Integration in Metabolism Flashcards

1
Q

Homeostasis is

A

A metabolic condition that is the result of dynamic processes to maintain a constant internal environment despite a changing external environment

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2
Q

What is considered a changing external environment?

A

Diet

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3
Q

What anabolic reactions are happening in the fed state

A

All the reactions are happening with different input of energy
Glucose+glucose=glycogen
Glycerol+FA=triglycerides ->adipose tissue
AA+AA=Protein

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4
Q

Why we are using storage during fasting state?

A

Because we do not have absorption

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5
Q

What is the dominant hormone during fasting and fed state?

A

Glucagon and insulin

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6
Q

What catabolic reactions are happening during fasting state?

A

Glycogen->glucose
TGs->Glycerol+FA
Protein->AA

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7
Q

What chemical and through what reaction protein is converted to AA?

A

Proteolysis performed by proteases

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8
Q

Two types of AA

A

Glycogenic and ketogenic

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9
Q

Can pyruvate be converted to AA?

A

Yes, but only for nonessential AA

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10
Q

Describe the pathway of AA breakdown

A

Glycogenic AA->pyruvate->acetyl CoA or glucose

Ketogenic AA->AcetylCoA->fat or TCA cycle

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11
Q

The other name for fed state

A

Postprandial

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12
Q

What is done to protein in the body( brief) during fed state

A

Protein->AA->1)first used to replace body proteins
2)synthesized in glucose or fat,depending on carbon skeleton
3)entering directly TCA cycle
Converted to urea as well

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13
Q

What happens when body switches from fed state to fasting state?

A

Liver and muscle glycogen stores->glucose->energy

Body fat stores->FA->energy

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14
Q

Describe the fed state CHO

A

CHO 1)glucose first goes to the liver. Increase in blood glucose is detected by the pancreas and the insulin is secreted .
2)insulin instructs liver and muscle store glucose as glycogen, cells to uptake glucose and the excess of glucose to convert into fat

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15
Q

Describe fat during fed state

A

TGs->chylomicrons->lymph->blood->giving away TGs->liver captures chylomicrons remnants->liver rearranges chylomicrons adding endogenous fat->VLDL->adipose tissue taking up TGs

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16
Q

What is the source of energy when fat is stored?

A

Glucose

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17
Q

When protein synthesize is bigger than protein break down?

A

During fed state

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18
Q

Describe what happens to the protein during fed state

A

After absorption protein goes to the liver first. Liver detects increase in protein concentration, liver increases protein synthesize.

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19
Q

When is the time when we are building protein

A

During fed state

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20
Q

3 ways how glucose is used during fed state

A

1) for their own metabolism
2) muscle and liver to store glycogen for short-term fast
3) for long term fast storage in adipose tissue

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21
Q

What is considered short term fast and long term fast

A

Short term fast- breakfast time

Long term fast- 24 hours-48 hours

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22
Q

Is there a sharp change between fed and short term fast?

A

No, there is a smooth change. When in the short term fast the dominant hormone is glucagon,insulin is still present

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23
Q

What is the preferable source of energy for brain?

A

Glucose

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24
Q

What happens to the protein and AA during short term fast?

A

AA pool gets smaller. Increase in protein break down to keep AA pool pretty steady(higher protein break down than synthesize)

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25
What happens to CHO during short term fast?
As we do nit absorb glucose->low blood glucose->pancreas detects it->glucagon secretion . Glucagon releases glycogen to feed the brain.(liver) Glycogen in muscles is used by muscles For Fly or Fight response in case
26
From what sources glycogen is used to feed the brain?
Liver
27
Why glycogen in muscles stays in muscles for energy?
Because they prefer to use glycogen instead of fat for source of energy
28
What happens to fat and TGs during short term fast?
Hormone sensitive lipase hydrolyses TGs from adipose tissue. FA+albumin->to the cells , where they enter TCA cycle for energy. Glycerol can be used to synthesize glucose
29
What happens during long term fast?
No more glycogen, glucose is a limiting agent, but brain still needs glucose. Increase in AA breakdown( especially glycogenic AA)->production of glucose Increased hydrolyses from adipose cells . MAINLY fat oxidation in the blood. Fat-based metabolism. A LOT OF acetyl CoA. NET LOSS of protein to synthesize glucose. Accumulation of acetylCoA, because it is produced faster than it can be removed by TCA cycle
30
To what compounds glucose can be converted and how we can get glucose?
Glucosepyruvate--->acetylCoA Glycerolglucose LactatePyruvateGlycogenic amino acids Fatty acidsAcetylCoa
31
How many carbons can be converted to glucose from TGs
3 out of 54
32
5 ways how AA can be used
1) synthesize of protein 2) glucose 3) pyruvate 4) acetylCoa 5) TCA cycle
33
Can TCA cycle "survive" only on acetylCoA
No, we need pyruvate as well.Without pyruvate TCA cycle gets stuck
34
Describe what happens to acetylCoA when it accumulates in the blood
2 acetylCoA->acetoacetate(ketone body) , which has both ketone and acid group
35
How can acetoacetate be used?
Can be converted to beta-hydroxybutyrate or acetone
36
What is the good thing and a bid thing about ketones in the blood?
Brain can oxidize ketone bodies and ketone spares protein (less protein break down). No break down of protein BUT beta-hydroxybutyrate and acetoacetate are acids.Metabolic acidoses,potentially fatal by lowering pH
37
What is ketogenic diet?
Extreme low in CHO to promote fatty acid oxidation in absence of glucose
38
What is the problem with ketogenic diet?
Very hard to maintain
39
What disease is treated with ketogenic diet?
Certain type of epilepsy
40
Why ketogenic is not for pregnant women?
Because fetus is using primarly glucose, no glucose , damage to fetus
41
What are the consequences of not enough glucose in the blood during ketogenic diet? 7 points
- Nausea - Constipation - Fatigue - Low blood pressure - High uric acid(gout) - Halitosis(bad breath) - Decreased energy expenditure
42
What do we wan to avoid when losing weight?
decreased energy expenditure
43
Why ketogenic diet is so popular and promoted?
Suppression of appetite
44
How many people are overweight or obese in US and Canada
70% of the population
45
What terms do malnutrition include?
Undernutrition and overnutrition
46
Three nutritional status
Undernutrition Well-nourished Overnutrition
47
Why undernutrition and overnutrition are dangerous?
Undernutrition- deficiency and immune-incompetence Overnutrition- toxicity from excess energy,obesity and co-morbidities(diabetes,joints)
48
What happens in the body when we have a deficiency
Primary deficiency or secondary deficiency->declining nutrient stores->abnormal functions inside the body->physical(outward) signs and symptoms
49
How can assess primary deficiency
Diet history
50
How can assess secondary deficiency
Health history
51
What can laboratory test assess
Declining nutrient stores and abnormal function sin the body
52
What is used to assess physical signs and symptoms?
Physical examination and anthropometric measures
53
What interest us in the body composition?
Adipose vs lean tissue How much fat Where is the fat
54
What is the proportion of fat vs lean tissue in men and women
Men- 15% fat and 85%Lean | Women- 25% fat and 75% lean
55
BMI index
Body Mass index kg/m^2
56
How much weight and from age do we start to gain weight?
From 20-50 a pound a year
57
Describe the ranges of BMI
``` Less than 18.5- underweight 18.5-25- Normal weight Overweight - 25-30 Obese class 1 30-35 obese class 2 35-40 obese class 3 40 and higher ```
58
Why the range between 18.5 and 25 is the normal range?
Because it a range where there is minimal or low risk of mortality
59
Why visceral fat is more dangerous?
It is more metabolically active and cause glucose resistance
60
The cut off for waist circumference
Men- less than 40 inches (102 cm) | Women (35 inches) 88 cm
61
What hormone is produced by adipose tissue and its effect
It produces adipokines | Released into plasma, promotes insulin resistance and inflammation
62
What are the screening test and their pros and cons
Waist circumference and BMI Pros- easy to do,cheap Athletes can be misdiagnosed, do not give you an idea what fat
63
What are the diagnostic tests?
``` Computerized tomography (CT Scan) Magnetic resonance imaging (MRI scan) ```
64
Two types of fat
- Subcutaneous | - Visceral
65
Modifiable risks for visceral fat
- Smoking and alcohol | - Stress, saturated fat
66
Non-modifiable risks for visceral fat
gender,genetics | Age/menopause
67
Can you have visceral fat without being overweight ?
Yes
68
With what diseases visceral fat is associated ?
CVD | T2DM