Changes in Phosphofructokinase and Pyruvate Kinase in
Rat Brain Regions during Alloxan-Induced Diabetes

Srivastava, Lalit K.; Baquer, Najma Zaheer

doi:10.1159/000469455

Cited by 5 publications

(4 citation statements)

References 13 publications

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“…[48] have also found that neonatal hypothyroidism decreases the flux of glucose into the glutamate, glutamine and GABA pools. In agreement with a depression of cerebral metabolism by hypothyroidism, phosphofructokinase and pyruvate kinase activities decrease in the cerebral hemispheres and cerebellum of hypothyroid rats [49].…”

Section: Discussionsupporting

confidence: 65%

Increased Oxidative Metabolism and Neurotransmitter Cycling in the Brain of Mice Lacking the Thyroid Hormone Transporter Slc16a2 (Mct8)

et al. 2013

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Mutations of the monocarboxylate transporter 8 (MCT8) cause a severe X-linked intellectual deficit and neurological impairment. MCT8 is a specific thyroid hormone (T4 and T3) transporter and the patients also present unusual abnormalities in the serum profile of thyroid hormone concentrations due to altered secretion and metabolism of T4 and T3. Given the role of thyroid hormones in brain development, it is thought that the neurological impairment is due to restricted transport of thyroid hormones to the target neurons. In this work we have investigated cerebral metabolism in mice with Mct8 deficiency. Adult male mice were infused for 30 minutes with (1-13C) glucose and brain extracts prepared and analyzed by 13C nuclear magnetic resonance spectroscopy. Genetic inactivation of Mct8 resulted in increased oxidative metabolism as reflected by increased glutamate C4 enrichment, and of glutamatergic and GABAergic neurotransmissions as observed by the increases in glutamine C4 and GABA C2 enrichments, respectively. These changes were distinct to those produced by hypothyroidism or hyperthyroidism. Similar increments in glutamate C4 enrichment and GABAergic neurotransmission were observed in the combined inactivation of Mct8 and D2, indicating that the increased neurotransmission and metabolic activity were not due to increased production of cerebral T3 by the D2-encoded type 2 deiodinase. In conclusion, Mct8 deficiency has important metabolic consequences in the brain that could not be correlated with deficiency or excess of thyroid hormone supply to the brain during adulthood.

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Section: Discussionsupporting

confidence: 65%

Increased Oxidative Metabolism and Neurotransmitter Cycling in the Brain of Mice Lacking the Thyroid Hormone Transporter Slc16a2 (Mct8)

et al. 2013

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“…Although phosphofructokinase was found in both types of brains, it has been reported that the levels of this enzyme are decreased in diabetic brains [27]. A number of cytoplasmic proteins were also identified in both the non-diabetic and diabetic brains: glycolipid transfer protein, a protein that accelerates the intermembrane transfer of various glycolipids [28]; ubiquitin protein ligase E3C, which is thought to be the component of the ubiquitin conjugation system most directly responsible for substrate recognition [29,30] and modulating the function of the synapse [31]; and heat shock protein 8 (HSP70).…”

Section: Resultsmentioning

confidence: 90%

Overexpression of myosin-IIB in the brain of a rat model of streptozotocin-induced diabetes

Calábria

Cruz

Nascimento

et al. 2011

Journal of the Neurological Sciences

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The Ca(2+)/calmodulin complex interacts with and regulates various enzymes and target proteins known as calmodulin-binding proteins (CaMBPs). This group of proteins includes molecular motors such as myosins. In this study, we show that non-muscle myosin-IIB is overexpressed in the brains of diabetic rats. We isolated CaMBPs from the brains of non-diabetic rats and rats with streptozotocin-induced diabetes and purified them by immobilized-calmodulin affinity chromatography. The proteins were eluted with EGTA and urea, separated by SDS-PAGE, digested and submitted to peptide mass fingerprinting analysis. Thirteen intense bands were found in both types of brains, two were found exclusively in non-diabetic brains and four were found exclusively in diabetic brains. A large fraction of the eluted proteins contained putative IQ motifs or calmodulin-binding sites. The results of the myosin-IIB affinity chromatography elution, western blot and RT-PCR analyses suggest that myosin-IIB protein and mRNA are expressed at high levels in diabetic brains. This is the first study that has demonstrated differential expression of CaMBPs in diabetic and non-diabetic brain tissue through a comparative proteomic analysis, and it opens up a new approach to studying the relationship between the expression of myosins in the brain, hyperglycemia and intracellular calcium regulation.

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“…It appears, therefore, that the observed decrease in the activity of Ala-AT in cerebral hemispheres could be due to a decreased glycolytic flux during diabetes. To this effect, the key glycolytic enzymes, name ly, phosphofructokinase and pyruvate kinase, have also been shown to decrease in cerebral hemispheres and cerebellum with no signifi cant change in brain stem [16].…”

Section: Resultsmentioning

confidence: 99%

Influence of Alloxan Diabetes and Insulin Treatment on the Activity of Alanine Aminotransferase in Rat Brain Regions, Liver and Heart

Kazmi¹,

Baquer²

1985

Enzyme

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Studies with brain alanine aminotransferase showed higher activity of the enzyme in the soluble fraction of cerebellum. Among the tissues, the liver soluble fraction was the richest source of the enzyme. Alloxan-induced diabetes caused both regional and timedependent variations in the activity of brain alanine aminotransferase. Significant among these changes were the decrease in both soluble and particulate enzyme from cerebral hemispheres and an increase in the soluble enzyme activity from cerebellum at early stages of diabetes. Brain stem did not show any marked change in enzyme activity. Liver and heart enzyme, however, increased significantly after 1-2 weeks of diabetes. Insulin treatment to diabetic animals caused an ‘over-shoot’ in soluble alanine aminotransferase activity, particularly in cerebellum and liver.

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Changes in Phosphofructokinase and Pyruvate Kinase in Rat Brain Regions during Alloxan-Induced Diabetes

Cited by 5 publications

References 13 publications

Increased Oxidative Metabolism and Neurotransmitter Cycling in the Brain of Mice Lacking the Thyroid Hormone Transporter Slc16a2 (Mct8)

Increased Oxidative Metabolism and Neurotransmitter Cycling in the Brain of Mice Lacking the Thyroid Hormone Transporter Slc16a2 (Mct8)

Overexpression of myosin-IIB in the brain of a rat model of streptozotocin-induced diabetes

Influence of Alloxan Diabetes and Insulin Treatment on the Activity of Alanine Aminotransferase in Rat Brain Regions, Liver and Heart

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