An individual's blood sugar is low. Assuming normal regulatory patterns, are the following ratios high or low? a. Active PFK-2: Active FBPase-2 b. Fructose 6-phosphate : Fructose 2,6-phosphate
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- Hemophilia B, an X-linked genetic disorder which highly affects males, is a condition in which levels of Factor VIII are significantly decreased. Please describe the physiologic pathway which utilizes Factor VIII and describe the consequences of missing this factor from a physiologic perspective.Novolog differs from "normal" insulin in that: Select one: a. An aspartic acid has been substituted for proline at B28 b. The proline at B28 and the lysine at B29 have been reversed c. A glycine has been substituten in at A21, and two new arginines have been added as B31 and B32 d. A "C-peptide" chain has been added e. The usual insulin molecule has been combined with zinc isophane(a) Predict the effect of a mutation that enhances the activity of the kinase associated with the PDH complex. (b) Predict the effect of a mutation that reduces the activity of the phosphatase associated with the PDH complex.
- Assume that the gene for PFK-2 is mutated and the mutated PFK-2 can no longer be phosphorylatedby protein kinase A (PKA). Do you think patients with such a gene mutation can efficiently increase theirblood glucose levels in response to starvation? Briefly explain your reasoning.Explain the mechanism by which statins lower “bad” cholesterol.Provide a diagram of the EPH RECEPTOR B2 (EPHB2) structure. Give annotations of binding sites and enzyme active sites.
- Inhibition of which enzyme/enzymes would inhibit the conversion of arachidonic acid to leukotrienes?a. cyclooxygenaseb. lipoxygenasec. phospholipase A2Lactic acidosis is a potential adverse side effect most commonly seen with which of these agents? Select one: a. Metformin (Glucophage) b. Glipizide (Glucotrel c. Repaglinide (Prandin) d. Miglitol (Glyset).Should teenagers be prescribed statins if they are diagnosed with hypercholesterolemia? Why or why not?
- Refer to Figure 3 which shows the relationship between phosphofuctokinase-1 (PFK-1) activity and fructose 2,6-bisphosphate. 100 +F2,6BP 80 60 40 -F2,6BP 20 0.05 0.1 0.2 0.4 0.7 1.0 2.0 4.0 EFructose 6-phosphate] (mm) Figure 3 (i) Explain the PFK-1 activity in the absence and presence of fructose 2, 6- bisphosphate. (ii) Explain the effect of increased ATP on PFK-I PFK-1 activity (% of Vma)What is the consequence of complete inhibition of all mutases in liver cells?a. Liver cannot provide free glucose to maintain blood glucose levelsb. Free glucose cannot be released from glycogenc. Glycerol cannot be converted to glucosed. The only fate of glucose-6-phosphate is to be converted to fructose-6-phosphateHow is cigarette smoking related to elastase function? Methionine sulfoxide is formed by cigarette smoke in the antitrypsin protein, which leads to the full manifestation of the disease in individuals heterozygous for emphysema. Oxidation of methionine 358 by cigarette smoke of the elastase inhibitor active site leads to an increased inhibition of elastase and subsequent overaccumulation of mucus in the lungs. The inhibitor of elastase is axidized by cigarette smoke so elastase doesn't function properly in healthy individuals. Cigarette smoke modifies the elastase methionine residues such that the enzyme activity is blocked.
