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Metabolism and Nutrition > Lecture 4 > Flashcards

Lecture 4 Flashcards

1
Q

PKU.

A

Lack of phenylalanine hydroxylase will cause a saturation of the blood brain barrier by phenylalanine, which affects protein synthesis and leads to mental issues.

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2
Q

Hemochromatosis.

A

A genetic disorder in which the blood contains too much iron.

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3
Q

Iodine.

A

Micromineral, necessary for thyroid function and synthesis of thyroid hormones (T3 and T4; the numbers refer to amount of iodine in the molecule).

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4
Q

Thyroid hormones.

A

Control carbohydrate and fat metabolism; ligands of TR receptor.

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5
Q

Sources of iodine.

A

Seafood, kelp, dairy products; most common source is iodized salt.

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6
Q

Cretinism.

A

Mental retardation.

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7
Q

Effects of iodine deficiency due to thyroid-related disorders.

A

Anemia, arthritis, ye enlargement and inflammation, hair loss, and pre-mature greying.

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8
Q

Goiter.

A

Caused by both excess and inadequate intake of iodine. When caused by iron deficiency: leads to impaired thyroid hormone synthesis. When caused by excessive iodine: causes inhibition of thyroid hormone production.

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9
Q

Iodine excess.

A

Kelp acne; issue in Japan. Impairs thyroid hormone synthesis and causes Goiter in response to decreased thyroid hormone concentration.

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10
Q

Major reason for acquired metabolic disorders.

A

Obesity; the problem is actually malnutrition.

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11
Q

Is obesity contagious?

A

In some ways, yes. Social influences, transmission o bacterial infections can all lead to obesity.

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12
Q

Obesity caused by bacteria.

A

An obese mouse (infected with the bacteria) housed with a lean mouse: both became obese.

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13
Q

Storage of excess fat.

A

Excess fat is stored in adipose tissue, which has a life span of 2-3 years.

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14
Q

Obesity and its associated metabolic diseases.

A

heart attack, atherosclerosis, stroke, kidney failure, etc.

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15
Q

High LDL concentration in the blood.

A

LDL is a risk factor for atherosclerosis; it transports cholesterol from the liver to the cells, where it is stored.

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16
Q

Where in the human body is cholesterol produced?

A

In the liver.

17
Q

Microbacteria and red meat.

A

A certain strain causes an increase in TMAO in meat eaters when the wrong bacteria is present.

18
Q

Inherited metabolic disorders.

A

Inborn errors of metabolism caused by genetic factors. Examples: PKU, Type I diabetes.

19
Q

Acquired metabolic syndromes.

A

Manifestation of overnutrition; there is a genetic factor, but it is not the main cause of the disease. Severity depends in gene variance.

20
Q

Super tasters.

A

Ability to taste better is caused by variations in the genes that code for taste receptors.

21
Q

Taste perception.

A

The sugar (for example) binds with the receptor due to conformational compatibility; we are then able to perceive the taste.

22
Q

Taste receptors and nutrient deficiencies.

A

People will not like certain foods, causing them to avoid them, which may lead to a nutrient deficiency.

23
Q

Lactose intolerance.

A

Not a disease; the gene just shuts itself off. Variations in the gene have led to a retention of lactose enzymes.

24
Q

Digestion of lactose.

A

LCT gene encodes lactose; this gene normally shuts down after weaning. Variations in the gene have led to lactase persistence.

25
Q

Gene responsible for lactase production.

A

LCT.

26
Q

LCT and MCM6 region.

A

Variations in lactose intolerance do not happen within the gene itself, but in a gene very far away: MCM6. SNPs in introns of MCM6 cause this variation.

27
Q

Gene responsible for lactase persistence.

A

MCM6 due to SNPs in the introns.

28
Q

Encode project purpose.

A

To identify the functions of introns; most of the genome is actually composed of regulatory elements.

29
Q

Chromatids.

A

Histone proteins and DNA.

30
Q

NPC1L1.

A

Controls cholesterol uptake of dietary cholesterol into the intestine. Cholesterol uptake can be inhibited by ezetimibe.

31
Q

T61M.

A

At position 61, threonine is replaced with methionine.

32
Q

Variations in NPC1L1.

A

Influence the quantity of nutrients available for metabolism.

33
Q

Genes control nutrient availability.

A

There is a sensing mechanism: certain transcription factors are activated in the presence of certain nutrients.

34
Q

Loss of sensitivity to nutrient cues.

A

Can result in inappropriate metabolic response to nutrient availability or deficiency.

35
Q

Cellular response to amino acid starvation.

A

The cell sends a signal to increase translation of the mRNAs coding for Fil1/ATF4, which is a stress gene. Once Fil1/ATF4 is activated, it will launch transcriptional programs that promote cellualr survival mechanisms.

36
Q

ATF4.

A

Controls autophagy: the cell eats itself.

37
Q

Are gain-in-function genes, like lactase persistence, common?

A

No, they are rare.

Metabolism and Nutrition (12 decks)

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