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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Glucose intolerance occurs in patients with sepsis, and resistance to insulin has been thought to be part of this process. To study this phenomenon, peritonitis was produced in rats by cecal ligation and puncture. One group was killed ten hours later (early sepsis). A second group of rats was killed 16 to 24 hours after ligation, just prior to their expected death (late sepsis). Insulin stimulated glucose uptake to the same extent in muscles from rats in early sepsis, late sepsis, and from control rats. Even at an insulin concentration that produced submaximal stimulation of glucose uptake, no difference in glucose uptake between the three groups of muscles was observed. Thus, there was no resistance to the stimulatory action of insulin on glucose uptake by skeletal muscle during early and late sepsis. However, basal glucose uptake by isolated soleus muscle from animals in late sepsis was significantly increased compared with controls when these muscles were incubated in an aerobic environment. Under anaerobic conditions, glucose uptake in these two groups of muscles increased to the same level. This indicates that there is some stimulus that increases glucose uptake in late peritonitis and may explain the hypoglycemia of late experimental or untreated sepsis. This stimulus could be hypoxia or some other factor resulting from decreased blood flow and increased anaerobic metabolism.
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PMID:Studies of peripheral glucose uptake during sepsis. 45 60

Six insulin-dependent diabetics were studied on their conventional insulin treatment and during continuous, dual-rate, subcutaneous insulin infusion for periods of up to 4 days. Dabetic control, as assessed by mean plasma glucose, range of plasma glucose values, M-value or range of M-values was improved significantly in 5 patients (mean +/- SD plasma glucose concentration on final infusion day 6.9 +/- 1.3 mmol/l, versus 11.3 +/- 3.2 mmol/l on conventional treatment). Once a suitable insulin dose was established blood glucose control could be maintained by continuous subcutaneous insulin infusion using the same daily infusion rate without frequent adjustment. In some case this was less than the daily dose on the conventional treatment. However, glycaemic control in one "brittle" diabetic, with unpredictable swings in blood glucose on her normal regimen, was not improved by continuous subcutaneous insulin infusion. During the period tested there was no sepsis at the cannula implantation site and patients did not find the system uncomfortable or unduly inconvenient.
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PMID:Continuous subcutaneous insulin infusion:good blood glucose control for up to 4 days. 46 48

Glucose intolerance has been commonly observed in sepsis and has been attributed to a multitude of endocrine and metabolic disorders. From 1977 to 1978, 19 patients were studied using intravenous glucose tolerance tests to evaluate this phenomenon; 15 patients presented with ongoing sepsis and four patients served as stress controls. Glucose intolerance was found to be a significant finding in less than 40% of the septic group. This state of intolerance was noted to be associated with a high mortality rate (60%), whereas glucose tolerance in sepsis was associated with a much improved mortality rate (10%). Hormone levels were correlated with glucose tolerance curves using the parameters of insulin, glucagon, growth hormone, cortisol, and epinephrine levels. Glucose intolerance and a high mortality rate were linked to sustained hyperglucagonemia, which was unresponsive to glucose challenge, and to marked suppression of growth hormone. This apparently represents a decompensated peripheral metabolic energy deficit, which results in the increased mortality rate.
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PMID:The sepsis-glucose intolerance riddle: a hormonal explanation. 47 28

Hormonal and substrate profiles and urinary nitrogen and urea excretion were measured in 78 underweight patients admitted for surgical investigation, who were placed into either a normo- or a hyperketonemic group, depending upon their levels of acetoacetate and beta-hydroxybutyrate. The two groups were otherwise similar in terms of weight loss, arm muscle circumference, triceps skinfold thickness, and serum protein levels. Before surgery only one-quarter of them were hyperketonemic displaying mean glucose, insulin, and glucagon levels characteristic of starvation-adaption, and excreted significantly less urinary nitrogen than in normoketonemic group. Those patients who underwent surgery tended to retain their presurgery hormonal and substrate profile. The normoketonemic group excreted significantly greater amounts of urinary nitrogen, depleted body protein to a greater extent as evidenced by larger changes in arm muscle circumference and serum protein levels, and mortality was greater. Interference with insulin-glucagon balance by sepsis and disease is suggested as a possible explanation for the failure of three-quarters of the patients to become starvation-adapted. The implications of this finding on the parenteral feeding of undernourished patients are discussed.
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PMID:Ketosis and nitrogen excretion in undernourished surgical patients. 57 67

Insulin glucose therapy can correct hyponatraemia and renal sodium retention in burns, sepsis and circulatory failure. A case of fulminant hepatic failure (F.H.F.) is described in which the same effect was observed. Insulin was thought to have corrected abnormal cell membrane permeability. The actions of insulin are discussed in relation to its possible role in the management of F.H.F.
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PMID:The effects of insulin glucose administration in fulminant hepatic failure. 69 Mar 22

Lactic acid is generated as the end product of anaerobic metabolism of glucose and is disposed by gluconeogenesis or oxidation. Changes in the lactate pyruvate ratio are not necessarily indicative of tissue hypoxia. The plasma lactate concentration is the result of lactate production and lactate removal (hepatic and renal gluconeogenesis; oxidation by muscle, liver and kidney). Lactic acidosis is defined as a state of metabolic acidosis (arterial pH less than 7.3) due to an increase in the blood concentration of lactate (greater than 2 mEq/l). Lactic acidosis may occur with evidence of tissue hypoxemia (type A) or in its absence (type B). Lactic acidosis has been described in association with phenformin therapy, hereditary enzymatic defects, hematological malignancy, prolonged fasting, shock with or without septicemia and occasionally without any underlying disease ("idiopathic" lactic acidosis). The therapy of lactic acidosis consists of administration of sodium bicarbonate and restoration of adequate tissue perfusion; hemodialysis may be helpful to control sodium excess and possibly to remove phenformin. The effectiveness of methylene blue, glucose and insulin are not yet established.
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PMID:Lactic acidosis. 87 61

Sixteen seriously septic patients were studied to determine whether proteolysis occurred to satisfy a deficit of peripheral fuel, as suggested by out previous experimental observations. Concentrations of glucose, lactate, free fatty acids,and alanine were measured in blood samples from the femoral artery and vein to determine extraction (+) and release (-) by the leg. Simultaneously, cardiac index (CI) was determined by thermal dilution, so that an estimate of uptake or production of fuel substrates could be made from the proportional relationship of cardiac index to peripheral blood flow. Due to the antilipolytic effect of elevated levels of insulin (42 +/- 4 muM per milliliter) in those patients with elevated cardiac indices (4.38 +/- 0.33 L. per square meter per minute), free fatty acid uptake (-0.59 +/- 0.021 mM.) was reduced. In low-flow septic shock (CI, 1.66 +/- .41 L. per square meter per minute), the majority of glucose taken up by the limb was converted to lactate (arterial lactate, 3.14 +/- 0.7 mM.; deltaA-V 0.68 +/- 0.17). Free fatty acid uptake also was impaired in low-flow sepsis. As opposed to fasting, arterial levels and uptake of ketone bodies were insignificant in sepsis. These findings suggest that there is a deficit of peripheral fuel with respect to glucose and fat. That protein is oxidized to fill this deficit is substantiated by the increased alanine release (-0.13 +/- 0.01, -0.33 +/- 0.12 mM.) in the high-flow and low-flow septic groups, respectively, whereas alanine production was three- and fourfold greater than that observed in fasting patients. Enhanced release of alanine reflects the magnitude of oxidation of branched-chain amino acids and accounts for the high rates of gluconeogenesis and proteolysis observed in sepsis.
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PMID:Proteolysis associated with a deficit of peripheral energy fuel substrates in septic man. 94 Oct 92

In conclusion, patients on chronic maintenance dialysis have an increased incidence of death from cardiovascular disease. Hypertension plays a major role, and these patients must be carefully monitored for complete control of blood pressure. Adequacy of ultrafiltration to maintain normal extracellular volume is an essential part of the dialytic treatment. Hypertensive patients should be screened for excessive renin secretion because of its possible role in unresponsive hypertension in patients on dialysis. Nephrectomy should be used when necessary, where dialysis and antihypertensive medication have not adequately controlled blood pressure. Patients must be monitored for the presence of pericardial disease to avoid subsequent pericardial effusion and the development of constrictive pericarditis with its adverse effect on myocardial function. When constrictive pericarditis is present, it obviously should be relieved by appropriate surgery. Efforts should be made to minimize cardiac output in hemodialysis patients. Whether or not routine transfusions to maintain a higher hematocrit are indicated is a question that cannot yet be answered. However, patients with marginal cardiovascular function who are accepted on hemodialysis and must have an arteriovenous shunt should be supported in any manner to minimize an increase in cardiac output. Early and aggressive treatment of known episodes of sepsis is important in the elimination of valvular endocarditis in this patient population. Perhaps one of the finer indicators of adequacy of hemodialysis will be K rate and peak immunoreactive insulin levels. Continued abnormality of these parameters may contribute to cardiovascular disease. Clearly, further study of the effect of abnormal carbohydrate metabolism on lipid metabolism is in order. Serum triglyceride, serum cholesterol and lipid electrophoretic pattern should be followed to evaluate the beneficial effects of drug therapy and changes in dialytic technique on the development of cardiovascular disease. Careful monitoring of calcium, phosphorus, bone films and parathyroid hormone levels is indicated to assess parathyroid status. The use of aluminum binders and parathyroidectomy to prevent vascular and myocardial calcification is important in the therapy of these patients. The use of cardiac catheterization, coronary artery arteriography, and possibly cardiac vascular repair, should be considered in the chronic hemodialysis patient with coronary artery disease if he is otherwise well. Adequacy of hemodialysis perhaps can be evaluated through its effect on all of the above parameters. Whether or not changes in artificial kidney treatments can correct the final vascular disease remains to be seen.
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PMID:Cardiovascular disease in uremic patients on hemodialysis. 109 1

The relationship of glucogenesis and other energy-requiring functions of the liver to the proteolysis which is characteristic of trauma and sepsis was studied in conscious pigs following laporotomy and after the induction of intraperitoneal sepsis. By means of appropriately placed thermal dilution catheters, portal and hepatic arterial blood flows, hepatic oxygen consumption, glucogenesis, and uptake of the fuel, substrates were measured. No animal was in shock. Despite significant increases of lactate and aminoacids delivered to the liver, the blood concentrations were maintained in the normal range. The rate of glucogenesis was proportional (r equals 0.71) to the sum of the glucogenic precursors (lactate, pyruvate, glycerol, and alanine) taken up by the liver. Higher rates of glucose production were accompanied by elevated blood insulin values. Hepatic oxygen consumption and the uptake of free fatty acids also were related directly to the glucogenic rate, the correlation coefficients being 0.69 and 0.74, respectively. In the absence of shock, the liver function and hepatic energy production remained normal in post-traumatic and septic states. Under the conditions insulin-resistant muscle in the presence of reduced free fatty acid availability mobilize protein to satisfy local energy requirements. Skeletal muscle can oxidize only branch chain aminoacids; other aminoacids, including alanine, are transported to the liver for glucogenesis or other purposed. This concept accounted for failure of glucose infusion to eliminate post-traumatic and septic proteolysis, since alanine is cleared only from blood by conversion in the liver to glucose. Thus it is concluded that in sepsis the release of glucogenic substrates because of altered metabolism in peripheral tissues determines the rate of hepatic glucogenesis. This relationship constitutes an important metabolic homeostatic mechanism.
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PMID:Liver metabolism and glucogenesis in trauma and sepsis. 114 47

The catabolism of glucose and amino acids has been studied in the normal, the fasted, and the fasted septic dog. The fasted septic dog oxidized more glucose and alanine, and had more gluconeogenesis from alanine and the five tritiated amino acids--glutamate, threonine, phenylalanine, leucine, and valine--as compared to the normal and equally fasted dog. Thus the total body protein catabolic state was characterized in biochemical terms. In contrast, following glucose infusion, the fasted septic animal responded much like the fasted animal in terms of decreased animo acid gluconeogenesis and decreased plasma concentrations of amino acids, fats and fat products, but considerably increased the oxidation of alanine. The increased alanine oxidation appeared to be primarily related to increased tissue clearance and increased plasma concentration. There was some suggestive evidence for enhanced oxidation of the tritiated amino acids including leucine and valine during glucose infusion. The protein catabolic state secondary to this sort of sepsis in dogs only on per os fluid support appears to be best characterized as a glucose catabolic state with alanine being oxidized directly. Such states are known to be ones of enhanced metabolic rate secondary to enhanced synthetic processes generally. This is probably related to enhanced sympathetic nervous system release of glucagon with insulin being normally responsive to glucose because of a normal plasma epinephrine.
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PMID:Turnover of amino acids in sepsis and starvation: Effect of glucose infusion. 125 26


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