Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Indirect calorimetry and nitrogen measurements suggest that uncomplicated abdominal surgery produces no significnat change in resting metabolic expenditure and only a slight loss of urinary nitrogen. More severe injury and infections produce larger increases in resting metabolic expenditure and nitrogen loss. Severe injuries can result in a 15 to 30% loss of body weight, but the protein contribution to caloric expenditure does not exceed 20% and is less than expected. The provision of calories and nitrogen can change the course of the septic patient. A continual conversion of alanine carbon to glucose occurs in septic patients, including those who are receiving exogenous glucose at the normal hepatic production rate. In sepsis, the release of glucogenic substrates from peripheral tissues may determine the rate of hepatic gluconeogenesis.
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PMID:Energy balance and carbohydrate metabolism in infection and sepsis. 88 81

Glucose kinetics and gluconeogenic precursors were studied in burned patients with or without gram-negative bacteremia. Gram-negative sepsis in burned patients impairs the increased rate of hepatic glucose production which characteristically occurs after thermal injury.
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PMID:Impaired gluconeogenesis in extensively injured patients with gram-negative bacteremia. 88 87

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

Fifteen thermally injured patients with positive blood stream cultures for gram-negative organisms demonstrated a decreased mass flow of glucose through the glucose space when compared with 17 patients without sepsis studied at a comparable time after injury. Amino acid concentrations determined in ten burned patients with sepsis and nine burned patients without sepsis revealed an increase in the gluconeogenic precursors alanine, glycine, methionine and phenylalanine in those patients with sepsis. The administration of alanine consistently increased serum glucose in seven patients without sepsis but exerted no effect on glucose concentrations in six person with sepsis. These data, taken together, indicate that gram-negative sepsis in burned patients impairs the increased rate of glucose production and flow to peripheral tissue which characteristically occurs after thermal injury.
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PMID:Impaired glucose flow in burned patients with gram-negative sepsis. 98 49

Enhancement of in vitro nitroblue tetrazolium dye reduction by human polymorphonuclear leukocytes may be mediated by a low molecular weight fluid phase component of the complement system. This occurs in the absence of phagocytosis and is associated with an increase in leukocyte hexose monophosphate shunt activity. The stimulatory component may be generated by activating the alternate complement pathway in serum, and shares many of the properties of human C5a. Thus, the enhanced spontaneous reduction of nitroblue tetrazolium by leukocytes from patients with bacterial sepsis may not necessarily be due to the phagocytic activity of these cells, but rather may occur as a consequence of in vivo complement activation by either intact microorganisms or their products.
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PMID:Enhancement of nitroblue tetrazolium dye reduction by leukocytes exposed to a component of complement in the absence of phagocytosis. 109 Jun 64

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 contribution of alanine to the synthesis of glucose and the oxidation of alanine was evaluated in normal and septic patients using (14C)L-alanine. The data indicate that there is a twofold increase in the conversion of alanine into glucose in sepsis and, further, this increase was observed while the patients were receiving a constant glucose infusion (100 mg/min) prior to and during the single injection of (14C)L-alanine. Failure of glucose to decrease this gluconeogenic response in these septic patients clearly indicates that the controlling mechanism for glucose synthesis is modified following injury and undoubtedly plays a role in the abnormal carbohydrate metabolism observed in injury. The contribution of alanine carbon to oxidation was the same in the control and septic group as measured by the per cent of the (14C)L-alanine dose expired in 3 h. Since the control subjects received glucose continuously during the study with and without amino acids, it is clear that nutritional intake and injury has minimal effect on the oxidation of alanine. This suggests that transamination is not affected by sepsis nor is there an inhibition of pyruvate oxidation following sepsis.
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PMID:Nonsuppressability of gluconeogenesis by glucose in septic patients. 125 Jan 57

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

This report describes a case of septicemia and meningitis secondary to dog bites by two different dogs on two consecutive days. The case is noteworthy because of the unusual characteristics of the etiologic agent and the inability to place the etiologic agent into any currently defined genus or to identify it by the existing systems of classification. The organism is a small, thin, Gram-negative bacillus after 24 hours of incubation on blood agar; after prolonged incubation, it becomes filamentous. The organism is catalase- and oxidase-positive, hydrolyzes esculin, and forms acid in glucose, xylose, and maltose after 21 days' incubation. The organism does not manifest lysis on sheep blood agar, and does not grow on MacConkey, Salmonella-Shigella, Centrimide, nutrient, or Kligler iron agars. The tests for urea, nitrate reduction, and indol are negative. The unidentified Gram-negative bacillus showed susceptibility to all antimicrobials tested except gentamicin.
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PMID:A previously undescribed gram-negative bacillus causing septicemia and meningitis. 126 16

Major thermal injury is associated with extreme hypermetabolism and catabolism as the principal metabolic manifestations encountered following successful resuscitation from the shock phase of the burn injury. Substrate and hormonal measurements, indirect calorimetry, and nitrogen balance are biochemical metabolic parameters which are useful and more readily available biochemical parameters worthy of serial assessment for the metabolic management of burn patients. However, the application of stable isotopes with gas chromatography/mass spectroscopy and more recently, new immunoassays for growth factors and cytokines has increased our understanding of the metabolic manifestations of severe trauma. The metabolic response to injury in burn patients is biphasic wherein the initial ebb phase is followed by a hypermetabolic and catabolic flow phase of injury. The increased oxygen consumption/metabolic rate is in part fuelled by evaporative heat loss from wounds of trauma victims, but likely also by a direct central effect of inflammation upon the hypothalamus. Although carbohydrates in the form of glucose appear to be an important fuel source following injury, a maximum of 5-6 mg/kg/min only is beneficial. Burn patients have accelerated gluconeogenesis, glucose oxidation, and plasma clearance of glucose. Additionally, considerable futile cycling of carbohydrate intermediates occurs which includes anaerobic lactate metabolism and Cori cycle activity arising from wound metabolism of glucose and other substrates. Similarly, accelerated lipolysis and futile fatty acid cycling occurs following burn injury. However, recent evidence suggests that lipids in the diet of burned and other injured patients serve not only as an energy source, but also as an important immunomodulator of prostaglandin metabolism and other immune responses. Amino acid metabolism in burn patients is characterized by increased oxidation, urea synthesis, and protein breakdown which is prolonged and difficult to reduce with current nutritional therapy. However, the current goal of nutritional support is to optimize protein synthesis. Specific unique requirements may exist for supplemental glutamine and arginine following burn injury but further research is needed before enhanced branched chain amino acids supplements can be recommended for burn patients. Recent research investigations have revealed the importance of enteral feeding to enhance mucosal defense against gut bacteria and endotoxin. Similarly, research has demonstrated that many of the metabolic perturbations of burns and sepsis may be due, at least in part, to inflammatory cytokines. Investigation of their pathogenesis and mechanism of action both at a tissue and a cellular level offer important prospects for improved understanding and therapeutic control of the metabolic disorders of burn patients.
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PMID:The metabolic effects of thermal injury. 129 Feb 69


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