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

Four patients from a larger group of 18 patients receiving dextrose-free isotonic (3%) amino acid solution as nutritional support, form the basis of this report. An additional seven patients received intravenous isotonic (5%) dextrose as their sole support in the postoperative period following major elective surgery (average nitrogen balance = -12.3 +/- 2.7 g). All patients were well-nourished as determined by anthropometric measurements. The nonseptic patients receiving infusions of isotonic amino acids demonstrated an improvement in nitrogen balance (= delta 8.5 +2, P less than 0.001) when compared to the postoperative use of 100 to 150 g of glucose. However, sepsis produced a decreased net utilization of the infused crystalline amino acids such that nitrogen balance was similar to the intravenous glucose group (- 10.6 +/- 2.1). This septic response was associated with decreased plasma free fatty acid concentrations and the absence of starvation ketosis and ketonuria. While the nitrogen balance was not different in the septic and the dextrose control groups, deficiencies in plasma amino acid concentrations were observed in the group receiving intravenous infusion of glucose.
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PMID:Effect of deep surgical sepsis on protein-sparing therapies and nitrogen balance. 40 78

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

Twenty-four chronic alcohol abusers hospitalized during a twenty-seven-month period were suspected of having "alcoholic ketoacidosis" because they had ketonuria or ketonemia with little or no glucosuria. Twenty-one had moderate or severe ketosis, with plasma 3-hydroxybutyrate of 5.2 to 22.5 mmol/L. Fifteen of this group were not diabetic, while six were later found to have mild postprandial hyperglycemia without glycosuria. Three patients who had continued to drink until shortly before admission, though at first suspected of having alcoholic ketosis, were found to have predominant lactic acidosis, with minor elevations of plasma 3-hydroxybutyrate. In contrast to previously reported patients with "alcoholic ketoacidosis", severe acidemia was uncommon in this series. Indeed, seven patients were alkalemic, because of coexisting respiratory or metabolic alkalosis. Most patients had eaten poorly for several days (and usually longer) and had allegedly decreased their alcohol intake during that period. That history, and the usual rapid clearing of ketosis simply by treatment with solutions of glucose and NaCl, suggested that acute starvation was an important factor in the pathogenesis of this disorder. Four patients were treated with insulin and four with NaHCO3 solutions. In retrospect, the need for either of these treatments was not clear. Two of the twenty-four patients died, one from circulatory failure secondary to hemorrhage and the other from pulmonary edema, but no patient died because of ketoacidosis per se.
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PMID:Alcoholic detosis. 80 36

We reviewed retrospectively a cohort of 80 patients with hyperemesis gravidarum hospitalized between 1976 and 1986 for the presence of abnormal liver enzymes and ketonuria. Thirteen (16%) had abnormal liver enzymes, generally less than four times the upper limit of normal. In this group, hyperemesis gravidarum began at the 14th week of pregnancy as compared to the 6th week in the normal enzyme group (p less than 0.01). Both groups were similar with regard to age, number of children and pregnancies, and duration of vomiting. Ketonuria was significantly more severe (p less than 0.01) in the abnormal enzyme group, implying a more severe state of starvation and dehydration. The correlation coefficient between the degree of ketonuria and level of liver enzymes was low for alkaline phosphatase (r = 0.18), GPT (r = 0.15), and GOT (r = 0.28). The concept that dehydration and starvation are important factors for the induction of liver cell injury is supported by our data. Lack of correlation between the degree of ketonuria and liver enzyme levels is suggestive of other mechanisms (hormonal, genetic) that may interact to produce transaminasemia.
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PMID:Abnormal liver enzymes and ketonuria in hyperemesis gravidarum. A retrospective review of 80 patients. 236 99

To study the influence of hypoglycaemia and starvation on mental functions eight healthy male students age 25-34 years with an ideal body mass of 99.9% +/- 2.5% (mean +/- SEM) were recruited. Hypoglycaemia was induced in random order by an insulin-glucose clamp technique (insulin: 2.4 mU/kg/min + glucose at variable rate) keeping the venous blood glucose at 2.2 mmol/l both after an overnight fast and after 72 h fasting. Mental alertness was assessed by measuring the recognition time, moving time and total reaction time to a visual signal and by a verbal mental clearness test and a synonym learning test during normo- as well as hypoglycaemia. Hypoglycaemia prolonged the total reaction time (p less than 0.05) and the time required for the mental clearness test (p less than 0.05). Compared with a control study performed at normoglycaemia the learning effect of the synonym test was reduced by hypoglycaemia. Fasting, which resulted in a body weight reduction of 2.6 +/- 0.3 kg and ketonuria prolonged the total reaction time (p less than 0.005) by increasing the moving time but did not affect the mental clearness test. When hypoglycaemia was preceded by 72 h fasting it did not increase the total reaction time, nor did it modify the mental clearness test. Moreover, the learning effect of the synonym test was less impaired. In conclusion, mental alertness was reduced by moderate hypoglycaemia after an overnight fast while similar hypoglycaemia did not reduce mental alertness after prolonged fasting. This may illustrate a decrease of the glucose dependency of the central nervous system during prolonged fasting.
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PMID:Mental alertness in response to hypoglycaemia in normal man: the effect of 12 hours and 72 hours of fasting. 331 61

During starvation for 72 h, tumour-bearing rats showed accelerated ketonaemia and marked ketonuria. Total blood [ketone bodies] were 8.53 mM and 3.34 mM in tumour-bearing and control (non-tumour-bearing) rats respectively (P less than 0.001). The [3-hydroxybutyrate]/[acetoacetate] ratio was 1.3 in the tumour-bearing rats, compared with 3.2 in the controls at 72 h (P less than 0.001). Blood [glucose] and hepatic [glycogen] were lower at the start of starvation in tumour-bearing rats, whereas plasma [non-esterified fatty acids] were not increased above those in the control rats during starvation. After functional hepatectomy, blood [acetoacetate], but not [3-hydroxybutyrate], decreased rapidly in tumour-bearing rats, whereas both ketone bodies decreased, and at a slower rate, in the control rats. Blood [glucose] decreased more rapidly in the hepatectomized control rats. Hepatocytes prepared from 72 h-starved tumour-bearing and control rats showed similar rates of ketogenesis from palmitate, and the distribution of [1-14C] palmitate between oxidation (ketone bodies and CO2) and esterification was also unaffected by tumour-bearing, as was the rate of gluconeogenesis from lactate. The carcinoma itself showed rapid rates of glycolysis and a poor ability to metabolize ketone bodies in vitro. The results are consistent with the peripheral, normal, tissues in tumour-bearing rats having increased ketone-body and decreased glucose metabolic turnover rates.
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PMID:Ketone-body metabolism in tumour-bearing rats. 395 47

The metabolic effects of oral ingestion of minute quantities of carbohydrate during prolonged starvation were studied in nine obese subjects. Measurements were made during a control period of total starvation, during the ingestion of 7.5 g carbohydrate daily, and finally during the ingestion of 15.0 g carbohydrate daily. Daily ketoacid excretion fell after carbohydrate ingestion and was significantly correlated (r = 0.62, P < 0.01) with the amount of carbohydrate administered. Despite this fall in ketoacids, the concentration of blood ketoacids, plasma free fatty acids, and serum insulin remained constant throughout the study. Urinary ammonium excretion, closely correlated with ketoacid output (r = 0.95, P < 0.001), also fell significantly after carbohydrate ingestion. No significant changes were present in extracellular or urinary pH. Urea nitrogen excretion did not change when urinary ammonium output fell. These results indicate that: the excretion of ketoacids and ammonium in starving man is exquisitely sensitive to minute amounts of ingested carbohydrate; the change in ketonuria appears to be due to increased renal ketoacid reabsorption after carbohydrate ingestion; and the nitrogen-sparing effect of reducing renal ammonium output in starvation can be dissociated from nitrogen sparing occurring because of changes in urine urea excretion.
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PMID:The effect of carbohydrates on ammonium and ketoacid excretion during starvation. 505 66

The metabolic response to human growth hormone (HGH) was studied in five obese subjects in the fed state and during prolonged (5-6 wk) starvation. In the fed state (three subjects), HGH induced an elevation in basal serum insulin concentration, a minimal increase in blood and urine ketone levels, and a marked reduction in urinary nitrogen and potassium excretion resulting in positive nitrogen and potassium balance. In prolonged fasting (four subjects), HGH administration resulted in a 2- to 3-fold increase in serum insulin which preceded a 50% elevation in blood glucose. Persistence of the lipolytic effects of HGH was indicated by a rise in free fatty acids and glycerol. The response differed markedly from the fed state in that blood beta-hydroxybutyrate and acetoacetate levels rose by 20-40%, resulting in total blood ketone acid concentrations of 10-12 mmoles/liter, ketonuria of 150-320 mmoles/day, and increased urinary potassium loss. The subjects complained of nausea, vomiting, weakness, and myalgias. Despite a 50% reduction in urea excretion during HGH administration, total nitrogen loss remained unchanged as urinary ammonia excretion rose by 50% and correlated directly with the degree of ketonuria. It is concluded that in prolonged starvation (a) HGH may have a direct insulinotropic effect on the beta cell independent of alterations in blood glucose concentration, (b) persistence of the lipolytic action of HGH results in severe exaggeration of starvation ketosis and interferes with its anticatabolic action by necessitating increased urinary ammonia loss, and (c) failure of HGH to reduce net protein catabolism in starvation suggests that this hormone does not have a prime regulatory role in conserving body protein stores during prolonged fasting.
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PMID:Metabolic response to human growth hormone during prolonged starvation. 554 Jan 76

To delineate the hormonal mechanism of dietary-induced changes in sodium balance, the role of insulin and glucagon in natriuresis of fast was evaluated in obese subjects submitted to a total starvation and given either glucagon or somatostatin infusion on day 4 of fast. While large amounts of glucagon (1 mg over 6 h) stimulated concomitantly ketonaemia, ketonuria and renal sodium losses, the ten-times lower amounts of glucagon induced an increase in renal ketone body and sodium excretion without any significant change in ketonaemia. It was concluded, therefore, that elevated plasma glucagon level may enhance renal sodium loss in ketotic states, through a direct renal effect reducing tubular ketone body reabsorption, hence increased ketonuria and natriuresis. It appears nevertheless that decreased insulin secretion, rather than an increase in plasma glucagon level must be considered as a key hormonal factor responsible for natriuresis attending starvation. Indeed, the concomitant reduction in plasma glucagon and insulin levels, resulting from somatostatin infusion on day 4 of fast, was followed by significant increase in natriuresis. The latter observation supports several previous studies indicating that insulin stimulates sodium reabsorption by the kidney and that the reduction in insulin secretion may induce an increase in renal sodium excretion. It was concluded, therefore, that not only sodium intake but also the carbohydrate content of the diet should be reduced in an attempt to induce a negative sodium balance and to correct hypertension in obese subjects.
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PMID:Influence of insulin and glucagon on sodium balance in obese subjects during fasting and refeeding. 611 18

Patients with type II diabetes mellitus (type II DM patients) are characteristically obese, hyperinsulinemic, and non-ketosis prone. Recently, we have encountered several obese type II DM patients with either diabetic ketoacidosis or significant ketonuria after insulin withdrawal. There was no evidence of infection, stress, or starvation to explain their ketonuria. Therefore, we assessed serum connecting peptide (C-peptide) response to oral glucose in 14 obese, insulin-treated type II DM patients: 6 with and 8 without episodes of spontaneous ketonuria. The group presenting with ketonuria had low to absent basal and stimulated serum C-peptide responses. The nonketonuric group had higher basal C-peptide (P less than 0.01) concentrations that increased significantly (P less than 0.001) after oral glucose compared with those of the ketonuric group. Clinical characteristics and biochemical control were similar in both groups. Our findings confirm that obese type II diabetes mellitus is a heterogeneous disease with variable fasting and stimulated C-peptide responses. Spontaneous ketonuria could be a feature in the clinical presentation of the patients especially in the presence of both low fasting and stimulated C-peptide levels. The significance of these findings is unclear but suggests individualization in the management of type II DM patients and cautious withdrawal of insulin therapy in such patients. Furthermore, serum C-peptide levels alone cannot be recommended to classify patients into either type I or type II diabetes mellitus.
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PMID:Significance of spontaneous ketonuria and serum C-peptide levels in obese type II diabetic patients. 638 58


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