NUTR1023 Lecture Notes - Lecture 5: Nicotinamide Adenine Dinucleotide Phosphate, Collagen, Intrinsic Factor

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redweasel913

28 May 2018

School

Department

Nutrition

Course

NUTR1023

Professor

Michael Leveritt

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NUTR1023 Health and Fitness Through Diet and Exercise

Summer Semester 2017

Module 5 – Micronutrients (PART 1)

Objectives

At the end of this module students will be able to do the following:

• Describe the functions of selected vitamins and minerals in the body

• Describe how selected vitamins and minerals are absorbed

• List symptoms and conditions associated with deficiency and toxicity of selected

vitamins and minerals

• List some rich food sources of specific vitamins and minerals

Vitamins

➢ Organic compounds occurring in small amounts in food

➢ Vitamins cannot be synthesised in the body (with some exceptions)

➢ Some vitamins are often available from foods in inactive forms known as precursors

or provitamins

➢ Fat soluble – A, D, E, K

o Often stored in the body’s tissue

➢ Water soluble – B vitamins, C

o Dispersed in the body without being stored

➢ Thiamin

o B vitamin

o Energy metabolism

o Transmission of nerve impulses

o Thiamine deficiency is common when energy intake is low and in alcoholics

o Beriberi – damage to the nervous system, heart and other muscles; muscle

wasting (dry) or oedema (wet)

o Wernicke – Korsakoff syndrome – a combination of cerebral beriberi and

psychosis

o Thiamin toxicity is rare

o Good food sources – pork, vegemite and whole grains

➢ Riboflavin

o B Vitamin

o Coenzyme in reactions of energy metabolism

o Flavin mononucleotide (FMN) and flavin adenine dinucleotide (FAD)

o Deficiency results in inflammation of the membranes of the mouth, skin,

eyes, GI tract

o Toxicity extremely rare

o Good food sources – milk, wholegrains, dark green vegetables

➢ Niacin

o B vitamin

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Document Summary

Nutr1023 health and fitness through diet and exercise. At the end of this module students will be able to do the following: describe the functions of selected vitamins and minerals in the body, describe how selected vitamins and minerals are absorbed. List symptoms and conditions associated with deficiency and toxicity of selected vitamins and minerals. List some rich food sources of specific vitamins and minerals. Organic compounds occurring in small amounts in food. Vitamins cannot be synthesised in the body (with some exceptions) Some vitamins are often available from foods in inactive forms known as precursors or provitamins. Fat soluble a, d, e, k: often stored in the body"s tissue. Water soluble b vitamins, c: dispersed in the body without being stored. Vitamin c: water soluble, collagen synthesis connective tissue, synthesis of carnitine, synthesis of hormones and neurotransmitters, general anti oxidant function.

Related Questions

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 âI canât, I canâtâ 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.

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NUTR1023 Lecture Notes - Lecture 5: Nicotinamide Adenine Dinucleotide Phosphate, Collagen, Intrinsic Factor

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