phosphocreatine and Diabetic-Ketoacidosis

phosphocreatine has been researched along with Diabetic-Ketoacidosis* in 4 studies

Other Studies

4 other study(ies) available for phosphocreatine and Diabetic-Ketoacidosis

ArticleYear
Effects of hyperglycemia and effects of ketosis on cerebral perfusion, cerebral water distribution, and cerebral metabolism.
    Diabetes, 2012, Volume: 61, Issue:7

    Diabetic ketoacidosis (DKA) may cause brain injuries in children. The mechanisms responsible are difficult to elucidate because DKA involves multiple metabolic derangements. We aimed to determine the independent effects of hyperglycemia and ketosis on cerebral metabolism, blood flow, and water distribution. We used magnetic resonance spectroscopy to measure ratios of cerebral metabolites (ATP to inorganic phosphate [Pi], phosphocreatine [PCr] to Pi, N-acetyl aspartate [NAA] to creatine [Cr], and lactate to Cr) and diffusion-weighted imaging and perfusion-weighted imaging to assess cerebral water distribution (apparent diffusion coefficient [ADC] values) and cerebral blood flow (CBF) in three groups of juvenile rats (hyperglycemic, ketotic, and normal control). ATP-to-Pi ratio was reduced in both hyperglycemic and ketotic rats in comparison with controls. PCr-to-Pi ratio was reduced in the ketotic group, and there was a trend toward reduction in the hyperglycemic group. No significant differences were observed in NAA-to-Cr or lactate-to-Cr ratio. Cortical ADC was reduced in both groups (indicating brain cell swelling). Cortical CBF was also reduced in both groups. We conclude that both hyperglycemia and ketosis independently cause reductions in cerebral high-energy phosphates, CBF, and cortical ADC values. These effects may play a role in the pathophysiology of DKA-related brain injury.

    Topics: Adenosine Triphosphate; Animals; Aspartic Acid; Brain Edema; Cerebrum; Diabetes Mellitus, Experimental; Diabetic Ketoacidosis; Diet, High-Fat; Hyperglycemia; Lactic Acid; Magnetic Resonance Spectroscopy; Phosphates; Phosphocreatine; Rats; Water

2012
Cerebral metabolic alterations in rats with diabetic ketoacidosis: effects of treatment with insulin and intravenous fluids and effects of bumetanide.
    Diabetes, 2010, Volume: 59, Issue:3

    Cerebral edema is a life-threatening complication of diabetic ketoacidosis (DKA) in children. Recent data suggest that cerebral hypoperfusion and activation of cerebral ion transporters may be involved, but data describing cerebral metabolic alterations during DKA are lacking.. We evaluated 50 juvenile rats with DKA and 21 normal control rats using proton and phosphorus magnetic resonance spectroscopy (MRS). MRS measured cerebral intracellular pH and ratios of metabolites including ATP/inorganic phosphate (Pi), phosphocreatine (PCr)/Pi, N-acetyl aspartate (NAA)/creatine (Cr), and lactate/Cr before and during DKA treatment. We determined the effects of treatment with insulin and intravenous saline with or without bumetanide, an inhibitor of Na-K-2Cl cotransport, using ANCOVA with a 2 x 2 factorial study design.. Cerebral intracellular pH was decreased during DKA compared with control (mean +/- SE difference -0.13 +/- 0.03; P < 0.001), and lactate/Cr was elevated (0.09 +/- 0.02; P < 0.001). DKA rats had lower ATP/Pi and NAA/Cr (-0.32 +/- 0.10, P = 0.003, and -0.14 +/- 0.04, P < 0.001, respectively) compared with controls, but PCr/Pi was not significantly decreased. During 2-h treatment with insulin/saline, ATP/Pi, PCr/Pi, and NAA/Cr declined significantly despite an increase in intracellular pH. Bumetanide treatment increased ATP/Pi and PCr/Pi and ameliorated the declines in these values with insulin/saline treatment.. These data demonstrate that cerebral metabolism is significantly compromised during DKA and that further deterioration occurs during early DKA treatment--consistent with possible effects of cerebral hypoperfusion and reperfusion injury. Treatment with bumetanide may help diminish the adverse effects of initial treatment with insulin/saline.

    Topics: Animals; Aspartic Acid; Brain; Brain Edema; Bumetanide; Cerebrovascular Circulation; Creatinine; Diabetic Ketoacidosis; Diuretics; Fluid Therapy; Hypoglycemic Agents; Infusions, Intravenous; Insulin; Lactic Acid; Magnetic Resonance Spectroscopy; Phosphocreatine; Rats; Rats, Sprague-Dawley; Sodium Chloride

2010
Brain metabolism in diabetes.
    Hormone and metabolic research. Supplement series, 1980, Volume: 9

    Topics: Adenine Nucleotides; Animals; Blood-Brain Barrier; Brain; Diabetes Mellitus; Diabetes Mellitus, Experimental; Diabetic Coma; Diabetic Ketoacidosis; Energy Metabolism; Glucose; Humans; Ketone Bodies; Oxygen Consumption; Phosphocreatine; Rats; Starvation

1980
Reduced high-energy phosphate levels in rat hearts. I. Effects of alloxan diabetes.
    The American journal of physiology, 1976, Volume: 230, Issue:6

    Significant alterations in heart carbohydrate and lipid metabolism are present 48 h after intravenous injection of alloxan (60 mg/kg) in rats. It has been suggested that uncoupling of oxidative phosphorylation occurs in the alloxanized rat heart in vivo, whereas normal oxidative metabolism has been demonstrated in alloxan-diabetic rat hearts perfused in vitro under conditions of adequate oxygen delivery. We examined the hypothesis that high-energy phosphate metabolism might be adversely affected in the alloxan-diabetic rat heart in vivo. Phosphocreatine and ATP were reduced by 58 and 45%, respectively (P is less than 0.001). Also, oxygen-dissociation curves were shifted to the left by 4 mmHg, and the rate of oxygen release from blood was reduced by 21% (P is less than 0.01). Insulin administration normalized heart high-energy phosphate compounds. ATP production was accelerated in diabetic hearts perfused in vitro with a well-oxygenated buffer. These studies support the hypothesis that oxidative ATP production in the alloxan-diabetic rat heart is reduced and suggest that decreased oxygen delivery may have a regulatory role in the oxidative metabolism of the diabetic rat heart.

    Topics: Adenosine Diphosphate; Adenosine Monophosphate; Adenosine Triphosphate; Animals; Blood Glucose; Blood Pressure; Diabetes Mellitus, Experimental; Diabetic Ketoacidosis; Diphosphoglyceric Acids; Erythrocytes; Ether; Fatty Acids, Nonesterified; Glucosephosphates; Glycogen; Heart Rate; Hydrogen-Ion Concentration; Insulin; Male; Myocardium; Oxygen; Pentobarbital; Phosphocreatine; Rats

1976
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