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Nutrition and Metabolism > Integration of Metabolism > Flashcards

Integration of Metabolism Flashcards

1
Q

What stimulates insulin secretion?

A
  • rise in blood glucose
  • rise in amino acid concentration
  • gut hormones (secretin)
  • glucagon
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2
Q

What inhibits insulin secretion?

A

Adrenaline

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3
Q

How is insulin secretion controlled?

A

Glucose enters beta-cell via GLUT2 receptor. Enters TCA cycle and releases ATP.
ATP blocks K+ channel - changes membrane potential of beta-cell.
Causes Ca2+ channels to open - influx of Ca2+ into cell, stimulates release of insulin in vesicles.

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4
Q

What stimulates glucagon secretion?

A
  • low blood glucose
  • high concentration amino acids in blood
  • adrenaline
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5
Q

What are the metabolic effects of insulin? (general)

A
  • promotes fuel storage
  • stimualtes glycogen synthesis and storage.
  • stimulates fatty acid synthesis and storage from carbohydrates
  • stimulates amino acid uptake and protein synthesis
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6
Q

What are the metabolic effects of insulin at a molecule level?

A
  • Activation of Akt protein kinase.
    1. Insulin binds - autophosphrylation of receptor
    2. Phosphorylation of IRS 1/2
    3. IRS 1/2 sctivates P13 kinase > kinase cascade
    4. Activation of PDK 1 kinase by PIP3.
    5. Triggers phosphorylation activation of phosphokinase B.
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7
Q

By what mechanism does insulin cause gycogen synthesis?

A

Activated Akt/PkB
- Phosphorylates glycogen synthase kinase (inactivated).
- Glycogen synthase remain active - catalyses glycogen synthesis.
Akt triggers GLUT4 receptors to fuse to membrane to increase glucose uptake into muscle cells.

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8
Q

By what mechanism is lipolysis inhibited by insulin?

A

Active Akt phosphorylates phosphodiesterase (ACTIVE)

cAMP converted to ATP - inactivation of protein kinaseA so hormone sensitive lipase is not activate by protein kinase A.

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9
Q

By what mechanism does insulin effect gene expression?

A

Through Ras and MAPK.
Autophosphorylation of insulin receptor - pathway occurs through Ras. Cascade of phosphorylation up to MAPKinase.
MAPK will activate/inhibit gene expression of different genes.

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10
Q

Which GLUT transporters are found in different tissues?

A

GLUT1 - Erythrocytes and brain (high affinity)
GLUT2 - Liver and beta-cells (non-dependent - low affinity)
GLUT3 - Neurons (high affinity)
GLUT4 - Adipose , Muscle (insulin dependent - low affinity)

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11
Q

What are the metabolic effects of glucagon?

A
  • mobilise fuel
  • activates glyconeogensis in the liver
  • activates glycogenolysis in the liver
  • promotes fatty acid release from adipose tissue
  • promotes fatty acid oxidation and ketone body formation in the liver.
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12
Q

What are the metabolic effects of adrenaline?

A
  • inhibits insulin secretion
  • stimulates glucagon secretion
  • Stimulates gluconeogenesis in muscle and liver
  • stimulates fatty acid release from adipose tissue
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13
Q

What are the metabolic effects of cortisol?

A
  • provides long term requirements
  • stimulates amino acid metabolism from muscle (catabolism)
  • stimulates gluconeogensis
  • stimulates fatty acid release from adipose tissue.
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14
Q

Which tissue(s) have priority for glucose?

A

Erythrocyte and the brain.
Brain can only use glucose as fuel source.
Erythrocyte can only use glucose as there is no mitochondria

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15
Q

What happens to excess glucose in the liver?

A

Glucose > acetyl CoA > TAG

TAG is transported in VLDL to adipocytes.

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16
Q

What occurs during fasting?

A

Hormone sensitive lipase is activated by glucagon and adrenaline.
Fatty acids are transported to the liver bound to albumin.

17
Q

Why is fatty acid not a gluconeogenic precursoe?

A

Pruvate > acetyl CoA is IRREVERSIBLE
Catalysed by pyruvate dehydrogenase.
PDH is activated by insulin and inhibited by insulin.

18
Q

How do ketone bodies form?

A

Fatty acid oxidation in hepatocyte - leads to high concentration of acetyl CoA - exceeds TCA capacity.
Excess are channelled into into ketone body formation.

19
Q

Name 2 ketone bodies.

A

Acetoacetate

B-hydroxybutarate

20
Q

What is the general function of ketone bodies?

A

Most tissue use glucose and ketone bodies as energy sources.

Ketone bodies cannot be used by erythrocytes and are only used by the brain if necessary.

21
Q

What metabolic pathways occur in prolonged starvation?

A

Body utilises more ketone bodies.
More KB are recovered from the kidney.
Inhibits breakdown of amino acids/muscle.

22
Q

What are the specific functions of ketone bodies?

A
  • act on the pancreas to stimualte insulin release
  • limits muscle proteolysis
  • limits adipose tissue lipolysis
23
Q

What is diabetes mellitus?

A

Unable to regulate blood glucose concentration. Can be type 1 or type 2.

24
Q

What is type 1 dibetes?

A

Autoimmune destruction of Beta-cells in the pancreas.

Body cannot produce insulin to regulate blood glucose.

25
Q

What are symptoms of type 1 diabetes?

A 
Polyuria, polydipsia
Excess eating
fatigue
weight loss
muscle wasting
weakness
26
Q

How is type 1 diabetes managed?

A

Chronic condition.

Monitoring of blood glucose levels and injecting with insulin when required.

27
Q

What causes type 2 diabetes?

A

Associated with diet and lifestyle e.g. obesity.

28
Q

Which type of diabetes has hyperglaecemia or ketoacidosis?

A

Type 1 = hyperglaecemia and ketoacidosis

Type 2 = hyperglaecemia but NO ketoacidosis

29
Q

How is type 2 treated?

A

Often responds to diet and oral hypoglaecemic agents.

30
Q

What is the difference between untreated diabetes mellitus and starvation?

A

In starvation, ketone body production stimulates insulin release which limits muscle breakdown.
In diabetes theres no insulin to be released so muscle breakdown continues hence muscle wasting occurs.

31
Q

Name 4 chronic complications of diabetes mellitus.

A

Microangiopathy - changes in walls of small blood vessels.
Retinopathy - blindness is 25x more common in diabetics.
Nephropathy - renal failure 17x more common in diabetics
Neuropathy - postural hypertnesion, impotence, foot ulcers.

Nutrition and Metabolism (11 decks)

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