SEARCH · Search PubMed

Results for “STARVATION”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

SourceResearch connectionFrom yearThrough year

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 325 records · Page 18Linked to original sources

PubMed1997

Adaptation to nutrient starvation in Rhizobium leguminosarum bv. phaseoli: analysis of survival, stress resistance, and changes in macromolecular synthesis during entry to and exit from stationary phase.

The nitrogen-fixing bacterium Rhizobium leguminosarum bv. phaseoli often has to survive long periods of starvation in the soil, when not in a useful symbiotic relationship with leguminous plants. We report that it can survive carbon, nitrogen, and phosphorus starvation for at least 2 months with little loss of viability. Upon carbon starvation, R. leguminosarum cells were found to undergo reductive cell division. During this period, they acquired the potential for long-term starvation-survival, levels of protein, DNA, and RNA synthesis were decreased to base levels, and pool mRNA was stabilized. The starved cells are ready to rapidly restart growth when nutrients become available. Upon addition of fresh nutrients, there is an immediate increase in the levels of macromolecular synthesis, pool mRNA destabilizes, and the cultures enter exponential growth within 5 to 8 h. The starved cells were cross-protected against pH, heat, osmotic, and oxidative shock. These results provide evidence for a general starvation response in R. leguminosarum similar to that previously found in other bacteria such as Escherichia coli and Vibrio sp.

Bacterial Proteins↗

PubMed1979

Insulin sensitivity of rat skeletal muscle: effects of starvation and aging.

The effects of starvation and of aging on the sensitivity of skeletal muscle to insulin were studied in the isolated perfused rat hindquarter preparation. As we have shown previously, starvation for 48 h had no effect on glucose uptake in hindquarters perfused with high levels of insulin (5 and 20 mU/ml). On the other hand, in the presence of physiological concentrations of insulin (50--200 muU/ml), glucose utilization was substantially greater in starved rats. Low concentrations of insulin had a greater effect on glucose uptake in fed young (100-g) than in fed older (350-g) rats. Starvation for 48 h enhanced glucose uptake in both young and older rats; however, the relative differences persisted. Starvation had similar effects on glucose utilization by the incubated soleus and extensor digitorum longus muscle. In addition, it augmented the stimulation by insulin of alpha-aminoisobutyric acid transport into the incubated extensor digitorum longus muscle. These results suggest that the in vitro sensitivity of skeletal muscle to physiological concentrations of insulin is enhanced during starvation. The basis for these findings and their physiological implications remain to be determined.

Aging↗

PubMed1980

Starvation in the rat. I. Effect of age and obesity on organ weights, RNA, DNA, and protein.

Previous studies have shown that obese man adapts to prolonged starvation with a conservation of body protein. In an attempt to delineate the biochemical and hormonal changes responsible for this adaptation, the effect of starvation was studied in rats with differing abilities to survive a fast and conserve protein. Sixteen-week-old rats made obese by fat feeding survived starvation for 25-30 dys, whereas 16-wk-old controls survived 11-12 days and the 8-wk-old controls for 6-7 days. Starvation decreased hepatic weight, RNA, and protein early in the fast in all three groups. In heart, the extensor digitorum longus muscle and some other organs decreases in RNA, protein, and weight occurred more slowly and were smaller in magnitude in the 16-wk-old control and obese rats. A pronounced loss of cardiac protein and RNA occurred in the 8-wk-old group. We conclude that 16-wk-old control and obese rats are better able to survive and conserve organ protein and RNA during prolonged starvation than younger rats. To what extent this reflects differences in the age and to what extent differences in adiposity remains to be determined.

Age Factors↗

PubMed1980

Starvation in the rat. II. Effect of age and obesity on protein sparing and fuel metabolism.

Sixteen-week-old control and obese rats survive longer than 8-wk-old control rats. In addition, unlike the 8-wk-old group, they conserve tissue RNA and protein. To evaluate the basis for this, the effects of starvation on circulating fuels and hormones and the urinary excretion of nitrogen and 3-methylhistidine (3MH) were compared in the three groups. Urinary nitrogen and 3MH diminished during prolonged starvation in 16-wk-old obese and control rats, suggesting that both groups are able to conserve protein and curtail muscle proteolysis. In contrast, urine nitrogen and 3MH did not decrease in 8-wk-old control rats. Protein conservation in the older rats was associated with diminished blood levels of alanine and increased levels of lipid fuels, ketone bodies, and free fatty acids. Although ketone bodies and free fatty acids were also increased during the first few days of starvation in 8-wk-old rats, there was no evidence of protein sparing. In all groups, as fat stores became exhausted terminally, blood lipid levels decreased and protein catabolism increased. Starvation caused insulin to decrease to comparable levels in all rats; however, minimal levels were reached later in the older groups. Thyroxine and triiodothyronine (T3) decreased during the fast in both control groups; however, T3 did not decrease in the obese rats. These findings support the contention that the conservation of protein during prolonged starvation requires the continued availability of lipid fuels. The role of insulin and thyroid hormone in modulating these adaptations is unclear.

Aging↗

PubMed1981

Adaptation to prolonged starvation in the rat: curtailment of skeletal muscle proteolysis.

Previous studies have established that 16-wk-old nonobese and obese rats conserve body protein during prolonged starvation. To determine the basis for this, protein synthesis and degradation in skeletal muscle were evaluated in the isolated perfused hindquarters of these rats, in the fed state and when starved for 2, 5, 10, and 11 days. Rats aged 4 and 8 wk were used as a comparison. The results indicate that the response to starvation depends on several factors: the age of the rat, its degree of adiposity, and the duration of the fast. An early event in starvation was a decline in muscle protein synthesis. This occurred in all groups, albeit this reduction occurred more slowly in the older rats. A later response to starvation was an increase in muscle proteolysis. This occurred between 2 and 5 days in the 8-wk-old rats. In 16-wk-old rats it did not occur until between 5 and 10 days, and it was preceded by a period of decreased proteolysis. In 16-wk-old obese rats, a decrease in proteolysis persisted for upwards of 10 days and the secondary increase was not noted during the period of study. The data suggest that the ability of older and more obese rats to conserve body protein during starvation is due, in part, to a curtailment of muscle proteolysis. This adaptation seems to correlate with the availability of lipid fuels.

Aging↗

PubMed1998

Altered expression of type 2 CRH receptor mRNA in the VMH by glucocorticoids and starvation.

In the rat, high-dose corticosterone (Cort) administration, the hypercortisolism of starvation, and adrenalectomy are all associated with decreased food intake and weight loss. We report here a study of the effects of high-dose Cort administration, starvation, and adrenalectomy on two peripheral hormones known to influence food intake and energy use, insulin and leptin. We also studied the impact of these interventions on the levels of type 2 corticotropin-releasing hormone receptor (CRHR-2) mRNA in the hypothalamic paraventricular nucleus (PVN) and ventromedial hypothalamus (VMH). The VMH is classically referred to as the satiety center because electrical stimulation of the VMH leads to inhibition of food intake, whereas CRHR-2 are thought to transduce the profound anorexogenic effects of CRH or its related peptide urocortin. Starvation and adrenalectomy each lowered plasma insulin and leptin levels and were associated with decrements in CRHR-2 mRNA levels in the VMH. Cort administration increased plasma leptin levels profoundly, as well as plasma insulin levels and the levels of VMH CRHR-2 mRNA. Under all experimental conditions, a positive correlation was seen between plasma leptin levels and VMH CRHR-2 mRNA. These data suggest that decreased food intake and weight loss after high-dose Cort administration at least partially depend on the profound impact of Cort on plasma leptin secretion in the rat; they suggest, moreover, an additional mechanism for the satiety-inducing effects of leptin, namely increasing CRHR-2 in the VMH. The concordance of a fall in plasma insulin and leptin levels with the fall in VMH CRHR-2 mRNA levels further supports the idea that compensatory responses during starvation and adrenalectomy include not only the disinhibiting effects of reduced insulin and leptin levels on appetite through already-described mechanisms but also via an effect of leptin on VMH CRHR-2. Neither Cort administration, starvation, nor adrenalectomy influenced the levels of CRHR-2 mRNA in the PVN, suggesting that these receptors are differentially regulated in different hypothalamic regions.

Adrenalectomy↗

PubMed1986

Lung mechanics, cellularity, and surfactant after prenatal starvation in guinea pigs.

Prenatal starvation in the guinea pig causes reduced pulmonary diffusing capacity and retarded alveolarization among neonates. To study the impact of such starvation on biochemical and mechanical properties of the neonatal lung, pregnant guinea pigs were fed ad libitum throughout gestation or starved with 50% rations during their last trimester. Neonatal body weight was 35% less due to starvation, and dry lung weight, DNA, and protein contents were decreased 26, 36, and 31%, respectively (P less than 0.001 for all). Hematological data indicated no anemia, hypoproteinemia, or altered glucocorticoid levels due to starvation. Total surfactant phospholipids in these neonates were reduced 61% in lavage and 35% in the neonatal lung tissue, although surfactant compositions were similar to controls. Specific lung compliance in the air-filled lungs was not altered, but the saline-filled lungs were more distensible over deflation pressures of 9-18 cmH2O (transpulmonary). Although starvation retarded both lung cellularity and surfactant, only that portion of lung elastic recoil attributable to tissue forces was affected.

Animals↗

PubMed1992

Effects of repeated cycles of starvation and refeeding on lungs of growing rats.

Adult male rats were subjected to four cycles of mild starvation (2 wk) and refeeding (1 wk) and were compared with a fed group. Starvation was induced by giving rats one-third of their measured daily food consumption. During each starvation cycle, rats lost approximately 20% of their body weight. Despite catch-up growth and overall weight gain, starved rats had lower final body weight than fed rats. Lung dry weight and lung volumes were also reduced in the starved group. The mechanical properties of air- and saline-filled lungs did not change significantly with repeated cycles of starvation. Mean linear intercept was similar in the two groups, but alveolar surface area was reduced in the starved rats. Total content of crude connective tissue and concentration per lung dry weight of hydroxyproline and crude connective tissue were reduced in starved rats. We conclude that lung growth is retarded in growing rats subjected to repeated cycles of mild starvation and refeeding, as manifested by smaller lung volume and reduced alveolar surface area. Because alveolar size is unchanged, a reduced number of alveoli is most likely responsible for decreased lung volumes.

Animals↗

PubMed1993

Effects of starvation and refeeding on adult male rat diaphragm contractility, fatigue, and fiber types.

The effects of 4.5 days of acute starvation, either alone or followed by refeeding (ad libitum), on diaphragm contractility, fatigue, and fiber types were studied in male rats. Contractility and fatigue resistance indexes were measured in an in vitro costal diaphragm strip preparation with direct stimulation at 37 degrees C. Compared with controls, starvation produced a 28 +/- 1% (P < 0.001) reduction in body weight and an 18 +/- 4% (P < 0.001) reduction in costal diaphragm weight. Twitch and tetanic tensions (normalized for weight or cross-sectional area) were not reduced by starvation. Starvation produced significant increases in fatigue resistance indexes after a 5-Hz stimulation paradigm but not after a 100-Hz paradigm, supporting the hypothesis that fatigue resistance is dependent on the energy demand of a given paradigm. The proportions of type I and type II fibers were similar between diaphragms of starved and control rats, but the cross-sectional area of type II fibers decreased significantly by 18 +/- 7% (P < 0.01). Thus, despite the significant decrease in diaphragm weight after starvation, contractility was preserved and fatigue resistance was increased (low-output paradigm). This is consistent with the decrease in type II fiber area. Refeeding restored all parameters so that there were no longer significant differences in body or diaphragm weight, contractility, fatigue, or fiber types.

Animals↗

PubMed1978

Effect of starvation on small intestinal enzyme activity in germ-free rats.

Starvation overnight and starvation for 48 h reduced the weight and the protein content of mucosal scrapings, but only minimally reduced the DNA content of the mucosal scrapings. The activity of sucrase and maltase was reduced by both periods of starvation. The activity of lactase and of acid and alkaline phosphatase, however, was less subject to starvation. There were striking differences in the response to starvation between the proximal, mid and distal third of the small intestine. The importance of the proper reference system was discussed.

Acid Phosphatase↗

PubMed1979

The response of adult rats weaned prematurely and normally to starvation.

Male rats were weaned normally (NW; day 30 after birth) or prematurely (PW; day 18) to a Purina Chow diet. Serum cholesterol levels and the activities of some enzymes of fatty acid and glucose metabolism were determined when the animals were 6 and 10 months old and, in the older group, also after 2 days of starvation. Blood cholesterol levels rose with age and at 10 months were higher in PW than NW rats. This difference disappeared after starvation. Hepatic pyruvate kinase (PK) activity was the same in fed NW and PW animals but was significantly higher in starved PW than NW rats. Hepatic phosphoenolpyruvate carboxykinase (PEPcK) activity was lower in NW than in PW rats, but this difference disappeared on starvation. In white fat, starvation caused a fall in PEPcK activity in both groups. In general, the effect of starvation did not accentuate the differences between the two groups. However, PEPcK activity in white fat increased with age about fourfold.

Adipose Tissue↗

PubMed1982

Effect of hyperventilation and starvation on rat lung mechanics and surfactant.

We studied the effects of hyperventilation and starvation on rat lung mechanics and surfactant. We hyperventilated lungs by excising and ventilating them at 3 times the normal tidal volume. Three days starvation reduced the alveolar pool of disaturated phosphatidyl choline by about 20% but did not significantly reduce the functional residual capacity. Air and saline deflation pressure-volume curves were performed in 4 groups: control lungs, lungs from starved rats, hyperventilated lungs, and hyperventilated lungs from starved rats. The area under each curve was calculated; this indicated the relative position of the curve in the pressure-volume diagram. We found that starvation did not change recoil, that hyperventilation increased surface recoil, and that combined starvation and hyperventilation increased it even more. We conclude that hyperventilation-induced dysfunction of surfactant is greater when the alveolar pool of surfactant is reduced by starvation. This effect might also occur clinically in the intensive care setting.

Air Pressure↗

PubMedDate not supplied

Decreased plasma fibronectin during starvation in man.

This study evaluated the effect of 5 days of starvation followed by 5 days of refeeding on immunoreactive plasma and serum fibronectin and associated opsonic activity as studied by peritoneal macrophage monolayer bioassay in 12 healthy women volunteers. The temporal alteration of fibronectin was compared with the serum albumin, total iron-binding capacity, and retinol-binding protein levels. Fibronectin concentration and opsonic activity were also determined in two cachectic patients who were 61 and 78% of their ideal body weight. Prior to starvation, plasma fibronectin was 292 +/- 20 micrograms/ml and serum fibronectin was 182 +/- 16 in all subjects. After 5 days of starvation, immunoreactive fibronectin decreased (p less than 0.05) by 20-25%. This decrease was not great enough to impair opsonic activity as tested by the in vitro macrophage assay. Starvation caused no decrease in serum albumin or total iron-binding capacity, although retinol-binding protein decreased by 35%. During refeeding, subjects were randomized to a diet with (n = 6) and without (n = 6) carbohydrate. After 5 days of refeeding, fibronectin levels were normalized on the carbohydrate-containing diet, but were still low (82% of normal) on the carbohydrate-free diet. Retinol-binding protein did not fully normalize after 5 days of refeeding. In the two cachectic patients, fibronectin levels prior to total parenteral nutrition were 25 and 75% of normal. Thus, starvation can lower fibronectin levels and this protein is rapidly restored with adequate nutrition.

Adult↗

PubMed1980

Starvation induces a partial failure of triiodothyronie to inhibit the thyrotropin response to thyrotropin-releasing hormone.

During starvation the response of TSH to TRH decreases in many subjects. This could be due to an increased sensitivity to TSH secretion to circulating thyroid hormones. To study this hypothesis, 13 subjects were starved twice for 2-day periods. After both starvation periods, a standard TRH test (200 micrograms TRH, iv) was performed; during 1 starvation period 15 micrograms T3 were injected iv 24 h before the TRH test. The TRH tests were also performed while on normal nourishment, once without pretreatment and once 24 h after the iv injection of 15 micrograms T3. The spontaneous decrease of the TSH response to TRH was seen in 10 of 13 subjects. In these 10 subjects it decreased from 18.0 +/- 1.9 to 9.7 +/- 1.2 microU/ml (mean +/- SEM; P < 0.001). The additional inhibition of the TRH test with T3 was small compared with the one observed under normal conditions. In starvation, T3 decreased the maximal TSH response from 9.7 +/- 1.2 to 8.4 +/- 1 microU/ml (P = NS), while during the control period the maximal TSH response fell from 18.0 +/- 1.9 to 11.4 +/- 1.3 microU/ml (P < 0.001). These data indicate a diminished effectiveness of T3 in inhibiting TSH secretion and are consistent with the hypothesis of a more generalized resistance of target organs to T3 during starvation in man.

Adult↗

PubMed1984

Metabolic alterations in normal and streptozotocin-diabetic rats in vivo: influence of prolonged starvation.

We studied the influence of prolonged starvation on carbohydrate metabolism in streptozotocin-diabetic rats compared with normal rats. In streptozotocin (STZ)-diabetic rats, the plasma glucose concentration decreased gradually during prolonged starvation, while it did not change in normal rats. In normal rats, glycogen depletion in the liver occurred within 24 hr of starvation, while in STZ-diabetic rats, glycogen content did not change even after 72 hr of starvation. Impaired glucose tolerance and glycogen deposition in response to oral administration of glucose were observed in STZ-diabetic rats compared with normal animals. STZ-diabetic animals generally had lower glycogen synthase and phosphorylase activities compared with normal rats during starvation. In normal animals, there is a significant correlation between the plasma concentration of free fatty acids and 3-hydroxybutyrate. On the basis of these findings, metabolic alterations in chemically-induced diabetic animals were discussed.

3-Hydroxybutyric Acid↗

PubMed1994

Effect of acute starvation on rat diaphragm function.

The effects of 130 h of acute starvation on diaphragm contractility fatigue were studied in isolated rat diaphragm strip preparations with phrenic nerve stimulation. Compared with controls, starvation produced a reduction in body and diaphragm weights. Twitch and tetanic tensions were reduced by starvation; however, when the force was calculated as the strength (normalized for the weight or muscle cross-section area of the diaphragm), no difference was observed between the control and experimental groups. Starvation induced a significant downward shift in the force-frequency relationship, and also increased diaphragm fatigability, but it had no effect on twitch contraction and relaxation time. We conclude that 130 h of acute starvation decreases diaphragmatic force and endurance, but the strength does not change, because of the reducing diaphragmatic mass.

Animals↗

PubMed2003

Starvation and diabetes reduce the amount of pyruvate dehydrogenase phosphatase in rat heart and kidney.

The pyruvate dehydrogenase complex (PDC) is inactivated in many tissues during starvation and diabetes to conserve three-carbon compounds for gluconeogenesis. This is achieved by an increase in the extent of PDC phosphorylation caused in part by increased pyruvate dehydrogenase kinase (PDK) activity due to increased PDK expression. This study examined whether altered pyruvate dehydrogenase phosphatase (PDP) expression also contributes to changes in the phosphorylation state of PDC during starvation and diabetes. Of the two PDP isoforms expressed in mammalian tissues, the Ca(2+)-sensitive isoform (PDP1) is highly expressed in rat heart, brain, and testis and is detectable but less abundant in rat muscle, lung, kidney, liver, and spleen. The Ca(2+)-insensitive isoform (PDP2) is abundant in rat kidney, liver, heart, and brain and is detectable in spleen and lung. Starvation and streptozotocin-induced diabetes cause decreases in PDP2 mRNA abundance, PDP2 protein amount, and PDP activity in rat heart and kidney. Refeeding and insulin treatment effectively reversed these effects of starvation and diabetes, respectively. These findings indicate that opposite changes in expression of specific PDK and PDP isoenzymes contribute to hyperphosphorylation and therefore inactivation of the PDC in heart and kidney during starvation and diabetes.

Animals↗

PubMed1999

Hepatic branched-chain alpha-keto acid dehydrogenase complex in female rats: activation by exercise and starvation.

The effects of acute exercise and starvation on hepatic branched-chain alpha-keto acid dehydrogenase (BCKDH) complex activity were examined in female rats fed high (30%)- or low (8%)-protein diets. The total activity of the complex was significantly higher in the high protein-fed rats than in the low protein-fed rats but was not affected by acute exercise and starvation in either diet group. The proportion of the active form of BCKDH complex was less than 10% in both diet groups. Acute exercise and starvation markedly increased the active form of the complex in both diet groups. The activity of BCKDH kinase, which is responsible for inactivation of the BCKDH complex by phosphorylation, tended to be decreased by acute exercise and starvation in both diet groups. These results suggest that the activity of the BCKDH kinase is an important factor determining the proportion of the active form of BCKDH complex in exercise and starvation, and that the female rat is a useful model for studying the regulation of hepatic BCKDH complex activity.

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