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Biochemistry > Integration of Metabolism > Flashcards

Integration of Metabolism Flashcards

1
Q

[YouTube Playlist]: Integration of Metabolism - Lectures by Dr. Amit

A

✔

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2
Q

[8-minute video]: Fed State - Armando Hasudungan

A

✔

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3
Q

[12-minute video]: Fasted State - Armando Hasudungan

A

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4
Q

[8-minute video]: Rapoport-Leubering Cycle

A

⚡

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5
Q

What is the primary energy source for the brain?

A

glucose

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6
Q

How much of the body’s total oxygen consumption does the brain use?

A

over 20%

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7
Q

What are the main byproducts of brain metabolism?

A

carbon dioxide and lactate

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8
Q

How does the brain adapt to low glucose levels?

A

The brain can adapt to low glucose levels by using ketone bodies as an alternative energy source.

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9
Q

What is the significance of lactate in brain metabolism?

A

Lactate can be used as an energy source by neurons and is involved in the metabolic coupling between astrocytes and neurons.

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10
Q

What is the normal range for glucose levels in the blood?

A

60 - 90 mg/ml

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11
Q

What is the primary metabolic pathway in erythrocytes?

A

glycolysis

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12
Q

Why do erythrocytes rely on anaerobic glycolysis?

A

They lack mitochondria and hence cannot perform oxidative phosphorylation.

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13
Q

Fed state metabolism

What triggers the release of insulin in the fed state?

A

elevated glucose levels in the bloodstream

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14
Q

Fed state metabolism

What is the primary glucose transporter in the liver during the fed state?

A

GLUT2 (insulin-independent)

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15
Q

Fed state metabolism

Which tissues use GLUT4 transporters for glucose uptake in the fed state?

A

Skeletal muscle and adipose tissue

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16
Q

Fed state metabolism

What is the main metabolic process in the liver during the fed state?

A

Glycogenesis (conversion of glucose to glycogen).

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17
Q

Fed state metabolism

How does insulin affect lipid metabolism in adipose tissue?

A

It promotes lipogenesis (fat storage)

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18
Q

Fed state metabolism

What is the role of insulin in protein metabolism in muscles?

A

It stimulates protein synthesis.

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19
Q

Fed state metabolism

Which glucose transporter is predominant in the brain during the fed state?

A

GLUT1 and GLUT3 (insulin-independent).

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20
Q

Fed state metabolism

What is the role of insulin in the brain during the fed state?

A

Insulin has minimal direct effect; glucose uptake is insulin-independent.

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21
Q

Fed state metabolism

Outline the effects of insulin on:
(a) Glucose metabolism
(b) Lipid metabolism
(c) Protein metabolism

A

(a) Glucose metabolism
✓ Increased Glucose Uptake: Insulin promotes the uptake of glucose into cells, especially in muscle and adipose tissue, via GLUT4 transporters.
✓ Glycogenesis: In the liver and muscle, insulin stimulates the conversion of glucose to glycogen for storage.
✓ Inhibition of Gluconeogenesis: Insulin suppresses the production of glucose from non-carbohydrate sources in the liver.

(b) Lipid metabolism
✓ Lipogenesis: Insulin promotes the synthesis of fatty acids and triglycerides in adipose tissue and the liver.
✓ Inhibition of Lipolysis: Insulin inhibits the breakdown of stored fats, reducing the release of free fatty acids into the bloodstream.

(c) Protein metabolism
✓ Protein Synthesis: Insulin stimulates the uptake of amino acids into cells and promotes protein synthesis, particularly in muscle tissue.
✓ Inhibition of Proteolysis: Insulin reduces the breakdown of proteins, preserving muscle mass.

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22
Q

Fasted state metabolism

What triggers the fasted state metabolism?

A

Decrease in serum glucose levels and insulin production, leading to an increase in glucagon, cortisol and epinephrine

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23
Q

Fasted state metabolism

What is the primary hormone that increases during the fasted state?

A

glucagon

24
Q

Fasted state metabolism

What metabolic process is stimulated by glucagon in the liver during fasting?

A

glycogenolysis

25
Q

Fasted state metabolism

Which metabolic pathway is activated to produce glucose from non-carbohydrate sources during fasting?

A

gluconeogenesis

26
Q

Fasted state metabolism

What are the primary substrates for gluconeogenesis?

A

amino acids, lactate, and glycerol

27
Q

Fasted state metabolism

What happens to fatty acids during the fasted state?

A

They are mobilized from adipose tissue and undergo beta-oxidation.

28
Q

Fasted state metabolism

What is beta-oxidation?

A

The process of breaking down fatty acids to produce acetyl-CoA.

29
Q

Fasted state metabolism

What role does cortisol play in the fasted state?

A

It promotes gluconeogenesis and the breakdown of proteins to amino acids.

30
Q

Fasted state metabolism

How does epinephrine affect metabolism during fasting?

A

It stimulates glycogenolysis and lipolysis.

31
Q

Fasted state metabolism

What happens to acetly-CoA produced from beta-oxidation in the liver?

A

It is converted to ketone bodies.

32
Q

Fasted state metabolism

Which tissues primarily use ketone bodies during prolonged fasting?

A

brain, heart, skeletal muscles

33
Q

Fasted state metabolism

What happens to muscle protein during prolonged fasting?

A

It is broken down to provide amino acids for gluconeogenesis.

34
Q

ANLS

What is the Astrocyte-Neuron Lactate Shuttle (ANLS)?

A

The ANLS is a hypothesis that describes how astrocytes supply neurons with lactate, which is used as an energy source for neuronal activity.

35
Q

ANLS

How do astrocytes produce lactate?

A

Astrocytes metabolize glucose through glycolysis to produce pyruvate, which is then converted to lactate by lactate dehydrogenase.

36
Q

ANLS

What happens to the lactate produced by astrocytes?

A

Lactate is released into the extracellular space and taken up by neurons, where it is converted back to pyruvate and used in oxidative metabolism to produce ATP.

37
Q

Insulin Transduction Pathway

What is the primary function of the insulin transduction pathway?

A

The insulin transduction pathway increases glucose uptake into fat and muscle cells and reduces glucose synthesis in the liver, maintaining glucose homeostasis.

38
Q

Insulin Transduction Pathway

What happens when insulin binds to its receptor?

A

Insulin binding to its receptor triggers autophosphorylation of the receptor’s intracellular tyrosine residues, initiating a cascade of downstream signaling events.

39
Q

What is the role of insulin receptor substrate (IRS-1) in the pathway?

A

IRS-1 is phosphorylated by the activated insulin receptor, creating docking sites for downstream signaling molecules like PI3K.

40
Q

How does the PI3K/Akt pathway contribute to glucose uptake?

A

The PI3K/Akt pathway promotes the translocation of GLUT4 vesicles to the plasma membrane, facilitating glucose uptake into cells.

41
Q

What is the significance of GLUT4 in the insulin signaling pathway?

A

GLUT4 is a glucose transporter that moves to the cell surface in response to insulin signaling, allowing glucose to enter muscle and adipose cells.

42
Q

What is diabetes mellitus?

A

Diabetes mellitus is a metabolic disorder characterized by chronic hyperglycemia due to defects in insulin secretion, insulin action or both.

43
Q

What are the main types of diabetes mellitus?

A

Type 1 diabetes (insulin-dependent)
Type 2 diabetes (non-insulin dependent)

44
Q

What causes Type 1 diabetes?

A

Type 1 diabetes is caused by autoimmune destruction of pancreatic beta cells, leading to an absolute deficiency of insulin.

45
Q

What causes Type 2 diabetes?

A

Type 2 diabetes is caused by insulin resistance and relative insulin deficiency, often associated with obesity and genetic factors.

46
Q

How is glycated haemoglobin (HbA1c) formed?

A

It forms when glucose in the blood binds to haemoglobin in red blood cells.

47
Q

How is HbA1c used as a diagnostic tool?

A

It is used to diagnose and monitor diabetes. Higher HbA1c levels indicate poorer blood sugar control.

48
Q

(a) What is the normal range for HbA1c levels?
(b) What HbA1c levels indicate prediabetes?
(c) What HbA1c levels are diagnostic of diabetes?

A

(a) HbA1c levels below 5.7% are considered normal.
(b) Levels between 5.7% and 6.4% indicate prediabetes.
(c) Levels between 5.7% and 6.4% indicate prediabetes.

49
Q

List 6 strategies for management of diabetes mellitus.

A

(1) Administering insulin itself in the case of Type 1 diabetes mellitus

(2) Increasing insulin secretion by the pancrease in Type 1 diabetes mellitus
(a) by use of secretagogues e.g. sulfonylureas such as Glimepiride and Glipizide. They increase release of insulin from the pancreas. (b) Non-sulfonylureas e.g. Repaglinide, Nateglinide and Mitiglinide. They inhibit (close) K-ATP channels and open calcium channels of beta cells causing release of insulin. Reduces glucagon secretion in alpha cells. They are generally known as Glinides.

(3) Increase sensitivity of target organs to insulin
Use of sensitizers which address the core problem of insulin resistance in Type II diabetes mellitus…
(a) Biguanides e.g. metformin (Glucophage) which decrease glucose output by inhibiting gluconeogenesis in the liver and also increase the uptake of glucose by tissues. Acts mainly in the liver. (b) Thiazolidinediones e.g. Pioglitazone which regulate glucose and fat metabolism by making better use of glucose by cells. They increase sensitivity by acting mainly on adipse tissue and muscle. They promote glucose entry.

(4) Decrease the digestion and absorption of glucose from the GIT
By use of alpha-glucose inhibitors e.g. Glucobay (Acarbose). They are antihyperglycemic agents. They lower blood glucose by delaying the digestion and absorption of complex CHOs. They are competitive inhibitors of the enzymes (lysosomal glucosidases) in the brush border of enterocytes that cleave complex carbohydrates to monosaccharides.

(5) Increase sugar loss through urination
(a) Use oral Glycosurics which inhibit SGLT-2 in kidneys i.e. SGLT-2 inhibitors aka. Gliflozins. Remove sugar through urine by providing lower glucose reabsorption in the kidneys. They are hypoglycemic drugs.

(6) Use of peptide analogues (injectable)
They are GLP-1 and GIP agnoists. They are incretin mimetics e.g. semaglutide. They are agents that act like incretin hormones such as GLP-1. They bind to GLP-1 receptors and stimulate insulin release. They suppress appetite and inhibit glucagon secretion. They are called Gliptins.

50
Q

Rapoport-Leubering Cycle

What is the Rapoport-Leubering cycle?

A

It is a metabolic pathway in red blood cells that produces 2,3-bisphosphoglycerate (2,3-BPG), which regulates oxygen release from hemoglobin.
[Diagram]

51
Q

Rapoport-Leubering Cycle

What enzyme catalyzes the formation of 2,3-BPG in the Rapoport-Leubering cycle?

A

Bisphosphoglycerate mutase.
[Diagram]

52
Q

Rapoport-Leubering Cycle

What is the main function of 2,3-BPG in red blood cells?

A

It decreases the affinity of hemoglobin for oxygen, facilitating oxygen release to tissues.

53
Q

Rapoport-Leubering Cycle

How does the Rapoport-Leubering cycle affect ATP production?

A

One mole of ATP is lost in the formation of 2,3-BPG from 1,3-BPG.
[Diagram]

54
Q

Rapoport-Leubering Cycle

What conditions can increase the levels of 2,3-BPG?

A

Hypoxia, high altitude, and certain types of anemia.
[Diagram]

55
Q

Rapoport-Leubering Cycle

Which enyzme converts 2,3-BPG to 3-phosphoglycerate in the Rapoport-Leubering cycle?

A

bisphosphoglycerate phosphatase
[Diagram]

56
Q

Which of the following pathways would not occur in the in the liver mitochondria?
(a) FA oxidation
(b) FA synthesis
(c) Ketone body (KB) synthesis
(d) Urea synthesis
(e) FA metabolism

A

(b) FA synthesis

Biochemistry (21 decks)

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