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Digestion and Renal Sciences > Fed, Fasted and Starvation > Flashcards

Fed, Fasted and Starvation Flashcards

1
Q

What is the absorptive state?

A

Food in the GI tract

Nutrients being absorbed into blood and 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 do absorbed nutrients enter first?

A

The portal blood

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4
Q

What organ do absorbed nutrients reach first?

A

Liver

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5
Q

What nutrients are in the portal blood?

A

Monosaccharides
Amino acids
Lipids

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6
Q

Which tissues are hormone-sensitive with regards to energy metabolism?

A

Liver
Muscle
Adipose tissue

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7
Q

Where will glucose in the blood end up?

A

Liver to store as glycogen
Adipose tissue to form triglycerides
Muscle to store as glycogen
Other tissues for krebs cycle

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8
Q

Where will amino acids in the blood end up?

A

In the liver to be converted to keto acids and release energy
In muscle to create proteins

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9
Q

Where will triglycerides in the blood end up?

A

In adipose tissue

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10
Q

What triggers a switch from post absorptive to absorptive state?

A

Increased glucose and insulin in the blood

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11
Q

What triggers release of insulin and from where?

A

Secreted by beta cells of the islets of Langerhans in the pancreas
Trigger is high blood glucose and amino acids

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12
Q

What takes up glucose into beta cells?

A

GLUT-2 transporter

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13
Q

What does uptake of glucsose into beta cells trigger?

A

Generation of ATP from glucose metabolism

Ca2+ influx

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14
Q

What causes insulin exocytosis?

A

Intracellular Ca2+ increase

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15
Q

Outline the feedback control of insulin after a meal

A 
Blood glucose concentration increases
Insulin secretion stimulated
Glucose uptake into cells by GLUT-4
Blood glucose concentration falls
Stimulus for insulin secretion removed
Blood insulin concentration falls
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16
Q

What do muscles and adipose tissue need for glucose entry to cells?

A

Insulin

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17
Q

Which transporter is stimulated by insulin?

A

GLUT4

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18
Q

What is the effect of insulin on GLUT4?

A

GLUT4 is a transporter stored within the cell

Insulin stimulates translocation to the plasma membrane

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19
Q

What concentrations of glucose are seen in diabetes patients?

A

High extracellular

Low intracellular

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20
Q

What does insulin promote?

A

Glucose disposal into muscle and adipose tissue

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21
Q

What enzymes does insulin activate in the liver?

A 
Glucokinase
Glycogen synthase
Phosphofuctokinase
Pyruvate dehydrogenase
Acetyl CoA carboxylase
Fatty acid synthase
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22
Q

What enzymes does insulin inhibit in the liver?

A

Glycogen phosphorylase

Glucose 6 phosphatase

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23
Q

What does insulin trigger in muscle?

A

Increased glucose uptake
Glycogen synthesis
Glycolysis

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24
Q

What enzymes does insulin activate in adipose tissue?

A

Pyruvate dehydrogenase
Acetyl CoA carboxylase
Lipoprotein lipase

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25
Q

What enzyme does insulin inhibit in adipose tissue?

A

Hormone sensitive TG lipase

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26
Q

What is utilised in the post absorptive state?

A

Glucose stores as none is being absorbed in the GI tract

27
Q

What are the two ways energy is obtained in the post absorptive state?

A

Glucose-supplying reactions

Glucose-sparing reactions

28
Q

What are glucose-sparing reactions?

A

Reactions which generate other energy substrates such as fatty acids and ketone bodies

29
Q

Why are reactions essential during the post absorptive stage?

A

To preserve plasma glucose levels for brain function

30
Q

In what two ways does the liver supply glucose?

A

Glycogenolysis

Gluconeogenesis

31
Q

What controls glucose-supplying reactions?

A

Fall in insulin levels

Increase in hormones

32
Q

What hormones are involved in glucose-supplying reactions?

A

Epinephrine
Glucagon
Cortisol
Growth hormone

33
Q

What effect does epinephrine have?

A

Increases glycogen breakdown in muscles, adipocytes and the liver

34
Q

What effect does glucagon have?

A

Increases glycogen breakdown and gluconeogenesis in the liver

35
Q

What effect does cortisol have?

A

Increase gluconeogenesis in the liver and decreases glucose uptake

36
Q

What does growth hormone do?

A

Decreases glucose uptake

37
Q

How much ATP is produced by beta-oxidation?

A

34

38
Q

Where are ketone bodies produced?

A

In the liver

39
Q

Where do ketone bodies go?

A

From the liver to tissues for use in the Krebs cycle

40
Q

What is a charecteristic of diabetes mellitus?

A

High blood sugar

41
Q

What happens to the ratio of hormones in someone suffering from diabetes mellitus?

A

Increased ratio of hormones that increase blood sugar to insulin
(glucagon, adrenaline, growth hormone)

42
Q

What is the cause of the shift in hormones?

A

Either insulin deficiency or insulin resistance

43
Q

What is type 1 diabetes?

A

Young onset
Destruction of beta cells and loss of insulin production
Metabolic derangement by inability to utilise glucose
Switch to other fuels leads to marked weight loss
Also hyperlipidaemia and ketoacidosis

44
Q

What is type 2 diabetes?

A

Prevalence increases with age
Insulin levels usually normal or high but with reduced action (resistance)
Treated with lifestyle changes, insulin stimulators or insulin
Less of an effect as some insulin action still present
Causes long-term damage due to high glucose levels and lipid abnormalities

45
Q

What is the relationship between obesity and type 2 diabetes?

A

Obesity is present in 55% of sufferers

46
Q

What happens in the liver of someone with diabetes?

A

Decreased glycogen synthesis

Increased glycogenolysis

47
Q

What happens in adipose tissue of someone with diabetes?

A

Decreased glucose uptake

Increased lipolysis

48
Q

What happens in the muscle tissue of someone with diabetes?

A

Increased extracellular

Breakdown of protein to amino acids as substrates for gluconeogenesis

49
Q

What happens to levels of acetyl coA in diabetes sufferers?

A

Increased by the b-oxidation of fatty acids

50
Q

What is the effect of increased acetyl coA levels?

A

Inhibits the Krebs cycle

Used for ketogenesis

51
Q

What is the effect of high ketone levels?

A

Acidosis

52
Q

What are clinical features of uncontrolled diabetes?

A 
Polyuria
Polydipsia
Blurred vision
Infections
Weight loss
Ketosis
Confusion
Coma
53
Q

How is uncontrolled diabetes treated?

A

Rehydration with intravenous saline
Insulin injections
Monitor serum electrolytes
Treatment of symptoms such as infection

54
Q

What is the impact of chronic diabetes?

A

Effects of high blood glucose
Thought to cause enzymatic glycation of proteins, altering their function
Sorbitol toxicity, sorbitol is produced from glucose by aldol reductase. Further glycation of tissues

55
Q

What is retinopathy?

A

Growth of friable and poor quality new blood vessels in the retina
Macular edema
Leads to severe vision loss or blindness

56
Q

What is nephropathy?

A

Damage to the kidney that can lead to chronic renal failure eventually requiring dialysis
Diabetes is the most common cause of adult kidney failure worldwide

57
Q

What is neuropathy?

A

Abnormal and decreased sensation in the feet and then fingers and hands
With damaged blood vessels it can lead to diabetic foot (delayed wound healing, infection, gangrene)

58
Q

What are the consequences of atherosclerosis?

A

Strokes
Heart attacks
Peripheral vascular disease

59
Q

What is hyperlipidaemia?

A

Common in diabetes
High circulating fatty acid concentration
Atherogenic

60
Q

What is hepatic steatosis?

A

Fatty liver

61
Q

What causes hepatic steatosis?

A

Fatty acids taken up by liver and converted to triaglycerol

Deposited in the liver

62
Q

What are long term treatments of diabetes?

A 
Lipid lowering drugs
Reduced blood pressure
Aspirin
Avoid smoking
Diet
Home monitoring
Adjustment of tablets/insulin
63
Q

Why is diabetes seen in cystic fibrosis patients?

A

CF gene creates CFTR protein
Blockage of pancreatic ducts
Ductal obstruction leads to pancreatic tissue distruction

Digestion and Renal Sciences (27 decks)

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