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Hexokinase deficiency (HKD) is a congenital disease that can disrupt intracellular glucose levels. Please provide an explanation of the diseases impact on intracellular glucose levels and the mechanism by which how GLUT1 regulates this disrupted glucose level.
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- Write a one-sentence explanation for each of the following statements.(a) In liver, glucagon stimulates glycogen breakdown via cAMP. Although you might expect glucagon to stimulate catabolism of the glucose formed as well, glucagon inhibits glycolysis and stimulates gluconeogenesis in liver.(b) An individual with a glucose-6-phosphatase deficiency suffers fromchronic hypoglycemia.(c) The action of phosphorylase kinase simultaneously activates glycogenbreakdown and inhibits glycogen synthesis.(d) The presence in liver of glucose-6-phosphatase is essential to the function of the liver in synthesizing glucose for use by other tissues.Write a one-sentence explanation for each of the following statements. (a) In liver, glucagon stimulates glycogen breakdown via cyclic AMP. Although one might expect glucagon also to stimulate catabolism of the glucose formed, glucagon inhibits glycolysis and stimulates glu- coneogenesis in liver. (b) An individual with a glucose-6-phosphatase deficiency suffers from chronic hypoglycemia. (c) The action of phosphorylase kinase simultaneously activates glycogen breakdown and inhibits glycogen synthesis. (d) The presence in liver of glucose-6-phosphatase is essential to the function of the liver in synthesizing glucose for use by other tissues.Which might be a physiological phenotype associated with loss of function of GLUT1? inability of glucose to enter the intestinal cells from the intestinal lumen and high glucose excreted accumulation of glucose in the intestinal epithelial cytoplasm loss of glucose transport into somatic tissues (such as neurons in the brain) low glucose levels in the bloodstream
- Mutations in glucokinase which lower the kcat for the enzyme or elevate the Km for glucose result in mild to moderate elevation of blood glucose. Explain how these mutations cause diabetes-like symptoms in patients.GluT transporters are responsible for passive transport of Glucose into the cell to yield G-6-P that cannot exit the cell; in liver cells this process is always regulated by insulin. True or FalseConsider fructose-1,6-bisphosphatase (FBP) when responding to Parts A, B, and C. When writing your response, please put A, B, or C in front of the answer for each part. NOTE: Each part can be answered in 3-4 sentences.A. State the effect (inhibition OR activation) of insulin signaling on the activity of FBP. Explain why this effect makes sense and make sure you identify the pathway where FBP participates.B. In a type 2 diabetic liver cell, when the blood sugar level is high, will the activity of FBP be HIGHER, LOWER, or THE SAME AS the activity in a nondiabetic liver cell under the same conditions? Explain your reasoning.C. Now think about the insulin and glucagon signaling pathways that control activity of FBP. When a nondiabetic liver cell is exposed to low blood sugar, indicate one specific way the insulin or glucagon signaling pathway could be disrupted so that the activity of FBP is not controlled correctly. Then, explain the reasoning for your answer.
- There are two types of diabetes. Mention their symptoms and causes.Identify if True or False The activated form of glucose that serves as glucose donor for glycogen synthesis is formed by the reaction of UTP and glucose 1-phosphate. True FalseGlycogen synthesis and breakdown are regulated primarily at the hormonal level. However, important nonhormonal mechanisms also control the rates of synthesis and mobilization. Describe these non- hormonal regulatory processes.
- Patients with a form of early-onset diabetes were found to carry a variety of mutations reducing the function of the glucokinase (GK) enzyme. These patients are heterozygous for one of the mutations, and thus show only partial rather than complete loss of GK activity. Answer the following questions about these patients. How would blood sugar lovolc likoly bo affoctod in CK nautatieWrite the name of different types of glycogen storage disorder and their enzyme deficiency.What would be the role of SAGA (Spt-Ada-Gcn5 acetyltransferase) in curing Diabetes Type I? asap