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28 Jan 2018

1a)How many ATP equivalents could be made from the oxidation of butanoic acid to Co2. AND explain how fatty acid oxidation is regulated in a few sentences.

1b) Explain how low blood sugar signals for the degradation of glycogen in the liver. Include a simple diagram if possible and use at least 4-5 sentences to explain.

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Related questions

Question 1
One complete cycle of the citric acid cycle is associated with therelease of (1 point)_CLO1

Question 2

Glycolysis is happening in __________whereas beta oxidation ishappening in__________________________(1 point)_CLO1

Question 3

How many Acetyl CoA are released from the beta oxidation of a 16C fatty acid? (1 point)_CLO1

Question 4

The citric acid cycle is producing three molecules of __________,two molecules of __________, one molecules of __________ and onemolecule of_____________________. (1 point)_CLO1

Question 5

Gluconeogenesis is likely to happen when (1 point)_CLO1

Question 9

If an individual is consuming 30g of carbohydrate daily, whichprocess may be predominant to cover energy needs? (1point)_CLO2

Question 10
If a food is having a low glycemic index, do you expect (1point)_CLO2

Question 11

Under aerobic conditions, the number of ATPs produced from 1molecule of glucose going through glycolysis and citric acid cycleis (1 point)_CLO1

Question 12
This is happening only in the liver: (1 point)_CLO1

Question 13
It is not digested but can be metabolized by bacteria in the colon(1 point)_CLO1

Question 14

Which of the following is a soluble fiber (1 point)_CLO1

Question 15

It is requiring ATP (1 point)_CLO1

Question 16

According to FNB guidelines, it is recommended to consume at least_____g of carbohydrates per day (1 point)_CLO2

Question 17

According to WHO guidelines, it is recommended to consume less than____________% of total energy intake as simple sugars per day (1point)_CLO2

Question 18
A glycemic index equal to 59 is considered as _______________(1point)_CLO2

Question 19

Describe two ways to produce glucose from fatty acids (2 points)_CLO1

rubyalligator107

(BIOCHEMISTRY QUESTION)

A. Gluconeogenesis is not just the reverse of glycolysis. Briefly describe one of the steps catalyzed by different enzymes in glycolysis and gluconeogenesis.

B. Explain how a biochemist might dicover that a certain enzyme is allosterically regulated.

C. What are the regulatory implications for the cell with regard to ATP & AMP, given the relative concentrations of ATP & AMP in a cell?

D. Describe the function of fructose 2,6-bisphosphate in overriding the control of gycolysis and gluconeogenesis in liver cells in response to lowered blood glucose levels.

E. The human disease beriberi is caused by a deficiency of thiamine in the diet. People with severe beriberi have higher than normal levels of pyruvate in their blood & urine. Explain this observation in terms of specific enzymatic reaction(s).

My Responses: Could you tell me if these are correct? If not, could you provide the correct answer and explanation?

A. Its a cellular process in which glucose is produced from pyruvate, amino acids, lactate, and other biogenic precursors.

B. They might learn that an enzyme is allosterically regulated if that protein or enzyme undergoes a conformational change modulated by the binding of one or more modulators/effectors to alternate sites on the protein, resulting in a change in its activity. And they usually have more than one polypeptide chain.

C. The regulatory implications for the cell would be that all activity would increase and concentrations would go up unless bound to PFK-1 and then the overall activity would drop.

D. Low blood glucose is when glucagon signals the liver to produce and release more glucose (gluconeogenesis) and stop consumption. Fructose 2, 6-bisphosphate mediates rapid hormonal regulation of glycolysis and gluconeogenesis.

E. Pyruvate is the product of both carbohydrate and amino acid catabolism that enters cellular respiration in the mitochondria when converted to acetyl-CoA catalyzed by the PDH complex. The first step in the PDH complex reaction is a decarboxylation reaction that cannot be catalyzed without the enzyme thiamine pyrophosphate (TPP). This coenzyme is a derivative of thiamine or vitamin B1.

sapphireswan33

Glycogen StorageDiseases

Glycogen storage diseases are so namedbecause a hallmark of the diseases is impaired glycogen storage dueto a deficiency of one of the enzymes involved in either glycogensynthesis or glycogen degradation. Several kinds of glycogenstorage diseases have been identified so far. Each type ischaracterized by the lack of a specific enzyme. An understanding ofglycogen metabolism is essential in the proper treatment of thisdisease, and identification of the deficient enzyme is requiredbefore a treatment protocol can be designed.

Your patient is a fifteen-year-oldCaucasian male named Joe K. Joe canât perform any kind of strenuousexercise. During his physical education classes, Joe could not keepup with his classmates and often suffered painful muscle cramps ifhe did attempt to exercise. He appeared to be normal if at rest orperforming light to moderate exercise. A physical examinationreveals that his liver appears to be normal in size, but hismuscles are flabby and poorly developed. A fasting glucose testshowed that Joe was not hypo- or hyperglycemic. A number ofbiochemical tests were carried out to identify the type of glycogenstorage disease in this patient.

Questions

1. You decide to try Joeâs response to glucagon. This testconsists of injecting a high dose of glucagon intravenously andthen drawing samples of blood periodically and measuring theglucose content of the samples. After the glucagon injection, Joeâsblood sugar rises dramatically. Is this the response you wouldexpect in a normal person? Explain.

2. Liver and musclebiopsies are taken from Joe and analyzed.

The biopsies revealed that glycogencontent in the liver is normal, but muscle glycogen content iselevated. The biochemical structure of glycogen in both tissuesappears to be normal. Suggest some possible explanations for theseobservations.

3. Next, you do another testwhere you have Joe perform ischemic exercise for as long as he isable to do so.

The ischemic exercise consists of thepatient squeezing a hand dynamometer at maximal strength for aspecific period of time, usually 1 minute, with an occlusionpressure cuff, which is placed on the upper arm and set at 250mmHg, blocking blood flow to the exercising arm. Blood is withdrawnfrom the patient every few minutes or so during the exerciseperiod.

a. Joeâs blood samples are tested forlactate and compared with a control sample of a patient who doesnot suffer from a glycogen storage disease. The results are shownin the plot to the right. Why does lactate concentration increasein the normal patient?

b. Why is there no correspondingincrease in Joeâs lactate concentration?

4. Urine tests after Joe has completedhis exercise reveal the presence of myoglobin in his urine.Myoglobin isnât normally found in the urine, but in muscle cells.Why does Joe suffer from myoglobinuria following ischemicexercise?

5. Joeâs enzyme deficiency does notcause him to suffer from either hypo- or hyperglycemia. Explainwhy.

6. As a treatment, you tell Joe thatthe best thing he can do is to avoid strenuous exercise. If he doeswish to exercise, you advise him to consume sports drinkscontaining glucose or fructose frequently while exercising. Whywould this help alleviate Joeâs suffering during exercise?