4 sketch the membrane of a neuron in a weight loss

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4. Sketch the membrane of a neuron in a weight loss circuit responding to leptin. How does this response alter the frequency of action potentials (nerve firing) in this cell? You may want to add a graph of a neuron in the weight loss circuit with an endogenous rhythm of action potentials before and after leptin interaction with the leptin receptor. 5a. Please add the 5 missing bars to the graph above which indicates muscle cell glucose uptake levels at fasting and elevated blood sugar levels. The mutants are: a K ATP loss of function mutant (K ATP - ), and a Glut4 loss of function mutant. The Glut4 gene codes for a glucose channel that is expressed in muscle cells. Enough information is provided in the graph to indicate which channel it is. Assume loss of function means no protein is present in these cases. 5b. Which loss of function mutation would lead to diabetes? Explain your answer. K ATP - Glut4 - Neither Both
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Bi212 Homework #4 Due Wednesday of week 9 @2pm page 3 The glucokinase mutation GCK-HH has an altered affinity for glucose. Trpm5 - mutants lack the Na + channel that is influenced by sweet taste receptors in pancreatic β -cells. 6a. Please add bars to represent the phenotype of the double mutant with both the altered affinity GCK gene and the missing Na + channel. 6b. Amazingly, the GCK-HH mutation is the result of a change in the amino acid sequence of the protein making it harder for an allosteric regulator to bind to the enzyme. Is the regulator an activator or an inhibitor? Defend your answer. 6c. How much insulin secretion would you expect in wild type b-cells in the presence of elevated blood sugar but no fructose present?
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