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PubMed1978

Muscle metabolism during exercise in diabetics and in obese during starvation.

The influence of exercise on forearm muscle metabolism was examined in 9 healthy subjects, in 16 diabetics and in 4 obese subjects during complete starvation. During exercise glucose uptake rose 7-8 fold in the controls. However, no increase of glucose uptake was observed in the other groups studied. Moreover, a glucose production from the working muscle took place in about 40 percent of both the diabetic patients and the starved obese subjects. The nonutilization of glucose during physical work in the diabetic like states was accompanied by a significantly diminished lactate output. The arterial concentration of FFA, glycerol beta-HOB and Acac was markedly elevated in the starved obese patients. The FFA-uptake at rest and during exercise, however, was not different from results of controls. Whereas an effux of beta-HOB has been observed during exercise, Acac uptake was increased in these patients. It is suggested that in maturity onset and starvation diabetes glycolysis is inhibited.

Adult↗
PubMed1988

Body weight and tissue composition in rats made obese by a cafeteria diet. Effect of 24 hours starvation.

Rat body size and tissue composition changes from pre-weaning to three months age resulted from voluntary hyperphagia triggered by offering a cafeteria diet. The effects of a 24 hour starvation period in both cafeteria and chow fed controls were compared. Obesity develops earlier in females than in males. This difference is related to the growth patterns in both sexes. Obesity occurs at the stages of development when growth rate decreases. Cafeteria fed female rats attained a 32% greater weight than their controls, with lumbar adipose cords that were 4 times heavier and brown interscapular adipose tissue 2 times heavier than controls. The overall cafeteria fed versus chow fed rat differences in the effects of a 24 hour starvation, were minor but less liver glycogen and much more skeletal muscle lipids were mobilized in the cafeteria fed rats than in controls.

Adipose Tissue↗
PubMed1987

Acute starvation affects rat adrenal steroidogenesis.

To determine how starvation affects adrenal steroidogenesis we measured the activities of 3 adrenal enzymes involved in corticosterone biosynthesis in a group of adult female rats. The animals were either starved for 7 days or fed ad libitum for the same period. Relative adrenal weight and plasma corticosterone levels were increased in the experimental group of animals compared to the control group (40 +/- 2 vs 27 +/- 1 mg/100 g body weight, P less than 0.001, and 45 +/- 4 vs 30 +/- 5 ng/dl, P less than 0.05 respectively). There were no differences in plasma ACTH levels between the groups (34 +/- 5 vs 26 +/- 4 pg/ml). 11-Hydroxylase activity was increased in the starved group of animals (18 +/- 3 vs 8 +/- 2 nmol/mg protein/min, P less than 0.01). 3 beta-Hydroxysteroid dehydrogenase and 21-hydroxylase activities were not different between the groups (19 +/- 2 vs 16 +/- 1 nmol/mg protein/min, and 100 +/- 10 vs 110 +/- 10 pmol/mg protein/min respectively). These results suggest that acute starvation in rats produces an increase in adrenal 11-hydroxylase activity.

3-Hydroxysteroid Dehydrogenases↗
PubMed1984

Starvation-induced secretory changes of insulin, somatostatin, and glucagon and their modification by 2-bromostearate.

The hypothesis was made of an increased oxidation of fatty acids (FFA) and a decrease of their esterification rate contributing to the islet secretory defect during starvation. 2-Bromostearate (BrS), a FFA-oxidation inhibitor, was therefore tested on the islet secretion of insulin, glucagon and somatostatin stimulated by glucose or palmitate under fasted or fed conditions. Starvation for 48 h blocked both the glucose-induced stimulation and inhibition of insulin and somatostatin and the glucagon secretion. BrS completely restored the insulin response and stimulated both somatostatin and glucagon-basal release, the latter inhibition by glucose being partially recovered. Palmitate transient stimulation of insulin and somatostatin and inhibition of glucagon release was turned into a sustained increase in all three cases by addition of BrS. The potentiation by BrS of palmitate secretory effects in "fed" islets and of hormone release in "fasted" islets, apparently suggest that inhibition of FFA-oxidation may play a role in the regulation of islet secretion.

Animals↗
PubMed1982

Effect of starvation on somatostatin content of pancreas and gastrointestinal tract of the guinea pig.

The effect of 48-hour starvation on the somatostatin contents of the pancreas and gastrointestinal tract was studied in the guinea pig. Somatostatin contents were higher in various portions of the stomach and pancreas of fed guinea pigs than in fed rats and unchanged after 48-hour starvation, in spite of the decreased blood glucose level. These results suggest that somatostatin may not play the same physiological role in nutrient homeostasis of guinea pigs as it does in other species.

Animals↗
PubMed1982

Starvation increases gastrointestinal somatostatin in normal and obese Zucker rats: a possible regulatory mechanism.

Normal, male Sprague-Dawley (S-D) rats and female, lean and obese Zucker rats were studied in the fed state and after 48 hours of food deprivation. Somatostatin-like immunoreactivity (SLI) was measured from acetic acid extracts of oesophagus-cardia, stomach, small and large intestine, pancreas, hypothalamus, pituitary and cerebellum. Within the CNS, the highest levels of SLI were found in the hypothalamus, while in the gut, these levels were highest in the stomach and pancreas. All Zucker rats displayed higher hypothalamic levels of SLI than did S-D rats. Obese Zucker rats in the fed state differed from their lean littermates in that SLI levels were lower in oesophagus-cardia, stomach and hypothalamus, while being higher in pancreas and pituitary. The response to starvation in both obese and lean Zucker rats was qualitatively similar, and included significant increases in stomach and oesophagus-cardia SLI, but with a significant fall hypothalamic SLI. We have concluded that the increase in gastrointestinal SLI with starvation in Zucker as well as in S-D rats may represent a significant regulatory mechanism in nutrient homeostasis. We postulate that gastric SLI may decrease the availability of intestinal insulin secretagogues in the fasting state. This adaptive mechanism appears to be intact in the obese Zucker rat.

Animals↗
PubMed1982

Degradation of intra- and extrahepatic protein by livers of normal and diabetic mice: differential responses to starvation.

Rates of total hepatic proteolysis were measured in normal and streptozotocin-diabetic mice during feeding and over 48 hr of starvation, during which livers in the two groups lost 37% and 54% of their protein content, respectively. Measurements were made in 15-min in situ cyclic perfusions from the linear accumulation of free valine in the presence of cycloheximide; rates were corrected for turnover of short-lived proteins because these components contribute negligibly to alterations in liver protein content. During deprivation, corrected rates, expressed on a per liver basis, remained constant in normal mice but increased markedly in the diabetic group, attaining twice prestarvation values by 48 hr. By contrast, degradation rates of long-lived intracellular proteins, calculated from the sum of their synthesis and the linear decrease in protein content, decreased predictably in both groups and in parallel with absolute rates of protein synthesis. The extra proteolysis, representing the difference between total and long-lived protein degradation, was small in fed animals but increased progressively during starvation. With diabetic mice, however, the increase was approximately 5 times that of the normal and, in absolute terms, roughly equaled the total loss of liver protein. We suggest that this fraction arose from intrahepatic breakdown of proteins that were ultimately derived from sources outside the liver. Acceleration of this novel process could play an important interim role in providing endogenous glucogenic substrate under conditions in which the demand for this substrate is high.

Animals↗
PubMed1998

Peroxisome proliferator-activated receptor alpha controls the hepatic CYP4A induction adaptive response to starvation and diabetes.

The hepatic CYP4A enzymes are important fatty acid and prostaglandin omega-hydroxylases that are highly inducible by fibric acid hypolipidemic agents and other peroxisome proliferators. Induction of the CYP4A enzymes by peroxisome proliferators is mediated through the nuclear peroxisome proliferator-activated receptor alpha (PPARalpha). Fatty acids have recently been identified as endogenous ligands of PPARalpha, and this receptor has been implicated in the regulation of lipid homeostasis. In the present report we characterized the induction of the hepatic CYP4A genes in rats during the altered lipid metabolism associated with starvation and diabetes. The mRNA levels of CYP4A1, CYP4A2, and CYP4A3 were induced 7-17-fold in the livers of fasted animals and 3-8-fold in the livers of diabetic animals. This was accompanied by corresponding changes in CYP4A protein levels and arachidonic and lauric acid omega-hydroxylase activity. Interestingly, feeding animals after the fasting period caused as much as an 80% suppression of CYP4A mRNA levels, whereas CYP4A protein levels and functional activity returned to control values. A second PPARalpha-responsive gene, acyl-CoA oxidase, was also induced in rat liver by diabetes and fasting. By using PPARalpha-deficient mice, we unambiguously demonstrated that PPARalpha is strictly required for hepatic CYP4A induction by starvation and diabetes. Similarly, induction of hepatic thiolase and bifunctional enzyme also required expression of PPARalpha. This represents the first evidence for the pathophysiologically induced activation of a nuclear receptor.

3-Hydroxyacyl CoA Dehydrogenases↗
PubMed2001

Starvation promotes nuclear accumulation of the hsp70 Ssa4p in yeast cells.

Nuclear import of proteins that are too large to passively enter the nucleus requires soluble factors, energy, and a nuclear localization signal (NLS). Nuclear protein transport can be regulated, and different forms of stress affect nucleocytoplasmic trafficking. As such, import of proteins containing a classical NLS is inhibited in starving yeast cells. In contrast, the hsp70 Ssa4p concentrates in nuclei upon starvation. Nuclear concentration of Ssa4p in starving cells is reversible, and transfer of stationary phase cells to fresh medium induces Ssa4p nuclear export. This export reaction represents an active process that is sensitive to oxidative stress. In starving cells, the N-terminal domain of Ssa4p mediates Ssa4p nuclear accumulation, and a short hydrophobic sequence, termed Star (for starvation), is sufficient to localize the reporter proteins green fluorescent protein or beta-galactosidase to nuclei. To determine whether nuclear accumulation of Star-beta-galactosidase depends on a specific nuclear carrier, we have analyzed its distribution in mutant yeast strains that carry a deletion of a single beta-importin gene. With this assay we have identified Nmd5p as a beta-importin required to concentrate Star-beta-galactosidase in nuclei when cells enter stationary phase.

Cell Nucleus↗
PubMed2002

Circadian modulation of starvation-induced hypothermia in sheep and goats.

Prolonged food deprivation is known to cause a fall in the core body temperature of homeotherms. In various species of small birds and mammals (body mass up to 2-3 kg), it has been shown that starvation-induced hypothermia is modulated by the circadian system, in the sense that hypothermia is observed primarily during the inactive phase of the daily activity cycle (i.e., during the night for diurnal animals and during the day for nocturnal animals), whereas relatively normal temperatures are recorded during the active phase. To investigate whether this modulation occurs also in larger animals, we investigated the effects of 4 d food deprivation on the body temperature rhythm of goats and sheep (body mass 30-40 kg). In goats, the body temperature rhythm was found to have a mean level of 39.0 degrees C with a mean daily range of excursion of 0.42 degrees C. The daily oscillation in body temperature persisted during the first day of fasting, but the rhythm was drastically damped, if not eliminated, over the next 3 d as body temperature descended from the baseline level of 39.0 to 38.2 degrees C. In sheep, the rhythm was found to have a mean level of 39.3 degrees C with a mean daily range of excursion of 0.34 degrees C. The daily oscillation in body temperature persisted through the 4 d of food deprivation, even though the mean level of body temperature gradually fell. Temperature fell more during the third and fourth nights than during the third and fourth days. Thus, circadian modulation of starvation-induced hypothermia was observed in sheep but not in goats.

Animals↗
PubMed1957

The cell in starvation; physiological and chemical observations.

Observations made on Amoeba proteus during total inanition revealed the following changes: Dry weight declined progressively, but at a decreasing rate to about 45 per cent of the initial levels when determined in surviving members of a dying population. Protein fell to about 70 per cent of the initial level. A hexane-alcohol extractable component fell during early starvation then rose to about its initial absolute level in the dying cells. While initially most of this component is probably lipide, it is not certain that other materials are not extracted during cell degeneration. Survival as a function of cell size was studied. No advantage in survival was apparent for any size class. Nucleate cell "halves" likewise showed no survival time differential, unlike a highly significant decrease in the survival of enucleate portions. The maintenance of the initial variance about the mean population weight (after hexane-alcohol extraction) during starvation, likewise supports the idea that survival depends largely on concentration parameters.

Amoeba↗
PubMed1958

The influence of age, sex, pregnancy, starvation, and other factors on the cytoplasmic ribonucleoproteins of rat liver.

Rat liver was homogenized in 0.88 M sucrose. The DNA and total RNA were determined, and the homogenate was fractionated by differential centrifugation. The pellets obtained between 30 minutes at 20,000 g and 180 minutes at 105,000 g were analyzed for RNA and nitrogen. The ribonucleoproteins were determined in the analytical ultracentrifuge. The non-pellet RNA was calculated by difference. The results are reported as amounts per 6.7 x 10(-9) mg. of DNA. In young, growing male rats the amounts of microsomal protein and ribonucleoprotein B (83S) increased with age. Non-pregnant adult females showed less non-pellet RNA and much more ribonucleoprotein C (63S) than did adult males. During pregnancy both of these cell constituents reverted to levels characteristic for male animals. Starvation for 5 days resulted in a reduction in the mass of liver tissue, the non-pellet RNA, the microsomal protein, and ribonucleoproteins B and C. During recovery from starvation the return of the liver to normal paralleled the rate at which body weight was restored. Treatment with cortisone, 25 mg. per rat per day for 5 days, caused an increase in microsomal protein and a decrease in ribonucleoprotein B. Treatment with 6-mercapto-purine, 50 mg. per kilo per day for 5 days, caused little change in liver composition in either males or females.

Animals↗
PubMedDate not supplied

Changes in blubber distribution and morphology associated with starvation in the harbor porpoise (Phocoena phocoena): evidence for regional differences in blubber structure and function.

To examine patterns of blubber loss accompanying a decline in body condition, blubber thickness of juvenile harbor porpoises in normal/robust body condition (n=69) was compared with that of starved conspecifics (n=31). Blubber thickness in the thorax of starved porpoises (9-11 mm) was only 50%-60% of that of normal animals (18-20 mm); however, very little tailstock blubber was lost during starvation. Adipocytes in thorax and tailstock blubber were measured in both groups (n=5) to determine whether thickness changes were homogeneous throughout blubber depth. In the thorax of normal porpoises, adipocytes near the epidermis (outer blubber) were smaller (0.11 nL) than inner blubber adipocytes (0.17 nL). Conversely, the size of tailstock adipocytes was uniform. Starved animals had fewer, smaller adipocytes in the inner thorax blubber, suggesting a possible combination of adipocyte shrinkage and loss. Lipids were withdrawn only from the inner layer of thorax blubber during starvation, supporting a hypothesis of regional specialization of function in blubber. Blubber of the thorax serves as the site of lipid deposition and mobilization, while the tailstock is metabolically inert and likely important in locomotion and streamlining. Therefore, some proportion of the blubber of small odontocetes must be considered structural/mechanical rather than an energy reserve.

Adipocytes↗
PubMed1989

Acute diaphragmatic changes induced by starvation in rats.

The aim of this study was to assess in an in vivo rat model the effects of total starvation for 4 d on diaphragmatic strength and endurance. Twenty-four rats were divided equally into a control (CTL) group and a starved (ST) group. Diaphragmatic strength was assessed and endurance index was calculated. Starvation induced a parallel decrease in body weight and diaphragmatic weight amounting to 18% of the control group. Diaphragmatic contractility was impaired in the ST group. This reduction was associated with a significant reduction in transdiaphragmatic pressure (Pdi) for all the frequencies of stimulation, except 20 Hz, in the ST animals as compared with the CTL animals; however, no significant difference in Pdi expressed per gram of diaphragmatic mass was observed. Endurance index was 0.63 +/- 0.01 1.4 +/- 0.02 in the ST and CTL animals (p less than 0.01), respectively. We conclude that a 4-d total fast produces a reduction in diaphragmatic weight, which is associated with a decreased diaphragmatic strength and reduced endurance capacity.

Animals↗
PubMed1990

Refeeding after fasting in rats: effects of duration of starvation and refeeding on food efficiency in diet-induced obesity.

Rats with diet-induced obesity starved for 8, 15, and 25 d lost liver and muscle glycogen, excess protein, and fat in proportion to duration of starvation. Fat-cell size decreased but fat-cell number did not. Upon refeeding, body fat was only partly restored, with further increase in adipocyte hyperplasia occurring in the starved obese rats. In contrast, fat-cell size was restored to near that of the prefasting value in the starved controls (dry-food-fed, fasted 4 d) after refeeding. With refeeding, food efficiency increased only if starvation had caused a reduction of adipocyte size below normal. Change in food efficiency was not associated with decreases in total carcass protein, specific tissue proteins, or glycogen stores but was correlated with degree of adipocyte filling. It is possible that adipose tissue status somehow modulates energy-dissipating mechanisms.

Adipose Tissue↗
PubMed1979

Interaction of glucocorticoid and insulin in the responses of rats to starvation-refeeding.

Experiments designed to determine whether the role of glucocorticoid (GC) in the induction of the enzyme overshoot response to starvation-refeeding was direct or permissive through insulin were conducted. Intact, adrenalectomized (ADX), and streptozotocin (STREP) treated rats with or without insulin and/or GC replacements were starved for 48 hours and refed a 65% glucose diet for 48 hours. The typical enzyme overshoot response to starvation-refeeding was observed in the intact rats, ADX rats given GC, STREP rats given insulin and ADX-STREP rats given glucocorticoid plus insulin. No overshoot was observed if glucocorticoid was absent whereas a modest increase in enzyme activity could be observed in insulin deficient rats treated with GC.

Adrenal Glands↗
PubMed1979

Effect of prolonged starvation on substrate uptake in the isolated perfused rat heart.

The pattern of substrate uptake by the heart in prolonged starvation, when lipid reserves are approaching depletion, has been examined. The classical Langendorff perfused heart preparation was employed to determine substrate uptakes in male rats fed ad libitum or starved for 7 days. Levels of metabolites in "arterial" and "venous" perfusion media and in heart tissue were determined by fluoroenzymatic assays, with the exception of palmitic acid which was analyzed by gas chromatography. It was found that glucose is the principal fuel of oxidation in perfused hearts of ad libitum-fed rats, whereas palmitate (FFA) is the major fuel of oxidation in perfused hearts of starved rats, followed by lactate, glucose, beta-hydroxybutyrate, pyruvate and alanine. Such changes might be related to some of the alterations in the metabolic pathway (e.g., glycolytic inhibition) in prolonged starvation.

Amino Acids↗
PubMed1980

Effects of prolonged starvation on plasma free fatty acid levels and fatty acid composition of myocardial total lipids in the rat.

Experiments were carried out on male rat fed ad libitum or starved for a period of 7 days. Plasma levels of free fatty acids (FFA) and the quantity and composition of fatty acids in total lipids of heart ventricular tissue in vivo were analyzed by gas liquid chromatography (GLC). In addition, FFA extraction ratios and uptake rates were determined in isolated perfused hearts using the classical Langendorff technique. After 7 days of starvation, distribution and concentrations obtained for total lipid fatty acids from heart ventricles of starved animals were substantially different from those of controls. In particular, 20:5 and 22:6 carbon polyunsaturated fatty acids were significantly elevated. Also, total plasma FFA level was elevated and FFA extraction ratios were increased as a result of prolonged starvation. Accumulation of 20- and 22-carbon polyunsaturated fatty acids observed in ventricles of starved rats may have resulted from increased availability and extraction of FFA.

Animals↗