Effects of starvation on lung mechanics and biochemistry in young and old rats

Two groups of rats (young and old) were food-deprived for 3 wk and were compared with age-matched fed groups. Final body weight and dry and wet weights of lungs were significantly reduced in both young and old starved rats. As determined by saline volume-pressure (VP) curves, lungs of young starved rats accepted significantly less volume at all pressure levels compared with lungs of young fed rats. When expressed as a percent of maximum lung volume, the VP curve in young starved rats was significantly shifted upward at low lung volumes. In the old rats, the VP curves were similar in fed and starved rats. Total lung content of protein, DNA, crude connective tissue, hydroxyproline, and elastin were significantly reduced in young starved compared with young fed rats, whereas in old starved rats only protein and DNA contents were lower than those in old fed animals. It appears that in rapidly growing young rats starvation leads to growth retardation, loss of connective tissue components, and possibly reduction in tissue elastic forces at low lung volumes, whereas starvation has no significant effects on lung mechanics and connective tissue in old rats.     

Effects of starvation and refeeding on elastase-induced emphysema

Adult rats received pancreatic elastase (75 U/100 g) intratracheally and were divided into three groups: fed, starved, and refed. Starved rats received one-third of their measured daily food consumption until they lost 40% body weight. The refed group was fed after 40% weight loss. A control group received saline intratracheally. Saline volume-pressure curve was shifted more significantly to the left of the control group in starved than in fed rats and was superimposed in refed and fed groups. Mean linear intercept was larger and alveolar surface area was smaller in starved than in fed rats compared with the control group; both were similar in fed and refed rats. Protein and hydroxyproline content of the lung were higher in fed than in control and in starved groups; after refeeding these returned to the control values. We conclude that starvation aggravates elastase-induced injury and that refeeding results in the complete recovery of the mechanical but only partial recovery of the morphometric changes induced by starvation.     

Lung mechanics and connective tissue proteins in diabetic Bio-Breeding/Worcester Wistar rats

We studied lungs of spontaneously diabetic Bio-Breeding/Worcester (BB/W) Wistar rats which resemble human insulin-dependent diabetes mellitus. Compared with the age-matched control group, the body weight of the diabetic rats tended to be smaller and lung wet and dry weight were similar, but lung dry weight, relative to body weight and to lung wet weight, was significantly larger. Both air and saline lung volumes were reduced in the diabetic rats, and volume-pressure (V-P) curves expressed as a percent of maximal lung volume were significantly shifted downward and to the right of those in the control group over the midportion. Total DNA and RNA contents were similar in both groups, whereas protein content and concentration and protein/DNA and RNA/DNA ratios were significantly reduced in the diabetic rats. In contrast, content and concentration of 4-hydroxy-L-proline, elastin, and crude connective tissue were significantly higher in the diabetic group. We conclude that the increase in connective tissue proteins in the BB/W rats is most likely responsible for the shift in the V-P curves.     

Radioglucose metabolism by richardson's ground squirrels in the weight-gain and weight-loss phases of the circannual cycle

Summary Captive fed, starved, and refed Richardson's ground squirrels in the weight-gain and weight-loss phases of the circannual cycle were injected with radioglucose and the activity of the label in skeletal muscle proteins and white adipose tissue lipids four hours after injection was used to determine if lean body mass and white adipose tissue would be rapidly restored when starved animals were refed. Starvation for six days reduced carcass mass 27–31% and white adipose tissue mass 23–24% (Table 1). Activity of the label in both tissues of weight-gain and weight-loss animals was reduced by starvation. After four days of refeeding activities retured to levels similar to those in fed animals, with the exception of lower activity in skeletal muscle proteins of weight-gain animals. Furthermore, activity in each tissue fraction of starved and refed weight-gain animals was similar to that in weight-loss animals when expressed as per cent of activity in the respective fed state (Table 2). Radioglucose incorporation indicated that when skeletal muscle and adipose tissue are depleted by starvation, distribution of the label upon refeeding is similar to that in the fed state. Four days after refeeding weight-gain phase ground squirrels had restored 5.5 g of lean body mass and 7.5 g of adipose tissue, including 1.4 g (6 kcal) of protein and 7.0 g (66 kcal) of lipid, respectively. These results are also consistent with the fed state, in which weight-gain animals were depositing more lipid than lean body mass.     

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.     

Further studies on the effects of dehydroepiandrosterone on hepatic metabolism in BHE rats

Two experiments were conducted to determine the effects of dehydroepiandrosterone (DHEA) on de novo fatty acid synthesis and oxygen consumption in BHE rats fed a 65% glucose diet. In Experiment 1, starved glucose-refed rats were injected ip with 120 mg of DHEA/kg body wt and hepatic de novo fatty acid synthesis was measured. DHEA-treated rats synthesized less fatty acid in response to starvation refeeding than nontreated rats. In Experiment 2, weanling rats were fed the glucose diet for 4 weeks. One-hundred twenty milligrams of DHEA/kg were injected daily for 3 weeks. Body weight gain, epididymal fat pad weight, and carcass lipid were less in the DHEA-treated rats than in the control rats. Mitochondrial respiration was less and liver size was greater in DHEA-treated rats compared with control rats. Whole body oxygen consumption was increased in DHEA-treated rats, suggesting that this steroid might be stimulating futile energy cycles involving lipid and protein turnover possibly through its effect on glucocorticoid and thyroid hormone function.     

Fatty acid synthetase in control, starved and refed Richardson's ground squirrels

1. Starvation for 6 days reduced whole body mass and total body lipids to 76 and 71%, respectively, of pre-starvation levels in weight-gain phase ground squirrels. After 4 days of refeeding, body mass increased to 86% of pre-starvation level but total body lipids had not changed from starvation levels. 2. Compared to the fed state, fatty acid synthetase (FAS) activity in white adipose tissue (WAT) was 15 and 31% in starved and refed 4-day animals, respectively, and in liver was 26 and 21% in starved and refed 4-day animals, respectively. Lipids depleted by starvation during prehibernatory fattening were not rapidly restored in Richardson's ground squirrels. 3. Changes in these parameters with starvation and refeeding were similar in weight-loss phase animals. 4. In control animals of both phases, WAT accounted for at least 90% of total FAS activity and liver nearly all of the remainder.     

Influence of starvation/refeeding transition on lipogenesis and NADPH producing systems in adipose tissue, mammary gland and liver at mid-lactation

Glucose-6-phosphate dehydrogenase, 6-phosphogluconate dehydrogenase and malic enzyme are enzymes involved in NADPH synthesis. Their specific activities and glucose utilization by isolated cell systems have been measured in adipose tissue and mammary gland from mid-lactating rats during starvation/refeeding transition. Starvation for 24 h produced a 75-90% decrease in the specific activities of these NADPH producing systems in mammary gland. Acinis isolated from the gland of starved rats had a lower production of CO2, fatty acids and triacylglycerols from (1-14C)glucose and (6-14C)-glucose than did gland from control rats. The activities of these enzymes in adipose tissue were very low and did not undergo any measurable alteration with starvation. The ability of adipocytes from well fed lactating rats to synthesize fatty acids from (1-14C)glucose was completely blocked. However, starvation is accompanied by a marked decrease in glucose incorporation into triacylglycerols. All the variations observed "in vivo" and "in vitro" in mammary gland returned almost to normal values by refeeding the starved lactating rats.     

Effects of streptozotocin-induced diabetes on lung mechanics and biochemistry in rats

Young and adult rats were given a single intraperitoneal injection of 75 mg/kg streptozotocin in citrate buffer and were compared with age- and weight-matched controls that received an equal volume of buffer alone. Studies done 8 wk after the injections showed that final body weight, lung dry weight, lung DNA content, and air and saline lung volumes were significantly lower in both young and adult diabetic rats compared with the controls. In young diabetic rats, volume-pressure (V-P) curves expressed as percent maximal lung volume (%MLV) were shifted downward and to the right of those in young control rats at 5 cmH2O transpulmonary pressure (PL) for air and at 4, 6, and 8 cmH2O PL for saline-filled lungs; specific lung compliance (CL) values obtained from both air and saline V-P curves were significantly reduced, and concentration of hydroxyproline relative to DNA was significantly increased. In adult diabetic rats, V-P curves expressed in %MLV, CL values, and concentrations of protein and hydroxyproline were similar to those in adult control rats. We conclude that in both young and adult rats, diabetic state leads to somatic and lung growth retardation. In addition in young diabetic rats lung distensibility is decreased. An increase in the concentration of some connective tissue proteins may be responsible for the latter observation.     

黑水虻幼虫的耐饥力及饥饿幼虫复食后的生物学特性

【目的】旨在明确黑水虻Hermetia illucens幼虫的耐饥力及饥饿幼虫复食后的发育、生殖力等生物学特性,为评估饥饿对黑水虻后续发育的影响并指导生产实践提供依据。【方法】将不同日龄或不同体重黑水虻幼虫进行不同时长的饥饿处理,测定和分析其耐饥力与日龄、百头重的关系;对7日龄幼虫进行不同时长的饥饿处理后再复喂,测定不同饥饿时长对其预蛹出现时间、总预蛹率、预蛹重、成虫繁殖等的影响。【结果】黑水虻幼虫饥饿后的半数致死时间(LT₅₀)与日龄成指数关系,与体重呈线性相关。7日龄幼虫的耐饥力较强,LT₅₀超过了50 d,饥饿30 d时存活率仍然达到了95%。百头重小于0.5 g的个体,其LT₅₀小于30 d;百头重在2～2.5 g的个体,其LT₅₀在45～70 d。幼虫超过8日龄时或百头重超过4.5 g时,多数个体在饥饿5 d时就提前进入了后续发育阶段。7日龄幼虫饥饿40 d内复食,其预蛹率未受到影响,但预蛹重显著增加;短期饥饿(0～10 d)对其成虫产卵量无显著影响,长期饥饿(30～40 d)使其成虫产卵量显著下降;饥饿长达30 d以上时,卵孵化率也显著降低。【结论】本研究明确了不同体重或不同日龄的黑水虻幼虫都具有一定的耐饥力;饥饿幼虫复食后预蛹重显著增加。     

The effect of starvation and refeeding on lipogenic enzymes in mammary glands and livers of lactating rats.

Lactating rats were starved for 48 h and refed a high-carbohydrate diet for a further 48 h. Starvation stops milk secretion, which resumes shortly after refeeding. Three lipogenic enzymes, fatty acid synthase, glucose 6-phosphate dehydrogenase (EC 1.1.1.49) and 'malic' enzyme (EC 1.1.1.40) all decrease in the mammary gland during starvation and are restored to the pre-starvation levels 48 h after refeeding. The same enzymes in liver also decrease during starvation, but increase to values significantly higher than those for the normal fed rats after refeeding the high-carbohydrate diet. For the fatty acid synthase these values were four times the pre-starvation values. Serum insulin and prolactin concentrations also increased upon refeeding the high-carbohydrate diet.     

Recovery growth following periods of restricted rations and starvation in rainbow trout Salmo gairdneri Richardson

Fingerling rainbow trout (6.9 to 11.6 cm fork length) maintained at 12° C were either: fed restricted rations (3% of dry body weight/day) for 16 weeks, or starved for 3 weeks (14.5% weight loss), or for 13 weeks (32.5% weight loss). Whole body wet weights and dry weights (as % of wet weight), and wet and dry weights of tissues (heart, spleen, liver, skin, gonad, gut, visceral fat, and 'carcase') resulting from these treatments were compared to corresponding weights of an 'initial sample'. Visceral fat was completely utilized during both short and long-term starvation and gut was significantly reduced in the extended starvation group.
During subsequent recovery growth on full rations, following food deprivation, fish grew at approximately the same rate as fully-fed controls, which had not suffered food deprivation, as regards body wet weight and condition ( K ), but tended to surpass controls in % dry weight.
Heart, liver, gonad, gut and visceral fat also increased during recovery growth in a manner suggestive of overcompensation in response to former food deprivation. Gut, skin and carcase dry weights were less in the control, and in the 14.5% weight loss groups following recovery growth than in those in 3% rations and in the severely starved group, indicating that the effects of slow growth resulting from limited rations resemble those of severe starvation more than those of limited starvation.     

The Liver Cells in Acute Starvation and Refeeding

A series of 52 young male white laboratory mice were starved for a maximum of five days, and 45 normally fed animals were used as controls. A group of experimental animals and a corresponding control group were sacrificed after two, three, and four days' starvation and after six, 12 and 17 days' refeeding. Even after two days the animals had lost weight, and the liver cells had diminished highly significantly. A return to the initial values was noted after 12 days' refeeding. In the experimental animals a strong negative correlation was noted between the cell count per field and body weight (r =–0.712, b =–7.520), while no such correlation was observed for the controls. The volume of the liver cells was reduced by 61.7 %, the volume of their nuclei by 16.2 % after four days' starvation. After two to three days' starvation the liver cells often showed a slight accumulation of fat. Mitoses were frequent in the liver cells during the stage of regeneration, when the cells had attained the same size as in the controls.     

Defense of body weight against chronic caloric restriction in obesity-prone and -resistant rats

Half of Sprague-Dawley rats develop and defend diet-induced obesity (DIO) or diet resistance (DR) when fed a high-energy (HE) diet. Here, adult male rats were made DIO or DR after 10 wk on HE diet. Then half of each group was food restricted for 8 wk on chow to maintain their body weights at 90% of their respective baselines. Rate and magnitude of weight loss were comparable, but maintenance energy intake and the degree of sympathetic activity (24-h urine norepinephrine) inhibition were 17 and 29% lower, respectively, in restricted DR than DIO rats. Restricted DIO rats reduced adipose depot weights, plasma leptin, and insulin levels by 35%. Restricted DR rats reduced none of these. When fed ad libitum, both DR and DIO rats returned to the body weights of their respective chow-fed phenotype controls within 2 wk. This was associated with increased adipose mass and leptin and insulin levels only in DIO rats. Thus DR rats appear to alter primarily their lean body mass, whereas DIO rats primarily alter their adipose mass during chronic caloric restriction and refeeding.     

Heterogeneity of glycogen synthesis upon refeeding following starvation.

1. Starvation of rats for 40 hr decreased the body weight, liver weight and blood glucose concentration. The hepatic and skeletal muscle glycogen concentrations were decreased by 95% (from 410 mumol/g tissue to 16 mumol/g tissue) and 55% (from 40 mumol/g tissue to 18.5 mumol/g tissue), respectively. 2. Fine structural analysis of glycogen purified from the liver and skeletal muscle of starved rats suggested that the glycogenolysis included a lysosomal component, in addition to the conventional phosphorolytic pathway. In support of this the hepatic acid alpha-glucosidase activity increased 1.8-fold following starvation. 3. Refeeding resulted in liver glycogen synthesis at a linear rate of 40 mumol/g tissue per hr over the first 13 hr of refeeding. The hepatic glycogen store were replenished by 8 hr of refeeding, but synthesis continued and the hepatic glycogen content peaked at 24 hr (approximately 670 mumol/g tissue). 4. Refeeding resulted in skeletal muscle glycogen synthesis at an initial rate of 40 mumol/g tissue per hr. The muscle glycogen store was replenished by 30 min of refeeding, but synthesis continued and the glycogen content peaked at 13 hr (approximately 50 mumol/g tissue). 5. Both liver and skeletal muscle glycogen synthesis were inhomogeneous with respect to molecular size; high molecular weight glycogen was initially synthesised at a faster rate than low molecular weight glycogen. These observations support suggestions that there is more than a single site of glycogen synthesis.     

Effects of pulmonary surfactant and surfactant protein A on phagocytosis of fractionated alveolar macrophages: relationship to starvation.

Pulmonary surfactant isolated from bronchoalveolar lavage fluid of rat lung contained a high content of surfactant protein A (SP-A) in starved for 2 days compared to fed controls, but this phenomena returned to baseline following more than 4 days starvation. As determined by immunoperoxidase staining of lung sections using SP-A antibody, SP-A could be consistently observed in nonciliated bronchiolar (Clara) cells, alveolar type II cells and some alveolar macrophages (AM). Fc receptor-mediated phagocytosis of AM was enhanced by SP-A, which was dependent on the dosis and reached a maximum at 10 micrograms of SP-A/ml. Antibody to SP-A completely inhibited the enhanced response of phagocytosis. When exposed AM subpopulations, separated into four fractions (I, II, III and IV) by discontinuous Percoll gradient, to SP-A or pulmonary surfactant prepared from rats fed and starved for 2 days enhanced their phagocytic activity in high dense cells (III and IV), particularly to SP-A and pulmonary surfactant from rats starved for 2 days. Whereas little change in lower dense fractions (I and II) were seen in all exposures except for SP-A that enhanced the cells of fraction II. These results supported the concept that pulmonary surfactant and its apoprotein, SP-A, are a factor to regulate lung defense system including activation of AM that undergo different processes following starvation.     

Changes in lung lysyl oxidase activity in streptozotocin-diabetes and in starvation.

The effects of streptozotocin-induced diabetes and of starvation on the lysyl oxidase activity of rat lung were investigated. Enzyme activity was elevated 2--3 fold in the lungs of streptozotocin-diabetic rats. In contrast, starvation of rats produced a rapid loss of lung lysyl oxidase activity, with levels approximating 25% of control values after 48--72 h of starvation. Enzyme activity was essentially fully restored to control values upon refeeding the 48-h starved animals for 3 h. These studies demonstrate the responsiveness of lysyl oxidase to these physiological states and suggest a component, enzymatic basis of change in lung function known to occur in the diabetic state.     

Changes in lung lysyl oxidase activity in streptozotocin-diabetes and in starvation

The effects of streptozotocin-induced diabetes and of starvation on the lysyl oxidase activity of rat lung were investigated. Enzyme activity was elevated 2–3 fold in the lungs of streptozotocin-diabetic rats. In contrast, starvation of rats produced a rapid loss of lung lysyl oxidase activity, with levels approximating 25% of control values after 48–72 h of starvation. Enzyme activity was essentially fully restored to control values upon refeeding the 48-h starved animals for 3 h. These studies demonstrate the responsiveness of lysyl oxidase to these physiological states and suggest a component, enzymatic basis of change in lung function known to occur in the diabetic state.     

Lysosomal enzyme activities in muscle following starvation and refeeding in the saithe Pollachius virens L

Saithe (Pollachius virens L.) were starved for 66 days at 10 degrees C and activities of aryl sulfatase, acid proteinase, beta-glucuronidase, RNAase and acid phosphatase measured in homogenates prepared from fast and slow myotomal muscles. In fed fish, hydrolase activities were generally higher in slow than fast muscles. With the exception of acid proteinase activity in slow muscle, the activities of all the lysosomal enzymes increased by 70 to 100% during starvation. In general, there was a proportionally larger increase in the hydrolase activities in fast than in slow muscle. In a second experiment, fish were starved for 74 days, and refed for up to 52 days. The increases in aryl sulfatase and acid proteinase activity produced in fast muscle with starvation were found to be rapidly reversed by refeeding. Lysosomal enzyme activities in fish sampled after 10 days refeeding were not significantly different from fed controls. Membrane fractions enriched in aryl sulfatase activity were prepared from the fast muscle of 66-day starved fish. These were capable of degrading both myosin heavy chains and actin to lower molecular weight peptides at acid (pH 5.0), but not at neutral pH. The results suggest a role for lysosomal enzymes in the breakdown of myofibrillar proteins during starvation.     

Effect of starvation and refeeding on autophagy and heterophagy in rat liver

Increase in the density of liver lysosomes after leupeptin administration was marked in starved rats but only slight in starved-refed rats. The levels of several intracellular enzymes in the liver lysosome fraction purified from leupeptin-treated rats were about 10 to 30 times more in starved rats than in refed rats. However, there was no difference between the intralysosomal levels of endocytosed FITC-labeled asialofetuin in starved and refed rats, indicating that refeeding after starvation markedly suppressed autophagy but not heterophagy in vivo. Immunohistochemical studies with cathepsin B and asialofetuin Fab'-peroxidase conjugates showed that refeeding after starvation markedly altered the cellular distribution of cathepsin B in the liver, resulting in a linear arrangement of the enzyme only on the periphery of hepatocytes. In contrast, endocytosed asialofetuin was found only in the periphery of hepatocytes of both starved and starved-refed rats. These results indicate that autophagy and heterophagy are regulated by different mechanisms in vivo.