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biochemistry > Anorexia, obesity and diabetes > Flashcards

Anorexia, obesity and diabetes Flashcards

1
Q

Which tissues take up glucose after a meal?

A
  • Liver
  • Brain
  • Erythrocytes
  • Adipose tissue
  • Muscle
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2
Q

Which tissues can store glucose as glycogen?

A
  1. Liver
  2. Muscle
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3
Q

What substances are used to make glucose in between meals?

A
  • Glycerol (Adipose)
  • Proteins (Muscle)
  • Lactate (Erythrocytes)
  • Glycogen
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4
Q

Which substances are used to make glucose during starvation?

A
  • Glycerol (Adipose)
  • Lactate
  • Proteins
  • NOT glycogen (=depleted)
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5
Q

Which energetic substance is preferred by the brain during starvation?

A

Ketone bodies produced from acetyl CoA

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6
Q

After how long are glycogen storages depleted?

A

After about a day

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7
Q

Where is most available glycose or glycogen at?

A

Muscle and liver

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8
Q

Where are most mobilizable proteins located?

A

Muscle

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9
Q

What is diabetes mellitus type 1?

A
  • Inability to produce insulin
  • Degradation of fat and muscle
  • Glucose levels far too high
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10
Q

Which other cells in the pancreas does insulin inhibit?

A

Alpha cells

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11
Q

Which glucose transporters are affected in people with diabetes type 1?

A

GLUT4

GLUT4 is not transported to the membrane

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12
Q

Which substances does glucagon mobilize?

A
  • Fatty acids
  • Amino acids
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13
Q

How does glucagon mobilize fatty acids from adipose tissue?

A
  1. Glucagon activates cAMP by binding to G protein coupled receptor
  2. Protein kinase A activated
  3. Protein kinase activates adipocyte tryglyceride lipase by phosphorylation
  4. Glycerol and fatty acids transported out of adipocytes
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14
Q

Which energy rich compounds are preferred during fasting and in people with diabetes type 1?

A

Ketone bodies

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15
Q

Which compond is needed to produce ketone bodies?

A

2 acetyl CoA molecules

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15
Q

Which compond is needed to produce ketone bodies?

A

2 acetyl CoA molecules

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16
Q

Describe the steps of Acetyl CoA to ketone bodies

A
  1. Acetyl CoA to acetoacetyl CoA
  2. Acetoacetyl CoA to 3-hydroxy-3-methylglutaryl CoA
  3. 3-hydroxy-3-methylglutaryl COA to acetoacetate
  4. Acetoacetate into acetone and D-beta-hydroxybutyrate (ketone)
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17
Q

What is diabetic ketoacidosis?

A

xWhen high levels of D-beta-hydroxybutyrate cause the pH to drop and acidosis to occur

hydroxybutyrate is the acid form of hydroxybutyric acid

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18
Q

How can type 1 diabetes be treated?

A

Well-timed insulin injections (Before a meal)

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19
Q

What is the difference between fasting and type 1 diabetes wiht regards to concentrations?

A
  • Insulin is absent in type 1, while low in fasting
  • Glucagon, glucose, ketone bodies are extremely high in type 1 but elevated or glucose below normal in fasting
  • free fatty acids are very high in type 1, while normal in fasting
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20
Q

What is catabolic state

A

Overall malnutrition

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21
Q

Name three types of catabolic states

A
  • Anorexia
  • Sarcopenia
  • Cachexia
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22
Q

What is sarcopenia?

A

Loss of muscle mass in elderly and immobilized

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23
Q

What is cachexia?

A

Loss of muscle and fat in people with different diseases

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24
Q

What are some differences between sarcopenia and cachexia?

A
  • Cachexia is pathological
  • Cachexia accompanied by inflammation
  • Fat mass decreased in cachexia
  • Protein degradation in cachexia
  • Cachexia is comorbid
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25
Q

What do inflamamtory cells thrive on?

A
  • Glucose
  • Glutamine

So when inflammation occurs, more glucose and AA’s are used

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26
Q

What is an effect of inflammation?

A

Muscle loss due to the fact that alanine is used to make more glucose for inflammatory cells.

Called Cachexia

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27
Q

What effect does infection have on muscle mass?

A

Muscle is lost

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28
Q

How are proteins selected for destruction?

A

E3-ligase catalyzes the ubiquitination of a protein

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29
Q

What kinds of enzymes destroy proteins?

A

Proteases

When a protien is ubiquitinated

30
Q

How are proteins degraded by 20 s proteasomes?

A
  1. 19 s regulatory particle binds to proteasome with ATP
  2. The protein is bound to the regulatory particle
  3. ATP needed for proteolysis
31
Q

How many regulatory particles can a proteasome bind to?

A

One or two

32
Q

How is the muscle-specific E3 ligase called?

A

Atrogin-1

33
Q

Atrogin-1 is inhibited by?

A

IGF-1

At a young age, so younger people have more strenght

34
Q

Atrogin-1 is induced by?

A

TNF-alpha

During inflammation to free up amino acids

35
Q

Which inflammatory cytokine influences the liver?

A

Interleukin-6

36
Q

What does interleukin-6 initiate?

A

Acute phase response

37
Q

What does the liver produce in the acute phase response?

A

Serum amyloid A CRP (liver-CRP)

38
Q

How is trauma/inflammation measured in the body?

A

By measuring serum amyloid a CRP

39
Q

What can cause sarcopenia?

A
  • Neurodegenerative disease
  • Genetics
  • Age-related
  • Disability
40
Q

What can cause cachexia?

A
  • Starvation
  • Proinflammatory cytokines
  • Hypermetabolic states
41
Q

What is the most effective treatment of cachexia?

A

EPA doses

42
Q

How does EPA regulate cachexia?

A
  • Inhibits inflammatory cytokines
  • Inhibits proteolysis
  • Inhibits PGE2 effects on appetite

PGE2 normally causes lack of appetite

43
Q

How can sarcopenia be treated?

A

GH and testosterone

44
Q

What is the normal range of fat in men and women?

A
  • Men: 15-20%
  • Women: 25-30%
45
Q

How many people with type 2 diabetes have generalized obesity?

A

71%

46
Q

How many people wiht type 2 diabetes have truncal obesity?

A

16%

47
Q

High mortality nowadays is due to which three factors?

A
  • Cardiovascular disease
  • Cancer
  • Type 2 diabetes
48
Q

How many people with diabetes live in low and middle income countries?

A

3/4

49
Q

Is more or less insulin produced in type 2 diabetes cases?

A

More

50
Q

Which signalling arm is disturbed in people with insulin resistance?

A

Metabolic arm

Mitogenic arm is intact

51
Q

How does genetic predisposition affect pathophysiology of type 2 diabetes?

A

Deranged insulin release also causes hyperglycemia

52
Q

In what form can glucose be toxic?

A

In hemoglobin A1c

53
Q

If HbA1c levels increase, risk of diabetic complications…?

A

Increase

54
Q

During pre-diabetes, how doe levels of blood glucose and insulin function change?

A
  • Glucose levels post meal and during fasting increase
  • Insulin levels and insulin resistance increases
  • Beta-cell function decreases
55
Q

How can GLUT4 be overruled if the cells become insulin insensitive?

A

Metabolite AMP via AMPkinase can induce GLUT4 mobilization to the membrane.

AMP is normally in abundance after exercise.

56
Q

Which treatment drug activates AMP-dependent kinase?

A

Metformin

57
Q

What does metformin inhibit?

A
  • Insulin secretion
  • FA synthesis
  • Cholesterol synthesis
  • Gluconeogenesis
  • Lipolysis
58
Q

What does metformin induce?

A
  • Glucose uptake
  • FA ocidation
  • Glycolysis
  • Expression of GLUT4
59
Q

The activation of what cells initiate type 1 diabetes?

A

Immune cells

In type 1, an autoimmune response initiates cascade

60
Q

In type 1 diabetes, which pancreatic cells are destroyed?

A

Beta-cells

61
Q

Insulin resistance … the levels of insulin in the first stage of type 2 diabetes?

A

Increases

62
Q

An increase in insulin during the first stage of type 2 diabetes has what effect on beta cells?

A

Beta cell dysregulation

63
Q

Beta cell dysregulation … glucose tolerance?

A

Impairs/decreases

64
Q

Insulin levels… in later stages of type 2 diabetes due to beta cell insufficiency?

A

Decrease

65
Q

What are two differences between type 1 and type 2 diabetes?

A
  • Lower production of glucagon in type 2 because insulin is present
  • Less keto acidosis, less protein breakdown and less glucose production in type 2
66
Q

When are type 1 and type 2 diabetes similar

A

When beta cells in type two are inefficient and no insulin can be produced

67
Q

Which two hormones respond to the brain about meal timing/size and energy

A
  • Leptin
  • Ghrelin
68
Q

What effect does leptin have on food intake and metabolic rate?

A

When leptin is increased, food intake decreases and metabolic rates increase

69
Q

What kind of tissue secretes leptin

A

Adipose tissue

70
Q

What is the relationship between obesity and leptin?

A

People with obesity are resitant to leptin

71
Q

Which system does leptin resistance activate?

A

Endocannabinoid system

72
Q

What is the endocannabinoid system?

A

A signalling network throughout the body concerning senses

73
Q

What does CB1 do in the endocannabinoid system?

A

Inhibits feeling of hunger and motivation to eat

biochemistry (13 decks)

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