Degradation of normal glycogen results to 97.2% glucose 1-phosphate and 7.2% glucose. Assuming a ratio of glucose 1-phosphate to glucose recorded in a glycogen sample from a patient with a liver disease was 100,  The patient’s most likely enzymatic deficiency is _________

384 Are there any negative allosteric regulators for glycogen phosphorylase?

Explain the mechanisms for the control of the citric acid cycle ? explain in more than 150 words typed please on the computer. thank you

Based on the image below, select the correct statements. Note: There may be more than 1 correct response. Ribose 5-phosphate ribose phosphate pyrophosphokinase (PRPP synthetase) glutamine-PRPP amidotransferase adenylosuccinate synthetase AMP -> PRPP 5-Phosphoribosylamine I adenylosuccinate lyase 9 steps Adenylosuccinate AMP IMP <-- ADP <- AMP <-- GMP <-- IMP IMP dehydrogenase <- GMP. XMP ADP ATP XMP-glutamine amidotransferase GMP يا Increased levels of ADP inhibit the production of PRPP. Increased levels of GMP inhibit the production of XMP. Increased ADP activates PRPP synthase to increase PRPP levels. Increased IMP activates glutamine-PRPP amidotransferase to further increase IMP levels.

In the clinical case scenario provided, match the defective enzyme in Column A with the consequence of this enzyme defect in Column B. IND OAD DH Autopsy results from individual X showed normal levels of glucose and pyruvate, very low levels of NAD+ and very high levels of NADH. Their blood oxygen levels were normal, although the cause of death was given to be a lack of oxygen. Option A B C D Defective enzyme Phosphofructokinase Pyruvate dehydrogenase Cytochrome oxidase Lactate dehydrogenase write your answer here Consequence of this enzyme defect Impaired ATP production Impaired NAD production Impaired respiration Impaired oxygen I L OORD ORD OND DORO G

hyperammonemia in patients is compounded by the reality of the normal regulatory controls in the urea cycle. Explain how increased GDH oxidative deamination activity will inhibit the urea cycle.