Metabolic Changes in Health and Disease Flashcards

(53 cards)

1
Q

Catabolism

A

Weight Loss

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2
Q

Anabolism

A

Weight Gain

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3
Q

How much body energy is lost as heat ?

A

60%

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4
Q

What does chronic, low-grade systemic inflammation cause ?

A

As a result of obesity :

Increases the risk of cancer, cardiovascular disease, osteoarthritis and other diseases.

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5
Q

What does obesity cause ?

A

Increases risk of developing metabolic syndrome and type 2 diabetes.

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6
Q

What controls appetitie enhancement / suppression?

A

Neuronal and hormonal factors regulate food intake

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7
Q

Describe the role of insulin in metabolism

A

Insulin :

Hypoglycaemic / Anabolic hormone

  • Acts to decrease blood glucose / fuel storage
  • Lock nutrients away in storage molecules
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8
Q

Describe the role of glucagon in metabolism

A

Glucagon :

Hyperglycaemic / Catabolic hormone

  • Acts to increase blood glucose levels
  • Mobilise energy stores
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9
Q

State the hyperglycaemic hormones

A

Glucagon
Adrenalin

Cortisol
Growth hormone
(not directly related to absorptive/postabsorptive events)

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10
Q

Give some functions of insulin

A

Stimulates :

  • glucose uptake by cells
  • amino acid uptake by cells
  • glucose catabolism for energy
  • lipogenesis & fat storage
  • protein synthesis

Inhibits :

  • gluconeogenesis
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11
Q

Give some functions of glucagon

A

Stimulates :

  • glycogenolysis
  • lipolysis and fat mobilisation
  • gluconeogenesis
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12
Q

Function of metabolic homeostasis

A

Aims to ensure a constant supply of glucose for the brain (which uses 60% of all glucose produced)

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13
Q

Why does the brain require a constant supply of glucose ?

A

It is unable to store glycogen or utilise fatty acids (due to blood brain barrier).

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14
Q

State the key regulator of blood glucose

A

Liver

Buffering via :

  • Glycogenesis
  • Glycogenolysis
  • Gluconeogenesis
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15
Q

State the normal blood glucose range

A

4-7 mmol/L

OR

70-110 mg/dL

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16
Q

How much energy does a 70kg person use per day ?

A

1600kcal/day

(up to 5000 active state)

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17
Q

How long do carbohydrate stores last ?

A

1 day or less - blood glucose will fall

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18
Q

Metabolic changes associated with short-term starvation

A

Proteins can yield glucose (deamination and gluconeogenesis), but need to be preserved as much as possible.

Muscle shifts to using fatty acids as primary fuel.

Triglycerides have limited ability to be converted to glucose.

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19
Q

Describe glucose sparing for the brain

A

Muscle shifts to using fatty acids as primary fuel.

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20
Q

Metabolic changes associated with long-term starvation

A

Ketone bodies build up

Over the 1st few days, the brain becomes more tolerant to lower glucose - uses ketone bodies

Over time the brain gradually increases the use of ketone bodies

The body preserves valuable protein reserves, as need for amino acids to fuel glucogenesis reduced (muscle preserved)

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21
Q

Describe a key feature of long term starvation

A

Ketone body build up
Brain increases use of ketone bodies (need for glucose reduced)

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22
Q

What is the cause of ketone body build up ?

A

A consequence of fatty acid breakdown of acetyl-CoA and reduced activity of the citric acid cycle.

23
Q

State the metabolic changes in fasting

A

Brain :

  • Can only use glucose and ketones for energy

Liver :

  • glycogen becomes glucose

Adipose :

  • Lipids become free fatty acids and glycerol that enter the blood.

Muscle :

  • Glycogen can be used for energy.
  • Muscle can use fatty acids
  • Muscle protein broken down to amino acids to enter blood
24
Q

Describe the function of the pancreas

A

Acts as both an endocrine and exocrine gland

25
Describe the exocrine function of the pancreas
Digestive enzyme production
26
Describe the endocrine function of the pancreas
Islets of Langerhans (endocrine cells) are embedded within exocrine tissue
27
Describe Islets of Langerhans
Composed of 4 cell types, secreting hormones directly into the bloodstream. - Glucagon in alpha cells - Insulin in beta cells - Somatostatin in delta cells - Polypeptides in PP cells
28
Exocrine cells
Acinar cells
29
Endocrine cells
Islets of Langerhans 2% of pancreas mass Found in clusters of cells
30
Amylin
Hormone which is involved in regulating appetite and inhibiting glucagon activity.
31
Insulin
Directs the events of the absorptive state - hypoglycaemic hormone
32
When are beta cells stimulated to release insulin ?
Rising blood glucose levels Glucose dependent insulinotropic peptide (GI tract hormone) Parasympathetic nervous system
33
When insulin binds to membrane receptors on target cells what is stimulated ?
Translocation of Glut transporters Facilitated diffusion - 20 fold increase in glucose uptake Glycogen synthesis (liver/muscle) Glycolysis Triglyceride and protein synthesis
34
Glucagon
Controls blood glucose levels in the post-absorptive/fasting state - hyperglycaemic hormone.
35
When are alpha cells stimulated to release glucagon ?
Secrete glucagon in response to low glucose
36
Where does glucagon act ?
Acts mainly on liver (muscle doesn't have glucagon receptors) : stimulating : - glyconeolysis - gluconeogenesis
37
What determines the state of metabolism ?
Circulating levels of insulin and glucose
38
What hormone dominates in the : a) fed state b) fasted state
a) Insulin b) Glucagon
39
Where is adrenalin & noradrenaline synthesised ?
The adrenal medulla (modified sympathetic ganglion)
40
Function of catecholamines (adrenaline / noradrenaline)
Targets mainly muscle for glucose Lower glucose uptake by muscle - metabolise fatty acids instead (glucose sparing) Increase glucagon secretion / inhibit insulin secretion
41
Function of the sympathetic nervous system ?
Plays a crucial tole in increasing glucose Adipose tissue also supplied with sympathetic fibres : growth hormone, thyroxine.
42
What is diabetes mellitus ?
Chronic metabolic disease resulting form deficient secretion or action of insulin.
43
How is diabetes mellitus characterised ?
BY elevated blood glucose / chronic hyperglycaemia.
44
What causes Type 1 diabetes ?
10% of cases An autoimmune condition in which Beta cells are destroyed - no insulin released. Genetic predisposition ? Environmental trigger
45
What causes Type 2 diabetes ?
90% of cases Mostly associated with lifestyle Genetic component (also)
46
Describe the results of Type 2 diabetes
Tissues become insensitive to the effects of insulin-resistance
47
Treatment of Type 2 diabetes
Lifestyle changes - diet + exercise Hypoglycaemic drugs (insulin)
48
Health consequences of hyperglycaemia
Lack of sensitivity to insulin (increase in blood glucose) Dehydration Tissue Injury Peripheral Neuropathy Autonomic Nerve Dysfunction
49
Describe tissue injury caused by hyperglycaemia
Prolonged hyperglycaemia damages blood vessels Poor circulation Increased risk for MI Stroke Kidney disease Blindness
50
Describe dehydration caused by hyperglycaemia
Osmotic pressures caused by glucose in renal tubules Decreased water reabsorption Polyuria Intra/extra cellular dehydration Increased thirst and hunger
51
Describe how excess urination occurs
XS glucose cannot be reabsorbed via the proximal convoluted tubules. Increased osmotic strength of urine - less water reabsorbed Urine volume greatly increases and this explains sweet urine. IN serve cases, acidic ketone bodies add to osmotic strength.
52
State the metabolic consequences of hyperglycaemia
Due to lack of insulin/insulin resistance, metabolism is similar to prolonged fasting/starvation. High glucose availability.
53
Describe what happens when there is an increased utilisation of fats
Glycolysis slows Gluconeogenesis stimulated (using amino acids) New glucose and ketone bodies circulate in blood Metabolic acidosis - increased ketone bodies