Fed, Fasted and Starvation Flashcards

(63 cards)

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
What enzyme does insulin inhibit in adipose tissue?
Hormone sensitive TG lipase
26
What is utilised in the post absorptive state?
Glucose stores as none is being absorbed in the GI tract
27
What are the two ways energy is obtained in the post absorptive state?
Glucose-supplying reactions | Glucose-sparing reactions
28
What are glucose-sparing reactions?
Reactions which generate other energy substrates such as fatty acids and ketone bodies
29
Why are reactions essential during the post absorptive stage?
To preserve plasma glucose levels for brain function
30
In what two ways does the liver supply glucose?
Glycogenolysis | Gluconeogenesis
31
What controls glucose-supplying reactions?
Fall in insulin levels | Increase in hormones
32
What hormones are involved in glucose-supplying reactions?
Epinephrine Glucagon Cortisol Growth hormone
33
What effect does epinephrine have?
Increases glycogen breakdown in muscles, adipocytes and the liver
34
What effect does glucagon have?
Increases glycogen breakdown and gluconeogenesis in the liver
35
What effect does cortisol have?
Increase gluconeogenesis in the liver and decreases glucose uptake
36
What does growth hormone do?
Decreases glucose uptake
37
How much ATP is produced by beta-oxidation?
34
38
Where are ketone bodies produced?
In the liver
39
Where do ketone bodies go?
From the liver to tissues for use in the Krebs cycle
40
What is a charecteristic of diabetes mellitus?
High blood sugar
41
What happens to the ratio of hormones in someone suffering from diabetes mellitus?
Increased ratio of hormones that increase blood sugar to insulin (glucagon, adrenaline, growth hormone)
42
What is the cause of the shift in hormones?
Either insulin deficiency or insulin resistance
43
What is type 1 diabetes?
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
What is type 2 diabetes?
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
What is the relationship between obesity and type 2 diabetes?
Obesity is present in 55% of sufferers
46
What happens in the liver of someone with diabetes?
Decreased glycogen synthesis | Increased glycogenolysis
47
What happens in adipose tissue of someone with diabetes?
Decreased glucose uptake | Increased lipolysis
48
What happens in the muscle tissue of someone with diabetes?
Increased extracellular | Breakdown of protein to amino acids as substrates for gluconeogenesis
49
What happens to levels of acetyl coA in diabetes sufferers?
Increased by the b-oxidation of fatty acids
50
What is the effect of increased acetyl coA levels?
Inhibits the Krebs cycle | Used for ketogenesis
51
What is the effect of high ketone levels?
Acidosis
52
What are clinical features of uncontrolled diabetes?
``` Polyuria Polydipsia Blurred vision Infections Weight loss Ketosis Confusion Coma ```
53
How is uncontrolled diabetes treated?
Rehydration with intravenous saline Insulin injections Monitor serum electrolytes Treatment of symptoms such as infection
54
What is the impact of chronic diabetes?
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
What is retinopathy?
Growth of friable and poor quality new blood vessels in the retina Macular edema Leads to severe vision loss or blindness
56
What is nephropathy?
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
What is neuropathy?
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
What are the consequences of atherosclerosis?
Strokes Heart attacks Peripheral vascular disease
59
What is hyperlipidaemia?
Common in diabetes High circulating fatty acid concentration Atherogenic
60
What is hepatic steatosis?
Fatty liver
61
What causes hepatic steatosis?
Fatty acids taken up by liver and converted to triaglycerol | Deposited in the liver
62
What are long term treatments of diabetes?
``` Lipid lowering drugs Reduced blood pressure Aspirin Avoid smoking Diet Home monitoring Adjustment of tablets/insulin ```
63
Why is diabetes seen in cystic fibrosis patients?
CF gene creates CFTR protein Blockage of pancreatic ducts Ductal obstruction leads to pancreatic tissue distruction