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Nutrition and Metabolism > Integration of Metabolism: the fed and fasting state > Flashcards

Integration of Metabolism: the fed and fasting state Flashcards

1
Q

Describe the demand and supply of fuel

A

The demand for fuel is constant but the supply intermittent

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2
Q

What do changes in the circulating concentrations of hormones allow the body to do?

A

Changes in the circulating concentrations of hormones
allow the body to:
1. STORE metabolic fuel
* when it is available
2. MOBILISE it in starvation,
* injury and stress

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3
Q

How are changes in metabolic pattern
achieved?

A
  1. variation in the amount of available substrate
  2. allosteric effects on enzymes
  3. covalent modification of enzymes
  4. changes in enzyme synthesis
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4
Q

Variation in the amount of available
substrate are
achieved by?

A

FA use in starvation

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5
Q

Allosteric effects on enzymes are
achieved by?

A

AMP and PFK in muscle
(Activation by phophorlation)

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6
Q

Covalent modification of enzymes are
achieved by?

A
  • phosphorylation of glycogen
  • phosphorylase and synthetase
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7
Q

Changes in enzyme synthesis are
achieved by?

A
  • Glucokinase and dietary CHO
  • HMG CoA reductase and cholesterol synthesis
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8
Q

Two Main hormones controlling intermediary
metabolism

A
  1. Insulin
  2. glucagon

Insulin and glucagon are the prime regulators of metabolism
* Insulin is the only hypoglycaemic hormone. (reduces BG)
* Glucagon is a hyperglycaemic hormone (Increases BG)

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9
Q

Other insulin counter-regulatory hormones?

A
  1. adrenaline (adrenal medulla)
  2. cortisol (adrenal cortex)
  3. growth hormone (anterior pituitary)
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10
Q

Location for metabolism?

Slide 5

A
  • Location of pancreatic islets reflects their functional role
  • Proximity of gut, prantantic and liver
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11
Q

What are the Islets of Langerhans?

A
  • The endocrine part of the pancreas
  • 2% of total pancreatic mass
  • adult pancreas contains about 1 million islets
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12
Q

What are Islets of Langerhans made up of?

A
  • β cells (60-70%) secrete insulin
  • α cells (30-40%) secrete glucagon
  • δ cells secrete somatostatin
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13
Q

How is Insulin secretion stimulated?

A
  • A rise in blood glucose
  • A rise in amino acid concentration in the blood
  • Gut hormones.
    – Secretin and other GI hormones released after food
    intake before blood glucose is elevated.
  • Glucagon.
    – glucagon leads to insulin secretion providing fine tuning of blood glucose homeostasis.
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14
Q

Control of insulin secretion?

A
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15
Q

Processing of pro-insulin into
insulin and C peptide?

A
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16
Q

How is secretion of glucagon is stimulated?

A
  • Low blood glucose
  • High conc of amino acids in the blood.
    – **prevents hypoglycaemia **after protein meal
  • Adrenaline.
    – In periods of stress glucagon secretion is stimulated
    regardless of blood glucose. (insulin secretion is
    suppressed)
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17
Q

What are the metabolic effects of insulin?

A
  • promotes fuel storage after a meal
  • promotes growth
  • stimulates glycogen synthesis and storage
  • stimulates fatty acid synthesis and storage from CHO when the intake exceeds glycogen storing capacity
  • stimulates aa uptake and protein synthesis
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18
Q

Structure of the insulin
receptor

A
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19
Q

Metabolic effects of insulin

A

Activation of Akt protein kinase

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20
Q

Effect of insulin on glucose transport (muscle and adipose) and glycogen synthesis in muscle and liver)

A
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21
Q

Inhibition of lipolysis in adipocytes by insulin through activation of Akt/PKB, and
inhibition of hormone sensitive lipase

A
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22
Q

effect of insulin on gene expression through Ras and MAPK

A
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23
Q

Insulin

A
  • promotes the appearance of GLUT4 (glucose transporters) in muscle and adipose tissue.
  • Brain liver, erythrocyte and pancreas** have GLUT** which are not insulin dependent
  • High concentrations of insulin lead to down regulation of its receptors
  • Insulin effects vary in time. Glc transport and enzyme activation are very rapid, synthesis of enzymes slow
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24
Q

Roles of Glucagon?

A
  • mobilises fuel
  • maintains blood glucose during fasting
  • activates glycogenolysis (liver)
  • activates gluconeogenesis (liver)
  • activates uptake of amino acids by the liver
    for gluconeogenesis
  • activates FA release from adipose tissue
  • activates FA oxidation and ketone body
    formation in the liver
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25
Q

Roles of Adrenaline?

A
  • mobilises fuel during stress
    – stimulates glycogenolysis (muscle and liver)
    – stimulates fatty acid release from adipose tissue
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26
Q

Roles of Cortisol?

A
  • provides for long term requirements
    – stimulates aa mobilisation from muscle
    – stimulates gluconeogenesis
    – stimulates FA release from adipose tissue
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27
Q

Graph of Blood glucose, insulin and glucagonafter a high carbohydrate
meal

A
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28
Q

Blood glucose, insulin and glucagon in a normal person over 24 hours of normal eating behaviour (mixed meals)

A
29
Q

metabolism in the fed state

A
30
Q

What is the fed (absorptive) state?
What occurs during this state?

A
  • 2-4 hours after a meal
  • increase in blood glc, amino acids and TAG as chylomicrons (1,2,3)
  • synthesis/storage of glycogen,TAG and protein
  • (6,11,13,14)
  • the liver is very important, it receives nutrients before other tissues from the hepatic portal vein
31
Q

What is the carbohydrate metabolism in the liver?

A

Liver engaged in gluconeogenesis at all times except the fed state (high ins/glucagon ratio)
* In the fed state glycolysis is activated through the
activation of GLUCOKINASE (5,6)
* (high Km for glucose and so no competition with the
brain when glc is low)

32
Q

What is the carbohydrate metabolism in the liver after glycolysis?

A
  • Glycogen synthesis is activated (6)
  • glycogen synthase is activated and phosphorylase inhibited
  • glycolysis is activated through PFK and pyruvate
    kinase (5)
    Gluconeogenesis is inhibited
33
Q

Process of liver fat metabolism in fed state ?

A
  • Fatty acid and TAG synthesis are activated (7)
  • Acetyl Co A carboxylase is activated (rate limiting step)
  • malonyl Co A inhibits carnitine transferase
  • in this way, newly synthesised FA does not enter the
    mitochondrion for oxidation but becomes esterified to
    TAG
34
Q

Metabolism in Brain and erythrocyte?

A
  • Both rely on glc. FA cannot cross the blood-brain
    barrier and erythrocyte has no mitochondria
  • glc transport into brain and erythrocyte is
    independent of insulin (glut1) (8,9)
  • This allows use of glc at both high and low
    concentrations
35
Q

Metabolism in Muscle during fed state?

A
  • glucose transport into muscle is increased (10)
  • GLUT 4 transporters increase in number
  • Glycogen synthetase is activated and
    phosphorylase inhibited as in liver (11)
  • amino acid uptake is activated and protein
    synthesis is increased (14)
36
Q

Metabolism of Adipose tissue?

A
  • Lipoprotein lipase is activated by insulin (12,13)
  • this allows entry of FA for esterification and storage of TAG
  • Glc transport is increased through glut4 (10)
  • glc is needed for production of glycerol phosphate and
    esterification of TAG
  • Hormone sensitive lipase in the adipocyte is inhibited so TAG is not degraded
37
Q

types of fuel reserves?

A
  1. glycogen (iver)
  2. glycogen (muscle)
  3. glucose
  4. TAG
  5. protein
38
Q

glycogen location?
quantity (g)?
Energy value (Kcal)?
Energy value MJ

A

Muscle - 300g - 1460Kcal - 6.1MJ
Liver - 80g - 330Kcal - 1.4MJ

39
Q

glucose location?
quantity (g)?
Energy value (Kcal)?
Energy value MJ

A

Body fluids - 15g - 60Kcal - 0.3Mj

40
Q

TAG location?
quantity (g)?
Energy value (Kcal)?
Energy value MJ

A

Adipose tissue - 15 kg - 140 000Kcal - 580Mj

41
Q

protein location?
quantity (g)?
Energy value (Kcal)?
Energy value MJ

A

muscle 6 kg - 26 000Kcal - 110Mj

42
Q

What is the fasting state?
What occurs during this state?

A

Post-absorptive state
* Blood glc concentrations peak an hour after eating
* they return to normal by two hours after a meal
* Blood glc is removed for oxidation or storage
* Concentration of insulin drops and glucagon rises

43
Q

Metabolism in the fasting state

A
44
Q

What are the early events of liver and adipose tissue?

A
  • The liver maintains blood glc concentrations at about 4 mM
  • Adipose tissue provides the greatest source of energy as TAGs
  • **Hormone sensitive lipase **activated by glucagon and adrenaline
  • FA transported to the liver bound to albumin
45
Q

Glucose production by the liver

A
  • The first supplier of blood glc is liver glycogen
  • gluconeogenesis follows from lactate
    (erythrocytes and muscle), glycerol (from adipose
    tissue) and amino acids (from muscle)
  • after 24 hours fasting all blood glc comes from
    gluconeogenesis
46
Q

Graph of Sources of blood glucose after ingestion of 100 g
glucose

A
47
Q

What can’t be used in gluconeogenesis?
Why?

A

Fatty acids are NOT gluconeogenic precursors
* Reaction catalysed by Pyruvate dehydrogenase is IRREVERSIBLE
* pyruvate acetyl CoA
* PDH is activated by insulin and inhibited by glucagon
* ensures that in fasting gluconeogenic substrates are channelled into glucose
production not acetyl CoA formation

48
Q

What occurs in liver during fed state?

A
  • glycolytic enzymes are activated
  • pyruvate ddehydrogenase is activated
  • excess acetyl CoA is channelled into FA synthesis bythe activation of acetyl CoA carboxylase

glc ———-> pyruvate ———>acetyl Co A ————>FA

49
Q

What occurs in liver during the fed state?

A

As FA can be used as fuel by liver adipose tissue and muscle, the draining of
gluconeogenic substrates into acetyl CoA is inhibited and conversion to glc is
favoured

50
Q

How does Ketone body (KB) formation take place?

A
  1. FA oxidation in the hepatocyte leads to high concentrations of Acetyl Co A
  2. it exceeds the capacity of the TCA cycle
  3. it is channelled into ketone body formation
  4. acetoacetate and β hydroxybutyrate are released into the bloodstream
    * most tissues oxidise a mixture of FA and KB
    * erythrocyte uses glc
    * brain uses glc and small amount KB
51
Q

What would happen to the body with prolonged fasting (starvation)?

A
  • If the early pattern were to continue in prolonged starvation body
    protein would be severely depleted
  • only about a third of body protein can be lost without severe or fatal
    consequences
52
Q

Graph of fuel concentration in the blood in prolonged
fasting?

A
53
Q

metabolism in starvation?

A
54
Q

Urea excretion in the fed and fasting state?

A
55
Q

What occurs as starvation continues?

A
  • more KB are recovered from the kidney
  • muscle uses FA rather than KB
  • FA concentrations plateau and KB rise
  • the brain can use more KB and less glc
  • the need for gluconeogenesis is reduced and muscle protein breakdown decreases
  • urea production decreases
56
Q

What is the role of Ketone bodies?

A
  • act on the pancreas to stimulate insulin release
  • this limits muscle proteolysis
  • and it limits adipose tissue lipolysis
  • so, muscle tissue is conserved
57
Q

When does death occur in fasting state?

A
  • amount of adipose tissue is an important determinant of survival
  • death comes from fuel exhaustion, loss of function from loss of protein and from
    impairment of the immune system
  • death from starvation is very often due to infection
  • about 40 days (young and fit, may be longer)
58
Q

Graph of Glucose tolerance curves of normal and diabetic
subjects?

A
59
Q

Who does Diabetes mellitus affect?
Consequences?

A
  • affects 6% of population in UK
  • 90% of all endocrine disorders
  • major cause of blindness, amputations, premature deaths
  • 10% of total health care budget
60
Q

Different types of Diabetes Mellitus?

A

* Type 1 or **Insulin dependent **diabetes mellitus (IDDM)
* **Type 2 or non-insulin dependent** diabetes mellitus (NIDDM)
* 10-20% of diabetics are type 1

61
Q

What is type 1 Diabetes?
How is it diagnosed?

A
  • autoimmune destruction of β cells
  • early onset
  • hallmarks are hyperglycaemia and ketoacidosis.
  • needs insulin treatment
62
Q

Symptoms of type 1 diabeties?

A
  • Polyuria, polydipsia, polyphagia, fatigue, weight loss, muscle
    wasting,weakness
63
Q

What is Diabetes type 2?
How is it diagnosed?

A
  • usually later onset
  • insulin resistance (target tissues non responsive
  • usually milder than type 1
  • association with diet and lifestyle e.g. obesity
  • major increase in incidence (including children)
  • hyperglycaemia but usually no ketoacidosis
  • often responds to diet and oral hypoglycaemic agents
64
Q

What is the Metabolic pattern in uncontrolled diabetes mellitus ?

A

Metabolic pattern in uncontrolled diabetes mellitus resembles that of starvation but the effects are more exaggerated

In starvation insulin is low
* In type 1 diabetes insulin is absent
* Glucagon acts unopposed
* KB produced in starvation stimulate insulin release
* this limits muscle protein breakdown, release of FA from adipocytes and the
uncontrolled production of KB.
* This important mechanism does not operate in diabetes

65
Q

Metabolism in diabetes?

A
66
Q

Chronic complications of diabetes mellitus?

A
  • Microangiopathy
  • changes in walls of small blood vessels seen as thickening of basement membrane
  • Retinopathy
  • blindness is 25 x more common in the diabetic patient
  • Nephropathy
  • renal failure 17 x more common
  • Neuropathy
  • postural hypotension
  • impotence
  • foot ulcers
67
Q

Treatment of type 1 diabeties?

A
  • exogenous insulin by injection
  • Important to balance dosage with amount of food to avoid hypoglycaemic incidents, the most common complication of insulin therapy
68
Q

Treatment of type 2 diabeties?

A
  • weight reduction, dietary modification, oral hypoglycaemic agents
  • biguanides increase the number of GLUT 4
  • sulphonylureas act on the β cell to improve insulin secretion
69
Q

What is metabolic syndrome?

A

Classified by the world health organisation as:
* High fasting glc/insulin resistance/diabetes type 2/impaired GT

Plus 2 of:
* Hypertension
* Dyslipidaemia (high TAG/low HDL
* Central obesity
* microalbuminuria

Nutrition and Metabolism (14 decks)

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