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DIG > Absorptive State > Flashcards

Absorptive State Flashcards

1
Q

What is the absorptive state?

A
  • Food in GIT
  • Nutrients being absorbed into blood + lymph
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2
Q

What is the post-absorptive state?

A
  • Fasting state
  • Nutrients not being absorbed
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3
Q

What blood system to absorbed nutrients enter and where is the first organ they visit?

A
  • Portal blood
  • Liver
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4
Q

Hormone-sensitive tissues of energy metabolism

A
  • Liver
  • Muscle
  • Adipose tissue
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5
Q

What causes the switch from the post-absorptive to absorptive state?

A

Increased glucose + insulin in blood

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6
Q

What is the transporter responsible for beta cell glucose uptake?

A

GLUT-2

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7
Q

Is GLUT-2 insulin sensitive or non-insulin sensitive?

A

Non-insulin sensitive

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8
Q

What does glucose entry through GLUT-2 trigger?

A
  • Generation of ATP from glucose metabolism
  • Ca2+ influx
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9
Q

What does the Ca2+ influx from GLUT-2 glucose transport cause?

A

Insulin exocytosis

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10
Q

What transporter moves glucose into tissues of the body requiring glucose?

A

GLUT-4

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11
Q

Is GLUT-4 insulin sensitive or non-insulin sensitive?

A

Insulin sensitive

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12
Q

Feedback control of insulin after a meal

A
  • Blood glucose concentration increases
  • Insulin secretion stimulated
  • Glucose uptake into cells (GLUT-4)
  • Blood glucose concentration falls
  • Stimulus for insulin secretion removed
  • Blood insulin concentration falls
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13
Q

How does insulin regulate access of glucose into muscle and fat?

A
  • GLUT-4 stored within the cell
  • Insulin stimulates translocation to plasma membrane
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14
Q

General action of insulin in the liver

A
  • Glycogen synthesis
  • Glycolysis
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15
Q

General action of insulin in muscle

A
  • Glucose uptake
  • Glycogen synthesis
  • Glycolysis
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16
Q

General action of insulin in adipose tissue

A
  • Glucose uptake
  • Glycolysis
  • Triglyceride synthesis
17
Q

Types of reactions in the post-absorptive state

A
  • Glucose-supplying reactions (make glucose)
  • Glucose-sparing reactions (make FA’s + ketone bodies instead)
18
Q

Glucose-supplying reactions producing glucose in the liver

A
  • Glycogenolysis
  • Gluconeogenesis
19
Q

Control of glucose-supplying reactions

A
  • Fall in insulin levels
  • Increase in other hormones:
    > Epinephrine (increase glycogen breakdown in muscle, adipocytes + liver)
    > Glucagon (increase glycogen breakdown + gluconeogenesis in liver)
    > Cortisol (increase gluconeogenesis in liver + decrease glucose uptake)
    > Growth hormone (decrease glucose uptake)
20
Q

What is beta oxidation?

A

Process by which fats are used to liberate energy

21
Q

How does beta oxidation liberate energy?

A
  • After cycle fatty acid is 2 carbons shorter –> acetyl CoA used in Krebs for energy
  • Energy released via FADH2 + NADH at some steps
22
Q

Classification of type 1 diabetes

A
  • Young onset
  • Destruction of beta cells –> loss of insulin
  • Severe metabolic derangement due to inability to utilise glucose
  • Switch to other fuels (AAs, lipids) leads to marked weight loss + metabolic disturbances (hyperlipidaemia, ketoacidosis)
23
Q

Classification of type 2 diabetes

A
  • Prevalence increases with age
  • Insulin levels normal/high but reduced action (ie. resistance)
  • Treated with lifestyle, tablets or insulin
  • Less severe metabolic derangements
  • Long-term damage due to high glucose levels + lipid abnormalities
24
Q

Effect diabetes has on processes in the liver

A
  • Decreased glycogen synthesis
  • Increased glycogenolysis
25
Q

Effect diabetes has on processes in adipose tissue

A
  • Decreased glucose uptake
  • Increased lipolysis
26
Q

Effect diabetes has on processes in muscle

A
  • Increased extracellular glucose
  • Breakdown of protein to AAs for gluconeogenesis (muscle wasting)
27
Q

How does diabetes cause ketoacidosis?

A
  • Increased lipolysis leads to increased circulating FAs
  • These are directed to the liver to be used in beta-oxidation, liberating energy + acetyl CoA
  • High acetyl CoA levels inhibit Krebs cycle and acetyl CoA is pushed towards ketogenesis
  • Ketones are then used as energy source in extra-hepatic tissues
  • Transported via blood, and acidic nature of ketones leads to acidosis
28
Q

Clinical features of uncontrolled diabetes

A
  • Polyuria/polydipsia
  • Dehydration
  • Blurred vision
  • Infections
  • Weight loss (muscle + fat wasting)
  • Ketosis
  • Confusion
  • Coma
29
Q

Treatment of uncontrolled diabetes

A
  • Rehydration with intravenous saline
  • Insulin (infusion or s/c / i/m injections)
  • Monitor +/- correct serum electrolytes (potassium disturbance common)
  • Treat underlying cause (eg. infection)
30
Q

Why is potassium disturbance common in uncontrolled diabetes?

A

Insulin normally activates Na+/K+ ATPases causing flux of potassium into cells

31
Q

Microvascular complications of diabetes

A
  • Retinopathy
  • Nephropathy
  • Neuropathy
32
Q

Macrovascular complications of diabetes

A
  • Atherosclerosis
  • Strokes
  • Heart attacks
  • Peripheral vascular disease
  • Hyperlipidaemia
  • Hepatic steatosis
33
Q

Long-term treatment of diabetes

A
  • Reduction in vascular risk:
    > Lipid lowering drugs
    > Reduced BP
    > Aspirin
    > Avoiding smoking
  • Tight regulation of blood glucose:
    > Diet
    > Home monitoring
    > Adjustment of tablets/insulin

DIG (19 decks)

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