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Let’s assume that for a prolonged period of time your diet was deficient in niacin; an essential vitamin which the human body cannot synthesize. What would be the direct effect of this deficiency on each of the following metabolic pathways? (A decrease in the activity, an increase in the activity or no effect)

Glycolysis

The Krebs cycle

The electron transport chain

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Deanna Hettinger
Deanna HettingerLv2
28 Sep 2019

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The people of Malaysia belong to three communities: the local people called Malays, immigrants from South India called Tamils, and immigrants from China. During the early 20th century, the Malays lived mainly in coastal villages, the Tamils worked on rubber estates, and the Chinese worked in tin mines. In general, the people were very poor and they consumed a limited variety of foods.[1] Rice was the staple diet of all three communities and therefore the key source of caloric and nutrient content. Malays typically grew their own rice and dehulled it before consuming it; dehulling partially removes the aleurone layer of the rice seed. Following their South Indian food habits, the Tamils ate parboiled rice, and the Chinese ate polished white rice imported from Thailand. It was found that among the three Malaysian communities, the Chinese community was much more prone to suffer from some degree of sub-optimal thiamin intake. Out of every 1,000 Chinese inhabitants, about 120 had mild thiamin deficiency, about 80 had severe thiamin deficiency, and about 16 people had died of it. Suboptimal intake of thiamin was rare in Malays and was not reported at all in Tamils.[1] Thiamin, also called Vitamin B1, is required for all tissues, and its deficiency causes the disease Beriberi. Less severe deficiency results in non-specific symptoms such as weight loss, malaise, irritability, and confusion. Although the origin of the word Beri-beri is disputed, it is believed to be a Philippine word meaning “I can’t, I can’t” and was probably coined to refer to the lack of neuromotor coordination in people afflicted with this disease.[2] Thiamin is water-soluble and is stable in the acidic medium. It is unstable to heat, oxygen, and UV light in neutral and alkaline medium. The active form of thiamin is thiamin pyrophosphate (TPP). This active form is a cofactor for pyruvate dehydrogenase and transketolase enzymes that are involved in the metabolism of carbohydrates. These enzymes play an important role in the biosynthesis of a number of cell constituents such as neurotransmitters, pentoses, and reduced equivalents, used in oxidant stress. The human body cannot store thiamin and therefore requires a continuous supply of the vitamin. The thiamin in an individual on a thiamin-free diet typically depletes in fewer than two weeks. Thiamin absorption is affected by compounds, called thiamin antagonists or anti-thiamin factors, that alter the structure of thiamin. These compounds include alcohols, polyphenols, flavonoids, and thiaminase, a heat labile enzyme found in certain foods.[2] In affluent countries, where the diet is rich in thiamin, the most common cause of thiamin deficiency is excessive alcohol consumption. Alcohol intake affects thiamin status in two ways. First, alcoholics get a significant percentage of their daily energy intake from alcoholic beverages, which are nutrient deficient. In other words, alcoholics replace their consumption of nutrient dense foods that are part of their normal diet with the consumption of nutrient deficient alcohol. Second, alcohol inhibits the intestinal ATPase involved in the absorption of thiamin.[4] Sub-clinical thiamin insufficiency associated with excessive alcohol consumption produces an encephalopathy called Wernicke-Korsafoff syndrome. Patients with this syndrome have a higher than normal incidence of abnormal transketolase, which has a very low binding affinity to TPP. This problem can be overcome by putting patients on high-dose thiamin therapy. Some patients, however, might have a form of abnormal transketolase that does not bind at all with TPP. Such people do not respond to high-dose thiamin therapy.[4] Thiamin deficiency is observed in individuals who have low thiamin intake and a diet rich in polished rice, especially if their diet also consists of anti-thiamin factors such as tea, coffee, raw fermented fish, and betel nuts. The minimum amount of thiamin needed by the body can increase because of increased physiological or metabolic demands arising from pregnancy and lactation, heavy physical exertion, illnesses like cancer, liver diseases, hyperthyroidism, and surgery. Since TPP is required for carbohydrate metabolism, the recommended dietary allowances for thiamin are based on the assumption that its intake is related to total energy intake. The recommended dietary allowance in the United States is 0.5 mg/1000 Kcal.

Questions
1. Thiamin deficiency was observed only in the Chinese community even though all three
communities had the same staple (rice) diet. Explain.
2. On packages of enriched rice sold in supermarkets, the rice preparation directions state that the
rice should not be washed before cooking. Explain.
3. Severe metabolic acidosis caused by high levels of lactate is often associated with thiamin
deficiency. Explain.
4. Provide two plausible explanations for what might cause above normal levels of pyruvate in blood
and urine. How can one determine which of the two explanations is correct?
5. Why does thiamin utilization increase among cancer patients?
6. A negative correlation exists between the need for thiamin and the amount of fat in the diet.
Explain.

(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.

Case Study Section 4 – Nitrogen Metabolism Based on “A Sickeningly Sweet Baby Boy: A Case Study on Autosomal Recessive Inheritance” by Jacqueline Washington and Anne Zayaitz (National Center for Case Study Teaching in Science) The Patient: Mathew Miller is a 7-day-old infant that is rushed to the emergency room by his parents Emma and Jacob Miller, Mennonites from Lancaster County, PA. Emma’s pregnancy and delivery with Mathew was normal but he started having trouble nursing and now has completely stopped feeding. By the time they reach the emergency room Mathew’s limbs were rigid and he had had a seizure. The initial examination showed no infection and his x-rays were normal. The family history collected by the Doctor revealed that Emma and Jacob had had a previous son, Samuel that died at 9 days-of-age. There also is a history of unexplained childhood mortality on both sides of the family; Emma’s mother had two sisters who died in the first year of their lives and Jacob’s father had a sister who died at 7 months of age. Emma also points out to the Doctor that Mathew’s diaper has a funny smell to it. Blood and urine samples were taken for testing and skin biopsies from Mathew, Emma, and Jacob were taken and tested for enzyme activity. The tests results showed that:

• Mathew’s urine had elevated levels of the branched chain amino acids and their α-keto acid derivatives (which caused the sweet smell in his diapers)

• Both Emma and Jacob’s skin biopsies had nearly normal levels of branched chain amino acid metabolism/enzyme activity

• Mathew’s enzyme activity was less than 2% of normal

Question 1: What is the most likely diagnosis for Mathew?

A. Argininemia

B. Diabetes mellitus '

C. Maple syrup urine disease

D. Phenylketonuria

Question2: What enzyme did the skin biopsy test measure?

A. Carbamoyl phosphate synthetase I

B. Alanine aminotransferase

C. Phenylalanine hydroxylase

D. Branched-chain α-keto acid dehydrogenase complex

Question 3: This enzyme functions VERY similarly to two other enzymes that we have discussed, what are they?

A. Phosphofructokinase-1 and fructose 1,6-bisphosphatase (FBPAse-1)

B. Pyruvate dehydrogenase complex and α-ketoglutarate dehydrogenase complex

C. Urease and arginase

D. Isocitrate dehydrogenase and malate dehydrogenase

Question 4: How did Mathew (and presumably Samuel) inherit the disease if both Emma and Jacob have normal enzyme activity levels?

A. Emma and Jacob must both be carriers for the disease but their one normal gene is enough to maintain enzyme activity levels.

B. The disease can happen spontaneously, there is no genetic link.

C. Jacob is not really the father of the boys.

D. The disease can skip generations.

Question 5: What would be the best diet for Mathew to follow to control his disease?

A. Atkin’s diet (low carbohydrates, high fat, and high protein)

B. Low protein

C. Low fat

D. No special diet will control the disease

Over the next 4 years Mathew’s metabolic disease is controlled by his special diet but he still suffers approximately 3 metabolic crises a year. These occur when amino acids accumulate in his blood leading to the swelling of his brain. Even something as simple as a cold or the flu can affect his amino acid levels and send his metabolism into crisis. Jacob and Emma decide that “We cannot continue to live in constant fear that a minor infection or a simple cold or ear infection could kill our son. Even though we are doing everything we are supposed to, he is still getting sick and we are afraid we may lose Mathew.” They learn that some children with Mathew’s disease have undergone liver transplants and are effectively cured.

Question 6: How/why would a liver transplant effectively cure Mathew’s condition?

A. A new liver would be able to spread it’s genes throughout the body and correct the genetic disorder.

B. A new liver would more effectively respond to metabolic hormonal control.

C. A new liver would express the functional enzyme needed to metabolize the amino acids causing Mathew’s condition.

D. A new liver would produce more hemoglobin to transport oxygen more effectively.

The family is directed to Dr. Morton of Children’s Hospital of Pittsburgh, where transplant experts agree to list Mathew for a liver transplant. Jacob and Emma learn that children who receive a liver transplant have to take strong immunosuppressive drugs for the rest of their lives. It was also clear that there was a 40% possibility that Mathew could reject the liver and need a second transplant (which also might be rejected) or he could die from surgical complications.

Question 7: Assuming the liver transplant was successful and Mathew did not reject the new liver, what type of diet would Mathew be able to/need to eat?

A. He would still need to eat his special diet but he would be at less risk of a metabolic crisis

B. He could eat a normal diet

C. He would need to change to a high protein diet like Atkin’s

D. He would be on an all liquid diet

Question 8: Emma and Jacob decide they want to try to have another child. What would be the chance that this child would also have the disorder that Mathew and Samuel have/had?

A. 0 %

B. 25%

C. 50%

D. 75%

E. 100%

Question 9: If Mathew grew up, got married, and decided to have children, what would be the chance that his children would have the disorder? A. 0%, the liver transplant would have cured him

B. 25%

C. 50%

D. 100%

E. It would depend on his wife, if she was normal than there would be a 0% chance of his children having the disorder but 100% would be carriers, if she was a carrier than there would be a 50% chance of his children having the disorder and a 50% chance that they would be a carrier.

Question 10: The disorder is found in 1 in 200,000 infants throughout the US but 1 in 200 in the Amish and Mennonites of Lancaster County, PA. Why is there such a difference in the prevalence of the disease?

A. There are environmental factors associated with being Amish or Mennonites that increase the prevalence.

B. There is a large amount of genetic similarity within these populations because they tend to marry within the population so recessive disorders such as this are more likely.

C. The gene mutation is preferentially carried in Caucasians so when you average the prevalence across all races in the US the prevalence drops.

D. It is unknown why the prevalence is so much greater in Amish and Mennonites.

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