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Query: UMLS:C0038187 (starvation)
 24,951 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In animals the pyruvate dehydrogenase reaction is mainly responsible for the irreversible loss of glucose carbon by oxidation. Regulation of this reaction is shown to be a major determinant of glucose conservation in starvation and diabetes. Estimates of conservation in man in starvation and diabetes are reviewed. The pyruvate dehydrogenase complex is inhibited by products of its reactions; it is also regulated by a phosphorylation-dephosphorylation cycle catalysed by a kinase intrinsic to the complex and by a more loosely associated phosphatase. Inactivation is largely accomplished by phosphorylation of the tetrameric decarboxylase component (alpha2beta2) to alpha2Pbeta2. Complete phosphorylation produces the (alpha2P3)beta2 form. Both forms are completely reactivated by phosphatase action but the initial rate of reactivation of a complex containing alpha2Pbeta2 is approximately three times that of (alpha2P3)beta2. The proportion of active (dephosphorylated) complex is decreased in rat tissues by starvation and diabetes and in perfused rat heart by oxidation of fatty acids and ketone bodies. In adipose tissue in vitro, insulin increases the proportion of active complex and lipolytic hormones may decrease this proportion. It is suggested that rates of oxidation of lipid fuels may be a major determinant of the activity of pyruvate dehydrogenase in tissues in relation to the actions of insulin and lipolytic hormones and the effects of diabetes and starvation. Phosphorylation and inactivation of the complex are enhanced by high mitochondrial ratios of [acetyl-CoA]/[CoA], [ATP]/[ADP], [NADH]/[NAD+] and low concentrations of pyruvate, Mg2+ and Ca2+, and vice versa.
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PMID:Regulation of pyruvate oxidation and the conservation of glucose. 37 69

A 24-h starvation markedly diminished the stimulant action of 8 mM glucose on insulin secretion from isolated perifused rat islets of Langerhans. The response to a supramaximal glucose stimulus (27.5 mM) remained normal, but prolonged fasting (48 or more) also reduced its efficacy. Refeeding of 24-h fasted animals resulted in complete restoration of glucose sensitivity within 24 h. The responses to glyceraldehyde (2 mM) and alpha-ketoisocaproate (8 mM) at concentrations which elicit approximately half-maximal stimulation were unaltered by a 24-h fast, while that to a half-maximally effective dose of mannose (15 mM) was decreased. Theophylline (5 mM) could not normalize the reduced secretory response to glucose seen in this state. The islets' ability to metabolize glucose, using various in vitro pretreatment protocols and different incubation times, was not affected by a 24-h fast. Mannose and glyceraldehyde metabolism were also unaltered. Prolonged fasting (48 h) reduced glucose metabolism by 25% at both 8 and 27.5 mM. The acute adaptive changes in islet sensitivity to moderate glucose and mannose concentrations during short term fasting (24 h) cannot be explained by an altered usage of the added hexoses.
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PMID:Starvation diabetes in the rat: onset, recovery, and specificity of reduced responsiveness of pancreatic beta-cells. 37 69

Mammalian pregnancy is characterized by progressive hyperinsulinaemia, raised plasma lipids and increased vulnerability to ketosis after food deprivation. The present investigations were performed to assess the role of two placental steroids, oestradiol and progesterone, in the development of these changes, since plasma titres of these hormones progressively increase during human gestation. In both human subjects and adult female rats it was demonstrated that these two steroids, separately or in combination, augment plasma insulin concentration in vivo, cause hypertrophy of pancreatic islets and promote exaggerated secretion of insulin, but not glucagon, by pancreatic islets in vitro. Hypertriglyceridaemia induced by oestrogen alone or combined with progesterone was associated with increased splanchnic production of triglyceride as well as altered tissue lipoprotein lipase (EC 3.1.1.34) and circulating apoproteins that influence activity of this enzyme. The combined regimen also increased hepatic glycogen storage and suppressed gluconeogenesis in vivo in the rat while accelerating the onset of ketosis during starvation in human subjects and in the animal model. Oestradiol and progesterone appear to effect metabolic changes in nonpregnant animals and human subjects that simulate maternal adaptations to advancing gestation, including altered endocrine pancreatic function, triglyceride metabolism and metabolic fuel storage and mobilization.
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PMID:The influence of hormonal changes of pregnancy on maternal metabolism. 37 20

Abomasal secretion has been collected from Grosskopftype pouches prepared in five adult Karrakul ewes. Feeding caused a marked increase in volume, acidity and pepsin activity, whereas these factors were reduced by starvation. Both insulin-induced hypoglycaemia and electrical stimulation of the vagal nerve supply to the pouch increased the volume, total acid and pepsin secretion. It is concluded that vagal activity is an important factor in the control of abomasal secretion in sheep.
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PMID:Neural and chemical control of abomasal secretion in sheep. 38

The effect of insulin on glucose entry has been studied in monolayer cultures of human diploid fibroblastic cells. Influence of insulin on total cell glucose incorporation was evaluated using [14C] glucose. Glucose incorporation was increased up to two-fold in the presence of insulin. Insulin action occurred within 30 minutes and could be observed with insulin concentrations as low as 10(-10) M (10 microU)ml). The action of insulin was enhanced by preincubation in glucose-free medium. After glucose starvation the cells converted glucose primarily to glycogen and nucleotides, and the stimulation by insulin was observed equally in both fractions. Influence of insulin on the kinetics of hexose transport was studied using 2-deoxyglucose and 3-0-methyl glucose. A large diffusion component was corrected using rho-chloromercuribenzoic acid or phloridzin. Km for facilitated diffusion averaged 1.9 mM for 2-deoxyglucose and 5.3 mM for 3-O-methyl glucose, and Vmax ranged from 10-24 nmoles/min/mg cell protein. Insulin resulted in a 150% increase in Vmax with no significant change in Km. The data suggest that human diploid fibroblasts can be a useful system for the study of insulin's glucoregulatory action.
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PMID:Insulin stimulation of glucose entry in cultured human fibroblasts. 39 2

The glycogen content of cultured chick embryo breast muscle cells changes during their development and can be reduced by starvation. It is demonstrated that the rate of glucose incorporation into glycogen and the degree of interconversion of glycogen synthase are controlled by the actual glycogen content. Stimulation of both corresponding activities by insulin is found in fused and in unfused cells. The insulin response depends on the extracellular calcium concentration and can be mimicked by the ionophore A 23187. These metabolic effects as well as calcium efflux data confirm the hypothesis that insulin acts on its enzyme target via increased cytoplasmic calcium concentration. Cytochalasin B is shown to inhibit the interconversion but does not interfere with the insulin-induced increase of the mitochondrial calcium pool or with the acceleration of the calcium efflux out of 45C-preloaded myotubes.
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PMID:Regulation of glycogen synthase interconversion in cultured muscle cells: actions of insulin, calcium, ionophore A 23187 and cytochalasin B. 40 13

Data are presented on the metabolic and endocrine effects of intravenous infusions in normal fasting man observed under highly controlled conditions over a period of six to eight days duration. There are comparative data on a variety of intravenous feeding programs. The data on total starvation are based on studies from the literature, some of which were carried out in this laboratory. The data on low dose glucose, high dose glucose, glycerol, fat emulsion, and amino acids, each given separately, demonstrate changes seen with simple infusion of a single substrate in fasting. These data are now compared with the utilization of amino acid infusions when accompanied by low dose glucose, high dose glucose, glycerol, and fat emulsion. In all, nine experimental intravenous feeding programs are presented, based on data from 35 subjects observed over a total of 370 subject-days. The findings show a strong interaction between glucose or lipid and protein metabolism. In fasting, glucose had protein sparing effect, most evident when given at high dose. Glycerol, in an amount equal to that contained in 2000 ml of ten per cent fat emulsion, had a mild protein sparing effect. Fat emulsion was no more effective. When amino acids were given alone, normal fasting human subjects were always in negative nitrogen balance with the daily nitrogen loss half that seen in starvation alone. Although amino acids given alone have a protein sparing effect, this is accomplished only at the expense of a high nitrogen excretion including an amount equivalent to the entire infusion plus an additional loss from the body's native proteins. The provision of energy yielding non-protein substrates with the amino acids markedly improved nitrogen economy in the following order: glycerol, low dose glucose, fat emulsion and high dose glucose. When caloric provision with glucose approached the isocaloric level for normal diet, the utilization of amino acids was maximized. When given with amino acids, fat emulsion was more effective than the available glycerol alone. THE ACCOMPANYING ENDOCRINE AND BIOCHEMICAL CHANGES SUGGEST THAT THE MILIEU FOR IDEAL UTILIZATION OF INFUSED AMINO ACIDS IS VARIABLE: ketones at low range (carbohydrate) or moderately elevated (fat emulsion); insulin elevated (carbohydrate) or unchanged (fat emulsion). The utilization of the infused amino acids was markedly improved in both endocrine settings, suggesting that it is the provision of energy as substrate as well as the endocrine setting that determines amino acid utilization. There were other changes in plasma intermediates, particularly fatty acids, glucose and urea, all consistent with the concept that when amino acids are given without other substrates, the amino acids must be maximally utilized for gluconeogenesis. When other substrates are provided (particularly glucose at high dose) then this mandate no longer exists and protein synthesis from the amino acids is favored. Several of the plasma amino acid concentrations responded to glucose when added to amino acid infusion. Amino acids alone produced increases in concentration of all the amino acids found in the infusion with the exception of alanine, arginine, and threonine. Many of these increases were abated by the addition of glucose to the amino acid infusion, suggesting an increased utilization rate. Glycerol and fat emulsion, while modulating increases in the plasma amino acid concentration, did so to a lesser extent than did glucose. This lowering of amino acid concentration was unaccompanied by an increase in urinary excretion. The assumption is therefore made that the provision of the added glucose favors the incorporation of amino acid into protein. There is no evidence from these data to suggest that a rising concentration of ketones in the blood favors amino acid utilization or protein synthesis.
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PMID:Substrate interaction in intravenous feeding: comparative effects of carbohydrate and fat on amino acid utilization in fasting man. 41 Mar 76

Long-term hyperinsulinemia and improved glucose tolerance were produced postoperatively by intravenous feeding with glucose or sorbitol. Raised immuno-reactive insulin (IRI) values persisted eight hours after carbohydrate infusions although the basal plasma glucose concentrations had returned to control values. Plasma glucose curves were normal at this time but were associated with an increased IRI response. These findings suggest that insulin secretion is modified by glucose not only in the short term but also by a separate effect acting over many hours. The combination of starvation and low dose glucose infusion to simulate the hyperglycemia of operation also produced high IRI values but these were associated with a rapid fall in the plasma glucose curve. Starvation alone reduced basal values of plasma glucose and IRI, and the IRI response to glucose infusion was also reduced, despite the plasma glucose curve being at a higher level. It is suggested that the high values of IRI reported in the postoperative period are mediated by a long-term effect of the small but sustained rise in basal plasma glucose. This specific role of glucose in the long-term potentiation of insulin secretion make it the carbohydrate of choice for the intravenous feeding in postoperative patients.
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PMID:Plasma insulin and surgery. II. Later changes and the effect of intravenous carbohydrates. 41 64

4 children with ketotic hypoglycemia (KH) showed during a fasting period over 24 hours significant higher decreases of serum alanine levels than normal controls. Insulin induced hypoglycemia was followed by only minimal increase of urine epinephrine secretion, while all controls showed more than 6 times higher increases. 2-desoxy-glucose-tests were pathological in all cases with KH. One can speculate, that there is a connection between the reduced availability of alanine and the adrenal medullary hyporesponsiveness. Epinephrine stimulates glycogenolysis in muscle cells. Lack of epinephrine reduces pyruvate production and subsequently alanine synthesis. Alanine however is essential for gluconeogenesis in liver cells especially during starvation. After some days administration of diazoxide the 2-desoxy-glucose-test was normalised in all patients. This observation could probably be of some interest in therapy of KH.
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PMID:[Pathogenesis of ketotic hypoglycemia (author's transl)]. 41 97

Physiological and behavioral responses of adult hamsters to starvation were studied by measuring food intake, weight recovery, serum concentrations of glucose, insulin, free fatty acids and beta-hydroxybutyrate, and ketonuria in animals subjected to different weight losses, diets, and durations of fast. Hamsters were debilitated by fasts longer than 12 h or leading to greater than 20% weight loss. Hamsters' feeding patterns were unmodified by fasts ranging between 5 and 12 h and showed no circadian periodicity. Hamsters predominantly recovered from weight losses without increasing their food consumption (unless they were offered a diet of pellets and seeds) and without changing their meal patterns, at a rate of weight gain proportional to the magnitude of preceding weight loss if provided with uninterrupted access to food. By 8 h of fast, blood metabolites were indicative of mobilization of body fat. Hamsters are thus behaviorally unresponsive to duration of fast, but compensate physiologically for weight losses with proportional increases in the rate of weight gain.
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PMID:Physiological and behavioral responses to starvation in the golden hamster. 42 Feb 82


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