5. Carbohydrate Metabolism (2) Flashcards

1
Q

Pathways of glucose metabolism during
fasting: (2)

A

 Glycogen breakdown (glycogenolysis)
 Gluconeogenesis

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2
Q

Glycogenolysis –
Gluconeogenesis –

A

Glycogenolysis – breakdown of glycogen stores to release glucose

Gluconeogenesis – de nova production of new glucose from substrates such as lactate, alanine and glycerol

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3
Q

Hormones that coordinate glucose homeostasis
Insulin vs Glucagon (5)

A
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4
Q
  • Other hormones that affect glucose metabolism:
    Adrenaline, Cortisol and ______ _______.
A

Thyroid Hormone

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5
Q

When glucose is _______ (i.e. post-meal) –
glucose is taken up and stored in liver as
glycogen

Between meals, when blood glucose is _____,
glycogen in liver is broken down to return
glucose to blood.

A

abundant
low

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6
Q

Breakdown of glycogen (glycogenolysis) (9)

A
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7
Q

Hormonal regulation of glycogen synthesis and glycogenolysis: (5)

A
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8
Q

Glycogen storage diseases: (3)

A
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9
Q

Gluconeogenesis (de nova glucose synthesis)
Non-carbohydrate sources in the liver (and kidneys) include: (4)

A
  • Amino acids (most important are alanine and aspartic acid)
  • Pyruvate
  • Lactate
  • Glycerol
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10
Q

Difference between glycolysis and gluconeogenesis:

A
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11
Q

What are the other substrates used for gluconeogenesis? (4)

A
  • Glycerol (3C)
  • Aspartate
  • Alanine
  • Lactate
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12
Q

What is the full cycle of gluconeogenesis? (9)

A
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13
Q

Pyruvate into the mitochondrion
* Pyruvate must enter the mitochondrion to be activated.
* Pyruvate carboxylase uses ____ and ____ to make
oxaloacetate (4C) - expression is increased by cortisol
and glucagon.
* Oxaloacetate is transported out of the mitochondrion
where it is ______ and ________ by PEP
carboxy kinase.
* PEPCK is the ____ ______ enzyme and its activity is
increased by glucagon, cortisol and thyroid hormone
and decreased by insulin.

A

ATP
CO2
decarboxylated
phosphorylated
rate limiting

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14
Q

What is The Cori cycle?

A

The means by which substances produced in the periphery, lactate (anaerobic waste) and amino acids (i.e. alanine) are transported to liver for further energy production or for gluconeogenesis when blood
glucose is low.

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15
Q

What is the full process of the Cori cycle? (2)

A

Cori cycle.
* Lactate produced by red blood cells and anaerobic glycolysis in muscles is released into the blood and transported to the liver,
* converted back to pyruvate and used for gluconeogenesis. The newly synthesised glucose is released into the blood and used again as a
substrate for anaerobic glycolysis.

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16
Q

What is the full process of The alanine/glucose-alanine cycle? (2)

A
  • When blood glucose is low, muscle protein is broken into amino acids. Amino groups from the amino acids are combined with pyruvate from glycolysis to form alanine, which is released into the blood.
  • In the liver alanine is converted back to pyruvate and used for gluconeogenesis. The new glucose is released into the blood and used again as a substrate for glycolysis.
17
Q

What are the fates of pyruvate? (4)

A
  1. When eating carbohydrate rich meal - high blood glucose, high insulin (low glucagon, low acetyl-CoA),
    a) pyruvate is converted to acetyl-Co-enzyme A by pyruvate dehydrogenase (PDH)
    b) energy generation in TCA cycle or fatty acid synthesis.
    c) pyruvate converted to acetyl-coA cannot be recovered for glucose synthesis.
  2. pyruvate converted to lactate in anaerobic cells – RBCs, muscle… – transported to the liver - converted back to pyruvate.
  3. In fasting (low blood glucose, low insulin, high glucagon), stress (high cortisol, high fatty acid catabolism leading to high acetyl-CoA) - pyruvate is converted to oxaloacetate for gluconeogenesis.
  4. In low blood glucose, muscle protein is broken down to amino acids. Amino groups are transferred on to pyruvate which is converted to alanine for transport to the liver for gluconeogenesis.
18
Q

Pyruvate dehydrogenase (PDH)
Catalyses the irreversible conversion of pyruvate to _____-_____.

A

Acetyl-CoA

19
Q
  • Regulation
    – Stimulated by:

– Inhibited by:

  • Once glucose oxidation passes through PDH, glucose cannot be recovered.
  • PDH is stimulated by insulin, ADP and Ca2+.
  • PDH is inhibited by acetyl-CoA and NADH and ATP
  • PDH activity requires ______ _______
    (derived from vitamin B1)
A
  • insulin
  • ADP
  • Ca2+
  • Acetyl-CoA
  • NADH
  • ATP

thiamine pyrophosphate

20
Q

What does Thiamine deficiency result in?

A

Results in decreased activity of PDH which causes beriberi.

21
Q

Beriberi is characterised by: (3)

A

increased plasma [lactate]
high output cardiac failure
neurological symptoms

22
Q

Beriberi is common in: (2)

A
  • Alcoholics: due to poor nutrition and ↓ absorption of thiamine (Wernicke-Korsakoff syndrome)
  • Populations that rely on polished rice.
23
Q

What is the Diagnosis of diabetes mellitus?

A
24
Q

Type 1 diabetes mellitus
* Total deficiency of ______ = “insulin-dependent diabetes mellitus (IDM)”
* Cause: inability of ___-____ of pancreas to produce insulin.
* ____ onset
* Requires insulin therapy.

A

insulin
β-cells
Early

25
Q

Type-2 diabetes mellitus
* Decreased response to insulin (insulin resistance)
= “non-insulin-dependent diabetes mellitus
(NIDDM)”.
* ____ onset
* Associated with obesity.
* Treatment involves drugs
* increase _____ receptor sensitivity to
glucose
* decrease glucose reabsorption via the
______ receptors in the nephron of the kidney

A

Later
GLUT4
GLUT2

26
Q

Caused by: (3)

A
  • decreased uptake of glucose by all cells (due to no
    insulin)
  • increased gluconeogenesis (due to “uninhibited”
    glucagon)
  • increased glycogenolysis (due to “uninhibited”
    glucagon) i.e. insulin: glucagon ratio is very low
27
Q

Clinical picture in patients with type 1 diabetes mellitus:

A
28
Q
  1. Regulation of glucose metabolism – the ‘metabolic see-saw’

The most important factor is: insulin: glucagon ratio

A