk of ischaemic heart disease and mortality from stroke by siege exposure. Odds ratios and means for several cardiovascular risk factors. RESULTS: Three to six decades after the siege, in men who experienced the siege around the age of puberty blood pressure was raised (mean difference in systolic 3.3 mm Hg, in diastolic 1.3 mm Hg) as was mortality from ischaemic heart disease (relative risk 1.39, 95% confidence interval 1.07 to 1.79) and stroke (1.67, 1.15 to 2.43), including haemorrhagic stroke (1.71, 0.90 to 3.22). The effect on mortality was partly mediated via blood pressure but not by any other measured biological, behavioural, or social factor. CONCLUSIONS: Starvation, or accompanying chronic stress, particularly at the onset of or during puberty, may increase vulnerability to later cardiovascular disease.

Adolescent↗
PubMed2006

Fuel metabolism in starvation.

This article, which is partly biographical and partly scientific, summarizes a life in academic medicine. It relates my progress from benchside to bedside and then to academic and research administration, and concludes with the teaching of human biology to college undergraduates. My experience as an intern (anno 1953) treating a youngster in diabetic ketoacidosis underscored our ignorance of the controls in human fuel metabolism. Circulating free fatty acids were then unknown, insulin could not be measured in biologic fluids, and beta-hydroxybutyric acid, which was difficult to measure, was considered by many a metabolic poison. The central role of insulin and the metabolism of free fatty acids, glycerol, glucose, lactate, and pyruvate, combined with indirect calorimetry, needed characterization in a near-steady state, namely prolonged starvation. This is the main topic of this chapter. Due to its use by brain, D-beta-hydroxybutyric acid not only has permitted man to survive prolonged starvation, but also may have therapeutic potential owing to its greater efficiency in providing cellular energy in ischemic states such as stroke, myocardial insufficiency, neonatal stress, genetic mitochondrial problems, and physical fatigue.

3-Hydroxybutyric Acid↗
PubMed2004

Modeling of lipid and protein depletion during total starvation.

This study presents a model describing lipid and protein depletion of an individual facing total starvation. The model distinguishes two compartments of body mass: a metabolic compartment and a structural compartment. It is considered that the lipids and the proteins of the metabolic compartment ensure the totality of physiological functions. The main assumptions of the model lie in the definitions of lipid mass and protein mass of the metabolic compartment, which are related to total lipid mass and total body mass, respectively. Under these assumptions, for a given individual, the ratio of lipid and protein utilization rates is proportional to the adiposity. The model accounts for the protein sparing observed at high adiposity levels and enables us to discuss the individual's survival in relation to the levels of lipid and protein depletion. The time course of changes in lipid and protein depletion rates can be calculated by introducing the energy expenditure of the individual. In simulations, it was assumed that specific energy expenditure was constant during starvation and that mortality occurred at a critical level of protein depletion. The most characteristic results derived from these simulations concern the kinetics of protein depletion, which depend markedly on initial adiposity. Accordingly, in obese subjects, the rate of protein losses remains fairly constant during fasting, whereas it increases from the onset of the fast in lean subjects, in agreement with experimental observations. In the model, protein and lipid depletion rates are both proportional to energy expenditure, which needs to be confirmed from complementary data.

Adipose Tissue↗
PubMed1979

Progesterone secretion and fetal development during prolonged starvation in the pig.

Roles of ovarian progesterone secretion and maternal nutrition in fetal development were investigated in a species that normally experiences considerable embryonic and fetal mortality. Pregnancies were maintained in 81% of Yorkshire pigs during prolonged starvation (e.g., 40 days; 0 kcal/day, water only) in either the middle third (days 30-70) or last third (days 70-110) of gestation compared with 100% in full-fed controls (7,028 kcal/day). In spite of severe maternal deprivation, fetal survival rates averaged 65% in starved dams and 63% in controls; mean number of living fetuses was 9.9 in starved and 9.6 in control dams. Fetal growth was reduced by maternal starvation during the middle third, but not the last third of pregnancy. Placental insufficiency was the primary cause of reduced fetal growth and resulted in abortion in a few of the dams. Progesterone in peripheral serum of dams starved either during middle or late pregnancy was maintained at levels similar (P greater than 0.05) to those in controls. Abortion occurred in starved dams only when serum progesterone concentrations dropped to less than 10 ng/ml within 3 days before loss of conceptuses.

Animals↗
PubMed1988

Effects of diabetes and starvation on skeletal muscle branched-chain alpha-keto acid dehydrogenase activity.

The activation state of branched-chain alpha-keto acid dehydrogenase (BCDH) was studied in rat hindlimb muscles during starvation and insulinopenic diabetes, conditions in which circulating branched-chain amino acids (BCAA) are increased and their oxidation is accelerated. Muscle BCDH is predominantly inactive (phosphorylated) in postabsorptive rats but is activated by increased circulating leucine. Diabetes (streptozotocin-induced and spontaneous BB/W) increased circulating BCAA four- to fivefold and BCDH activity approximately threefold. Insulin treatment caused near normalization of circulating BCAA without correcting BCDH activity. Adrenalectomy of diabetics decreased (without normalizing) circulating BCAA and BCDH activation. Starvation caused mild, progressive increases in circulating BCAA and significant activation of BCDH only after 4 days. Leucine infusion activated BCDH in muscle but the activation by leucine was markedly blunted by diabetes. In isolated perfused hindlimbs (control and diabetic) insulin did not affect BCDH significantly; perfusion with leucine activated BCDH, and this response appeared blunted in diabetics. Activation of muscle BCDH may contribute to increased BCAA catabolism in diabetes; the blunted activation response to hyperleucinemia may spare BCAA and contribute to their persistent elevation in plasma.

3-Methyl-2-Oxobutanoate Dehydrogenase (Lipoamide)↗
PubMed1990

Selective reduction of alpha 2-adrenergic responsiveness in hamster adipose tissue during prolonged starvation.

The influence of fasting on the dual adrenergic control of adipose tissue lipolysis was investigated in hamsters because in this species the adipocytes exhibit both beta-stimulatory and alpha 2-inhibitory adrenergic responses. In adipocytes from fed animals, the number of alpha 2-receptors (identified with [3H]clonidine and [3H]RX 821002) was greater than that of beta-receptors. As in humans, the alpha 2-adrenoceptor number was greater in adipocyte membranes from subcutaneous (inguinal and popliteal) than from internal (perirenal and epididymal) adipose tissues. Despite this difference in alpha 2-adrenoceptor number, the antilipolytic responses to the alpha 2-agonists clonidine and UK 14304 were similar in the two tissues. Food deprivation for a period of 1-6 days induced a net depletion of both adipose tissues. In 6-day starved animals the number of adipocyte alpha 2-adrenoceptors and the maximal antilipolytic effect of UK 14304 were less than 50% of those in fed controls. In contrast, the antilipolytic responses to phenylisopropyladenosine or prostaglandin E1 remained unchanged. Starvation induced a decrease in alpha 2-adrenoceptor number and an increase in beta-adrenergic sensitivity that were greater in adipocytes from subcutaneous than from internal fad pads. The data suggest that the adipocyte beta- and alpha 2-adrenoceptors are independently regulated during starvation. In the adipocyte, the alpha 2-antilipolytic responses and the alpha 2-adrenoceptor levels are dependent on the extent of the adipose mass; they are particularly reduced in emaciated hamsters.

Adenosine Deaminase↗
PubMed1995

SAM prevents impairment of glucose-stimulated insulin secretion caused by hexose deprivation or starvation.

Succinic acid monomethyl ester (SAM) was recently proposed as an insulinotropic tool in non-insulin-dependent diabetes mellitus. Three models were now used to investigate whether SAM protects the B-cell against the impairment of glucose-stimulated insulin release caused by either glucose deprivation or starvation. In the first model, preincubation of the islets for 180 min at low glucose concentration in the presence of SAM prevented the decrease in the secretory response to D-glucose otherwise observed during a subsequent incubation. In the second model, an impaired secretory response to D-glucose was observed after 3-day culture at low (2.8 or 5.6 mM) as distinct from high (11.1 mM) hexose concentration and the presence of SAM in the culture medium again protected against this anomaly. In the third model, the infusion of SAM for 3 days to starved rats restored the secretory potential of isolated islets to a level comparable to that otherwise found in fed rats. Thus, during glucose deprivation or starvation, SAM is indeed able to maintain B-cell responsiveness to D-glucose.

Animals↗
PubMed1996

Regulation of lipid metabolism in adipose tissue during early starvation.

We studied changes in lipid metabolism in adipose tissue in 24 healthy adults during early starvation (14-20 h) by cannulating the venous drainage of the subcutaneous adipose tissue of the anterior abdominal wall. Net nonesterified fatty acid (NEFA) efflux from adipose tissue increased steadily from 1,790 +/- 300 to 2,360 +/- 290 nmol.100 g-1.min-1 (P = 0.03), due to increasing transcapillary efflux of NEFA (release from adipocytes; P < 0.01). The reesterification rate after an overnight fast was close to zero; thus, reduction in the rate of reesterification played no part in the increased transcapillary efflux of NEFA. One-quarter of the net efflux of NEFA after an overnight fast arose from the action of lipoprotein lipase (LPL), although this relative contribution decreased during the study (P < 0.02). The increased transcapillary efflux of NEFA reflected a significant increase in the rate of action of hormone-sensitive lipase (HSL; P = 0.03). There was a strong relationship between mean arterial NEFA concentration and net NEFA release from adipose tissue (P < 0.001), implying that the particular depot studied reflects the behavior of adipose tissue as a whole. Thus the increasing efflux of NEFA from adipose tissue observed during early starvation is due to an increased rate of action of HSL, which may in turn be regulated by a fall in the plasma insulin concentration.

Adipose Tissue↗
PubMed1986

Lung mechanics and connective tissue levels in starvation-induced emphysema in hamsters.

The effect of starvation on lung mechanics, morphometry, and levels of connective tissue components was determined in young adult golden Syrian hamsters. A base-line control, fed control, and starved group were studied. Fed group animals increased body weight by 13%, but dry lung weight did not increase above that of the base-line controls. The total lung capacity when transpulmonary pressure was at 25 cmH2O (TLC25) also increased by 20% above base-line controls. The mean TLC25 of the starved group was greater than that of the base-line control group but less than that of the fed control group (P less than 0.05). Volume-corrected air-filled volume pressure (VP) curves of the three groups were similar. Volume-corrected saline-filled VP curves were identical in the three groups. Total lung collagen, elastin, glycosaminoglycan, and protein were similar in the three groups. Air space size was significantly increased and mean internal surface area was significantly decreased in the starved group compared with the base-line and fed controls. No evidence of alveolar wall destruction was evident by light or electron microscopy. We conclude that severe starvation of young adult hamsters produces air space enlargement without changes in lung elastic recoil. The mechanism of alveolar wall remodeling is not yet understood in this model of emphysema.

Air↗
PubMed1986

Environment and hamster reproduction: responses to phase-specific starvation during estrous cycle.

Reproductive capacity of female hamsters, as estimated by the ovulatory response, is particularly susceptible to interference by food deprivation. Previous studies showed that hamsters generally fail to ovulate if deprived of food for one or two estrous cycles. The present work demonstrates that starvation which is specific to the 2 days immediately after ovulation will block the next expected ovulation in approximately 80% of the animals. Such phasic starvation also resulted in significantly smaller ovarian follicle sizes. When placed with vigorous males, anovulatory animals failed to show lordosis behavior unless exogenous estradiol benzoate (EB) was supplied. With EB provided, all animals showed short-latency lordosis. These bioassay data suggested that poorly developed follicles were secreting insufficient estradiol for the facilitation of lordosis. Exogenous luteinizing hormone (LH) given 6 h before lights off on cycle day 4 failed to elicit ovulation, further suggesting that the follicles were not mature. Radioimmunoassay of LH and follicle-stimulating hormone (FSH) levels during the ovulatory gonadotropin surge showed that LH was vastly reduced, whereas FSH was in the low-to-normal range. Estradiol levels, assayed immediately before the gonadotropin surge, were low compared with controls, whereas progesterone levels were higher than normal. The results suggest that ovulatory failure in response to phasic food deprivation is a joint function of absence of an ovulatory LH surge and a set of immature follicles.

Animals↗
PubMed1988

Effect of starvation and food intake on sympathetic activity.

These studies have examined the effect of fasting and nutrient loads on sympathetic firing rate in three groups of rats that develop widely divergent degrees of obesity when eating a high-fat diet. Starvation of Sprague-Dawley rats for 24 or 48 h was associated with a decrease in basal sympathetic activity of nearly 25% in the first 24 h and of slightly greater than 30% in 48 h. This decline in sympathetic activity paralleled the loss of body weight and reduction in adipose tissue mass. After starvation for 48 h, Osborne-Mendel rats, which readily develop obesity when eating a high-fat diet, showed a greater decrease in basal sympathetic activity than did the diet-resistant S 5B/P1 rats. A single liquid 36-kcal intragastric meal was associated with an acute 30% increase in sympathetic firing rate in the overnight-fasted Sprague-Dawley rats. The values 3 h after the meal had returned halfway to normal, and by 6 h they were more than 85% of the way to normal. An intravenous injection of glucose produced a greater rise in sympathetic activity in diet-resistant S 5B/P1 rats than in the diet-sensitive Osborne-Mendel rats. These data are consistent with the hypotheses that sympathetic activity is positively related to nutrient status, that it varies between strains of rats, and that it can be acutely increased by an intragastric meal or by intravenous glucose.

Adipose Tissue↗
PubMed1995

Starvation-induced increase of hepatic alanine uptake is related to changes in sensitivity to SH-group reagents.

Changes in L-alanine transport in plasma membrane vesicles from livers of control and 24- and 48-h starved adult rats and the sensitivity of alanine uptake to sulfhydryl group reagents [N-ethylmaleimide (NEM) and p-chloromercuribenzenesulfonate (p-CMBS)] were studied. The portal concentration of certain amino acids was measured, and the relationship between L-alanine transport kinetic parameters and amino acid levels was analyzed. Starvation only induced a decrease in portal concentration of these amino acids that are mainly carried by Na(+)-dependent systems (85 and 61% for 24- and 48-h starved rats, respectively). Portal alanine concentration was lower in 24-h starved animals than in control rats (370 vs. 587 microM) and further decreased after 48 h of fasting (228 microM). Starvation induced an increase in maximum velocity (Vmax) values of Na(+)-dependent L-alanine transport (7.19, 8.97, and 12.38 pmol.U 5'-nucleotidase-1.10 s-1 for control and 24- and 48-h starved rats, respectively) with slight, but not significant, changes in the apparent Michaelis constant (Km) values (3.35, 2.63, and 2.20 mM for control and 24- and 48-h starved rats, respectively). Portal alanine showed a directly close correlation with Km values and inverse with Vmax values. The mean affinity constant values for the effects of NEM and p-CMBS on Na(+)-dependent L-alanine transport were lower in 48- (2.57 and 0.13 mM, respectively) and 24-h starved rats (3.59 and 0.32 mM, respectively) than in control rats (8.56 and 0.59 mM, respectively) and showed a directly strong correlation with kinetic characteristics of L-alanine transport and portal alanine concentration.(ABSTRACT TRUNCATED AT 250 WORDS)

4-Chloromercuribenzenesulfonate↗
PubMed1998

Impact of starvation-refeeding on kinetics and protein expression of trout liver NADPH-production systems.

Herein we report on the kinetic and protein expression of glucose-6-phosphate dehydrogenase (G6PDH), 6-phosphogluconate dehydrogenase, and malic enzyme (ME) in the liver of the trout (Oncorhynchus mykiss) during a long-term starvation-refeeding cycle. Starvation significantly depressed the activity of these enzymes by almost 60%, without changing the Michaelis constant. The time response to this nutritional stimulus increased with fish weight. The sharp decline in G6PDH and ME activities was due to a specific protein-repression phenomenon, as demonstrated by molecular and immunohistochemical analyses. Also, the dimeric banding pattern of liver G6PDH shifted from the fully reduced and partially oxidized forms, predominant in control, to a fully oxidized form, more sensitive to proteolytic inactivation. Refeeding caused opposite effects in both protein concentration and enzyme activities of about twice the control values in the first stages, later reaching the normal enzyme activity levels. Additionally, the partially oxidized form of G6PDH increased. The kinetics of these enzymes were examined in relation to the various metabolic roles of NADPH. These results clearly indicate that trout liver undergoes protein repression-induction processes under these two contrasting nutritional conditions.

Animal Feed↗