Metabolism of Carbohydrates ,Proteins Flashcards

1
Q

explain the role of glucose
( line to Krebs )
(1)

A

glucose –> pyruvate –> Acetyl CoA–> Krebs =ATP

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2
Q

what does insulin do?

4

A

Insulin regulates blood glucose levels :
reduces blood glucose levels via :
1-increases glucokinase which increases glucose 6 phosphate & glucose uptake into cell
2-Glycogen synthetase = increases glycogen storage
3-Gluconeogenesis decreases
4-Glycogenolysis decreases

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3
Q

what does glucagon do?
(3)

where is it produced and what can stop the secretion

A

produced by Alpha cells in the islet of Langerhan cells
stimulated by increased circulating AA as well
1- Less storage of glucose Stimulated by low blood glucose levels
2-Glucogneogensis
3-Glycogenolysis increases
(glucagon receptor signalling causes an increase in cAMP, PKA to stimulate glycogen phosphorylase promoting glycogen break down)

Somatostatin = stops glucagon secretion

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4
Q

what do glucocorticoids and adrenaline and other hormones do?
GANGC
(5)

A

Growth hormone= decreases glucose uptake by muscle, lipolysis increases, gluconeogenesis increases
Adrenaline=increases glycogenolysis and lipolysis
Noradrenaline=increases lipolysis, glycogenolysis
Glucagon=decreases glucose uptake into cells
Cortisol= increases lipolysis, gluconeogenesis, decreases glucose uptake

They all increase glucose in Blood

they are protective of Hypoglycaemia ( low blood sugar )

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5
Q

what osmotic changes does hyperglycaemia cause

4

A

1-increased blood glucose causes an increase in OSMOLARITY of ECF so water moves out from cells to ECF
2-high blood glucose also causes an increase in OSMOLALITY of renal tubular fluid=more urine loss
3-increase in blood osmolarity causes ADH to be secreted
4-we become more thirsty and try to increase body water.

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6
Q

ketoacidosis
what causes the smell?
(3)

A

Decreased amounts of insulin –>fat metabolism –>beta oxidation of fatty acids –>ketone ( fruity smell like acetone )

NOTE :
Normally the acetyl CoA goes to Krebs and combines with oxaloacetate, but when it doesn’t = KETONE BODIES

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7
Q

predict the effects of hypoglycemia

5

A
1-Glycosuria ( glucose in urine)
2-Dehydration =polyuria , Polydipsia
3-Tired= brain is starved
4-dizzy 
5-hungry
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8
Q

distinguish between type 1 and type 2 diabetes

2

A

Type 1 =not enough insulin due to beta-cell dysfunciton

Type 2 =insulin resistance ( receptors don’t recognise body insult anymore) most common =90%

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9
Q

outline carbohydrate metabolism

2

A

dietary carbs :
1-fructose, galactose converted in the liver to glucose 6 phosphates –>glucose via Glucose 6 phosphatase

2- glucose can also be made via B oxidation + amino acids in gluconeogenesis

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10
Q

what are the 4 receptors for glucose and where are they found?
(4)

A

1- GLUT 1= most tissues, it takes up glucose
2-GLUT2 = less efficient, found in liver, pancreatic B cells ( removes excess glucose only when glucose is HIGH )
3-GLUT3= CNS = very sensitive to Glucose uptake
4-GLUT4=takes glucose into Skeletal muscle, adipose tissue= insulin causes these receptors to increase in number

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11
Q

what is the islet of Langerhans?
(2)
what do they secrete?

A

endocrine cells which secrete hormones in liver
Beta-cell =insulin
Alpha cell = glucagon

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12
Q

how is glucose filtered in the kidney

A

1-SGLT1/2 Co transporter and then GLUT2

  • Na+ and glucose into the tubule
  • Glucose –>GLUT2 = blood
  • Na+ taken out via pump back out into blood
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13
Q

what is the islet of Langerhans?
(2)
what do they secrete?

A

endocrine cells which secrete hormones in the liver
Beta-cell =insulin
Alpha cell = glucagon

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14
Q

how is glucose filtered in the kidney

4

A

1-SGLT1/2 Co transporter and then GLUT2
2-Na+ and glucose into the tubule
3-Glucose –>GLUT2 = blood
4-Na+ taken out via pump back out into blood

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15
Q

How does diabetes cause a switch to fat metabolism?

4

A

1- increases hormone sensative lipase wihc is normally inhibited by insulin
2-lipolysis = glycerol + fatty acids
3-Fatty acids = beta oxidation =ketone bodies =ketoacidosis
4-acid= increased H+ in blood so more K+ moves into blood causng hyperkalemia

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16
Q

what is teh last reosrt fro enegry ?

2

A
1- PROTEIN = decreased insulin causes increase of protein+ fat
2-untreated TD1:
-rapid weight loss
-lack of energy
-increased appetite 
-tissue wasting
17
Q

How does diabetes cause a switch to fat metabolism?

4

A

1- increases hormone sensitive lipase which is normally inhibited by insulin
2-lipolysis = glycerol + fatty acids
3-Fatty acids = beta-oxidation =ketone bodies =ketoacidosis
4-acid= increased H+ in blood so more K+ moves into blood causing hyperkalemia

H+/K+ ATPase in DCT , H+ is excreted in urine (lumen ) and more K+ is reabsorbed back into the blood .

18
Q

what is the last resort for energy?

2

A
1- PROTEIN = decreased insulin causes increase of protein+ fat
2-untreated TD1:
-rapid weight loss
-lack of energy
-increased appetite 
-tissue wasting
19
Q

what is glucose toxicity?

A

glucose reacts with proteins to cause tissue damage

20
Q
how do we diagnose diabetes
(5)
urinary glucose?
fasting glucose range?
Fasting plasma insulin?
A
1-urinary glucose x>10mmol/L
2-Fasting Blood Glucose 3.4-6.2 mmol/L
3-Fasting Plasma insulin =10mu/mL
4-Glucose tolerance test( delayed decrease in glucose after intake )
5-Ketoacidosis