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Biomedical subjects

E E Gordon

Publications and source records attributed to E E Gordon.

At least 37 records · Page 2Linked to original sources
PubMed1984

Effects of noncarbohydrate substrates on protein synthesis in hearts from fed and fasted rats.

An overnight fast reduced RNA content and resulted in lower rates and efficiency of protein synthesis when rat hearts were perfused in vitro and supplied glucose as oxidizable substrate. Decreased efficiency of synthesis was associated with development of a block in peptide chain initiation in hearts of both fed and fasted rats. Provision of pyruvate increased the rate and efficiency of protein synthesis in fasted but not fed tissue, and partially overcame the initiation block in both groups. A mixture of glucose, pyruvate and insulin increased the efficiency of protein synthesis and decreased ribosomal subunit content to similar values in both groups of hearts. Noncarbohydrate substrates, including pyruvate, lactate, acetoacetate and beta-hydroxybutyrate, supported higher rates of protein synthesis than glucose in hearts of fasted, but not fed rats. However, mixtures of glucose and either pyruvate, acetoacetate or beta-hydroxybutyrate increased the synthetic rate in fed tissue. Provision of noncarbohydrate substrates increased energy availability, as indicated by higher creatine-P/creatine ratios in both groups of hearts, but the synthetic rate increased as a function of creatine-P/creatine ratio only in the fasted tissue. Octanoate and leucine accelerated protein synthesis and increased energy availability in the fed tissue. The mixtures of glucose and noncarbohydrate substrates or octanoate elevated glucose-6-P content. These studies indicate that an overnight fast decreased the capacity for protein synthesis and modified the regulation of synthesis by noncarbohydrate substrates.

3-Hydroxybutyric Acid↗
PubMed1984

Aortic pressure, substrate utilization and protein synthesis.

An increase in aortic pressure from 60 to 120 mmHg in Langendorff perfused hearts increased oxygen consumption, glucose utilization, pyruvate oxidation and protein synthesis. These changes were not prevented by insertion of a ventricular drain that prevented intraventricular pressure development. Arrest of the heart with tetrodotoxin markedly reduced oxygen consumption; under these conditions an elevation of aortic pressure did not increase oxygen consumption. Elevation of aortic pressure in arrested-drained preparations supplied either glucose or pyruvate as oxidizable substrate increased protein synthesis to a comparable extent. Energy availability, as assessed by measurements of the creatine-P/creatine ratio, increased as aortic pressure was raised in hearts provided glucose, but not pyruvate, suggesting that greater energy availability was not the factor linking higher aortic pressure to faster rates of synthesis. These results focus attention on stretch of the ventricular wall, as the mechanical factor responsible for the effects of aortic pressure on several metabolic activities of the heart.

Animals↗
PubMed1984

Aortic perfusion pressure as a determinant of cardiac protein synthesis.

Mechanical parameters and intracellular mediators that may control protein synthesis have been studied in isolated rat hearts subjected to increased aortic pressure or induced to perform cardiac work. Elevation of aortic pressure from 60 to 120 mmHg in Langendorff preparations with glucose, glucose plus insulin, or pyruvate raised the rate of protein synthesis during the 2nd h of perfusion. These effects involved faster rates of both peptide chain initiation and elongation. In working hearts supplied glucose or glucose plus insulin, higher rate of synthesis were observed in both the 1st and 2nd h of perfusion, compared with Langendorff preparations perfused at 60 mmHg. Intracellular levels of glucose 6-phosphate, ATP/ADP ratio, adenylate energy charge, or creatine phosphate/creatine did not correlate with the rate of protein synthesis in beating control hearts. When ventricular pressure development was prevented by ventricular draining and hearts were arrested with tetrodotoxin, protein synthesis still increased as a function of perfusion pressure. Oxygen consumption increased as aortic pressure was raised in beating-drained hearts but was unaffected in arrested-drained hearts. These results indicate that intraventricular pressure development, cardiac contraction, oxygen consumption, glucose 6-phosphate, energy availability, and coronary flow could be dissociated from the stimulatory effect of higher aortic pressures on protein synthesis and suggested that stretch of the ventricular wall, as a consequence of increased aortic pressure, could be the mechanical parameter most closely related to the increase in protein synthesis.

Animals↗
PubMed1983

Altered oligosaccharides as the initiating autoantigen in rheumatoid arthritis.

The linkage of rheumatoid arthritis (RA) to infection though vague has remained a persistent notion for the past fifty years. The hypotheses that streptococcus was responsible; then M. Pneumoniae; the implication of a viral pathogenesis and, more especially, the Epstein-Barr virus, have all not withstood the test of Koch's postulates. Today, autoimmunity holds the field in the pathogenesis of RA. We know in fair detail what happens after failure of self-recognition develops. Why does synovial tissue become antigenic? Altered receptors of cell surface may be the loci of change, namely, glycoproteins and glycolipids. A hypothesis is constructed based on alteration by viral DNA of these cell surface markers that are then recognized as alien. Evidence is drawn from insulin dependent juvenile diabetes, glomerulonephritis, and Landsteiner blood groups. The initial lesion may be initiated by an infectious agent leading to a chain of events, the first link constituting change of the specific glycoprotein or glycolipid of a cell to one of antigenic challenge, thus stimulating an autoimmune reaction. The ultimate destructive-proliferative sequences of RA are then set in motion.

ABO Blood-Group System↗
PubMed1981

Handling of insulin by the isolated perfused rat kidney.

The organ clearance of insulin calculated from the rate of disappearance of immunoreactive insulin from the perfusate averages 0.76 ml.min-1.g kidneys wt-1, a value greater than the simultaneously measured glomerular filtration rate. Clearance does not fall when hormone concentration is as high as 7 X 10(-8) M (10,000 microunits/ml). Fifteen percent of the cleared insulin is excreted in the urine; the remainder is chemically modified and appears in the perfusate both as low molecular weight fragments and as high molecular weight species. In the process of clearing the hormone, kidney tissue accumulates both intact insulin and 125I-labeled insulin degradation products. the organ clearance of insulin is not curtailed when the glomerular filtration rate is sufficiently reduced (by lowering perfusate pressure) to cause urine flow to cease. Studies using hyperglycemic perfusates and kidneys taken from starving or streptozotocin-diabetic animals provided no evidence that the kidney plays a role in the regulation of plasma glucose by modulating the rate of insulin degradation.

Animals↗
PubMed1978

Neurophysiologic syndromes in stroke as predictors of outcome.

Outcomes in self-care following rehabilitation in 226 patients were correlated with 11 stroke syndromes, reflecting several pathophysiologic disturbances subsequent to either infarction or hemorrhage in cerebral or vertebro-basilar vessels. Self-care was scored on a 20-point scale for bed movements, transfers, feeding, dressing, personal hygiene, and bathing. Interjudge error among therapists did not exceed 2.5%. Mean score in left cerebral infarction without aphasia was used as a referent value. Scores in left cerebral infarction with aphasia and right parietal lobe syndrome with and without spatial agnosia were similar to the referent. Brain stem dysfunction with spasticity and right cerebral infarction with paresis and spatial agnosia fell below the referent value (Pless than 0.05). Higher levels were achieved in the syndromes of left and right anterior cerebral artery territories, brain stem dysfunction with ataxia, and left parietal lobe syndrome with comprehension aphasia, although t-values were not significant. Length of stay among the 11 groups was fairly uniform except for the group with brain stem dysfunction with spasticity and the group with left hemiplegia with spatial agnosia. These groups indicated rather severe disabilities. Aside from neurologic dysfunction the range of scores was influenced by associated cardiopulmonary involvement.

Activities of Daily Living↗
PubMed1976

Insulin resistance and acanthosis nigricans. Report of a case with antibodies to insulin receptors.

A 64-year-old black man presented with the syndrome of acanthosis nigricans and insulin-resistant diabetes mellitus requiring up to 3000 units of insulin per day. The patient's plasma contained circulating antibodies to insulin receptors thought to be responsible for the insulin resistance. The marked insulin resistance, the manifestations of acanthosis nigricans, the evidence of immunologic dysfunction by the absence of expected circulating antibodies to insulin, and the demonstration of circulating antibodies to insulin receptors put this patient in Kahn's category B of insulin resistance and acanthosis nigricans. There was no evidence of malignancy, lipodystrophy, or endocrine abnormality. The occurrence of acanthosis nigricans with insulin resistance due to binding of cell membrane insulin receptors by antibodies has been reported exclusively in women. This case report is the first description of a male patient with the syndrome of insulin resistance and acanthosis nigricans and focuses attention on features that might mislead one to suspect other causes of insulin resistance.

Acanthosis Nigricans↗
PubMed1975

Relationship of energy production to gluconeogenesis in renal cortical tubules.

Isolated tubules prepared by collagenase treatment of rat renal cortex retained their ultrastructural integrity and responded to added lactate and succinate with an increase in gluconeogenesis and respiration. Inhibition of the mitochondrial respiratory chain with rotenone, or energy conservation sites with oligomycin caused a marked reduction in respiration and ATP content thereby completely inhibiting net gluconeogenesis. Dissociation of gluconeogenesis from respiration was accomplished with quinolinic acid and hydrazine, inhibitors of gluconeogenesis. At 5 times 10(-3) M quinolinic acid, gluconeogenesis from succinate was inhibited approximately 50% and from lactate nearly 100%. This concentration of quinolinic acid did not affect oxygen uptake or the ATP content of tubules in the presence or absence of substrate. Hydrazine at 10(-3) M resulted in approximately 75% inhibition of glucose formation from succinate and complete inhibition from lactate without interfering with respiration or ATP content. The increased mitochondrial energy generation, as manifested by accelerated respiration was independent of gluconeogenesis. The unchanging cell ATP concentration with a higher respiratory rate upon addition of exogenous substrate bespeaks increased ATP turnover. ATP utilization for the substrate-induced enhancement of gluconeogenesis could not account for the increment in ATP hydrolysis.

Adenosine Triphosphate↗
PubMed1975

Inhibition of renal gluconeogenesis by guinolinate and hydrazine in diabetic rats.

Renal as well as hepatic gluconeogenesis is inappropriately accelerated in the diabetic state when plasma glucose levels are elevated. Known regulatory mechanisms influence gluconeogenesis in both organs. However, under certain circumstances gluconeogenesis may be affected in one organ and not the other. Recent studies with the tryptophan metabolite, quinolinate, suggest that hepatic gluconeogenesis in the diabetic is unaffected by this agent, whereas gluconeogenesis is blocked in the normal liver. These experiments have been interpreted as providing evidence for the lack of a specific physiologic repressor for gluconeogenesis in diabetic liver. In the present study quinolinate and hydrazine are shown to be effective inhibitors of the accelerated gluconeogenesis in the renal cortex of diabetic rats. Thus, the renal gluconeogenic mechanism in diabetics retains the capacity to recognize quinolinate as an inhibitor, but may be influenced by the depressed conversion of tryptophan to quinolinate in the intact diabetic organism.

Animals↗
PubMed1975

Experimental hyperosmolar diabetic syndrome. Ketogenic response to medium-chain triglycerides.

The clinical features of the experimental hyperosmolar diabetic (EHD) rat model resemble those seen in the human syndrome--extreme hyperglycemia without ketoacidosis is common to both. The absence of ketoacidosis in the syndrome has been ascribed to both substrate (free fatty acid) deficiency and to interference with hepatic ketone body synthesis. The potential for hepatic ketone body synthesis in the experimental model has been directly assessed by challenging the EHD animals with medium-chain triglycerides (MCT) administered intragastrically. This neutral lipid, largely consisting of C8 and C10 fatty acids, leads to a dose- and thime-related increase in the plasma concentration of acetoacetate and beta-hydroxybutyrate. The EHD rats respond to MCT with an increase in plasma ketone bodies that rises to levels that are twice as high as those observed in normal rats receiving MCT and are equivalent to the levels seen in untreated ketoacidotic animals. These data indicate that hepatic medium-chain fatty acid oxidation and ketogenesis are unimparied in the EHD animal. An analysis of the factors responsible for the greater ketogenic response in the EHD rat reveals that moderate diabetes and dehydration enhance MCT-induced ketone body accumulation, while cortisol is without effect. The plasma free fatty acid concentration in EHD animals does not differ from normal rats, but is significantly lower than that seen in diabetic ketoacidosis. These data support the concept that a principal reason for the absence of ketoacidosis in the EHD syndrome is the limitation in availiability of substrate, free fatty acids, for ketone body synthesis.

Acetoacetates↗