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Articles by Q Hu
Total Records ( 3 ) for Q Hu
  X Yu , Y Huang , Q Hu and L. Ma

Homocysteine is an intermediate in the sulfur amino acid metabolism. Recent studies suggested that there might be links between hyperhomocysteinemia and insulin resistance. In the present study, we investigated the effect of homocysteine on glucose metabolism. We demonstrated that the levels of insulin were significantly higher in mice with hyperhomocysteinemia than those in the normal mice after administration of glucose. The effect of insulin on glucose output was significantly blocked in the homocysteine-treated hepatocytes. In addition, the expression of phosphoenolpyruvate carboxykinase (PEPCK) gene was elevated in the liver of mice with hyperhomocysteinemia and primary mouse hepatocytes treated with homocysteine. The action of homocysteine was suppressed by H89, a protein kinase A (PKA) inhibitor. Thus, hyperhomocysteinemia may be considered as a risk factor that contributes to the development of insulin resistance with respect to elevated glucose output and upregulation of PEPCK, probably via the PKA pathway. Our study provides a novel mechanistic explanation for the development of insulin resistance in hyperhomocysteinemia.

  Y Wang , M Zhang , C Moon , Q Hu , B Wang , G Martin , Z Sun and H. Wang

FE65 is expressed predominantly in the brain and interacts with the C-terminal domain of β-amyloid precursor protein (APP). We examined hippocampus-dependent memory and in vivo long-term potentiation (LTP) at the CA1 synapses with isoform-specific FE65 knockout (p97FE65–/–) mice. When examined using the Morris water maze, p97FE65–/– mice were impaired for the hidden platform task but showed normal performance in the probe test. To further discriminate the role of FE65 in acquisition and memory consolidation, we examined p97FE65–/– mice with temporal dissociative passive avoidance (TDPA) and contextual fear conditioning (CFC). p97FE65–/– mice showed impaired short-term memory for both TDPA and CFC when tested 10 min after training. After multiple TDPA training sessions, the crossover latency of some p97FE65–/– mice reached the cutoff value, but it significantly decayed in 8 d. At the Schaffer collateral-CA1 synapses, p97FE65–/– mice showed defective early-phase LTP (E-LTP). These results demonstrate novel roles of FE65 in synaptic plasticity, acquisition, and retention for certain forms of memory formation.

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