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Metabolism II > 18/19 - Integration of Metabolism > Flashcards

18/19 - Integration of Metabolism Flashcards

1
Q

Give the metabolic goals and main energy sources in the following states:

Fed
Post-absorptive
Fasting
Exercise

A

Fed

  • Remove glucose from blood and store for later (insulin)
  • Glucose is main energy source

Post-absorptive

  • Provide glucose to the tissues that need it (eg. brain) and provide energy to other tissues via fatty acids
  • GLucagon

Fasting

  • glucagon
  • Same as PA
  • Reduce glucose requirements as much as possible

Exercise

  • Epinephrine
  • Provide energy to muscle
  • Increase oxygen supply to muscle
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2
Q

Give the MAIN source of glucose during fast-feed cycle (eg. after meal)

A
  • Exogenous (just ate)
  • Liver glycogen (8 hours after meal)
  • Gluconeogenesis (2 days after meal, no more glycogen)
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3
Q

True or false, glucagon acts on muscle to provide energy

A

False, there are no glucagon receptors on muscle cells. There are insulin receptors, however.

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4
Q

How does epinephrine cause different effects in the liver and muscle?

A

Liver: provide glucose for other tissues during fasting (glucagon) or stress (epinephrine) with cAMP signalling increasing glycogenolysis and gluconeogenesis

Muscle: cAMP signaling to increase glycogenolysis and glycolysis

Different isoforms of phosphofructokinase and pyruvate kinase in liver and muscle lead to different effects of epinephrine in muscle than effects caused by glucagon or epinephrine in other tissues

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5
Q

Give sources for ATP as the duration of an activity increases

A

Short: ATP

Moderate (10 s): phosphocreatine (eg. sprints). Can re-phosphorylate ADP

Few minutes: glycolysis

Longer: oxidative phosphorylation

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6
Q

Why is diabetes mellitus associated with increased thirst and urination?

A

Because the osmolarity of the blood is disrupted by extra glucose

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7
Q

What is a common diagnostic test for diabetes?

A

Administering lots of glucose and then looking at blood glucose levels before and after. A lack of insulin/insulin sensitivity will lead to very very high blood glucose

You can also just look for elevated fasting plasma glucose

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8
Q

In what type of diabetes is ketoacidosis common? Why?

A

Type I, increased breakdown of TAGs leads to accumulation of free fatty acids which are converted to acetyl-CoA in the liver, which is subsequently converted to ketone bodies.

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9
Q

Which type of diabetes has a strong genetic link and responds to oral agents?

A

Type II

Type I generally only treated with extra insulin.

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10
Q

Give the etiology of type I diabetes

A
  1. Initiating event (eg. exposure to a virus or toxin that starts autoimmune destruction of beta cells)
  2. Slow beta cell destruction over a period of years.
  3. Clinical disease manifests when insulin secretory capacity falls below a certain threshold.
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11
Q

Describe the metabolic changes associated with diabetes and carbohydrates

A

Hyperglycemia

  • Decreased glucose uptake into muscle and adipocytes
  • Ongoing gluconeogenesis (high glucagon)
  • GLycogen breakdown in liver
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12
Q

Describe the metabolic changes associated with diabetes and amino acids

A
  • Amino acid uptake and protein synthesis are not stimulated leading to many gluconeogenic precursors
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13
Q

Describe the metabolic changes associated with diabetes and fatty acids

A

No insulin and high glucagon leads to increased hormone sensitive lipase activity (increased TAG metabolism and fatty acid conversion to acetyl-CoA in the liver)

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14
Q

Describe the metabolic changes associated with diabetes and lipoproteins

A
  • Insulin inhibits VLDL secretion and activates lipoprotein lipase
  • If there is no insulin decreased clearance of TG-rich lipoproteins and increased VLDL secretion occurs
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15
Q

Give the etiology of type II diabetes

A
  1. Genetic predisposition and environment, lifestyle and obesity factors contribute to insulin resistance
  2. Hyperinsulinemia (insulin tries to compensate with increased synthesis)
  3. Beta cell exhaustion
  4. Hyperglycemia
  5. Type II diabetes
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16
Q

How do you calculate BMI?

A

kg/m^2

weight/height squared

17
Q

Which type of body shape is linked to insulin resistance, CV disease and overall mortality?

A

Apple shaped, more visceral fat around organs. Whereas pear shaped is more subcutaneous fat

18
Q

How can the risk for diabetes be relatively low even if the BMI is high?

A

If there is a low waist to hip ratio (eg. bodybuilders would have high BMI and low WHR)

19
Q

List the four things that adipocytes secrete

A

Leptin
- Signals energy sufficiency and decreases appetite. Obesity associated with leptin resistance

Adiponectin

  • Enhances insulin sensitivity
  • Increases glucose in muscle
  • Decreases influx of FFA into liver and hepatic glucose output
  • Increase fatty acid oxidation
  • Secretion decreases in obesity, especially in abdominal fat

Free fatty acids
- Activate protein kinase C and upregulate inhibitory serine/threonine phosphorylation of IRS-1 (increased in obesity)

Inflammatory cytokines

  • TNFalpha and IL-6 can lead to decreased insulin sensitivity, possibly by increasing serine/threonine phosphorylation of IRS-1 and IRS-2 and repression of genes involved in adipocyte fatty acid uptake and storage. Increased in obesity.
  • During obesity, macrophages infiltrate the adipose tissue and also secrete inflammatory cytokines
20
Q

How can unesterified fatty acids induce insulin resistance?

A
  • At insulin receptor, stimulating serine/threoning phosphorylation by protein Kinase C and decreasing tyrosine phosphorylation. Signal transduction is less efficient and the response to insulin is muted.
21
Q

Adiponectin promotes AMP activated kinase (AMPK) activation, what are the consequences of this?

A

Anti-diabetic effects!

  • HMG-CoA reductase inhibited (cholesterol biosynthesis inhibited)
  • Acetyl-CoA carbxoylase inhibited (fatty acid biosynthesis decreased)
  • mTor (decreased protein synthesis)
  • glycogen synthase inhibition (glycogen synthesis inhibited)
  • Hormone sensitive lipase inhibited (lipolysis decreased)
  • GLUT4 upregulated
  • PFK2 upregulated in heart, increasing cardiac glycolysis
  • Mitochondrial biogenesis and oxidative metabolism increased
22
Q

What does the agouti gene do?

A

signalling peptide

  • Yellow fur
  • Inhibits melanocortin signalling (leading to obesity)

methylation of this gene keeps the above expressions silent. Methyl rich diet can induce this in offspring.

23
Q

What is leptin (from adipocytes) action on the hypothalamus?

A

Promotes

  • Melanocortin (decrease food intake) from POMC neurons
  • Activation of SNS (thermogenesis) through adrenergic beta receptors

Inhibits
- NPY (increased food intake) and AgrP have orexic effects

Obesity is often characterised by leptin resistance.

24
Q

What does ghrelin from the stomach do to hypothalamus? INsulin?

A

Ghrelin: Stimulates NPY/AgrP neurons in the hypothalamus

Insulin: Along with leptin, inhibits NPY/AgrP neurons and stimulates POMC/CART neurons

25
Q

How does loss of leptin/leptin receptors promote obesity?

A

Leptin does the following

  • Stimulates SNS
  • Muscle: increaes glycogeolysis, glycolysis, energy expenditure and fatty acid oxidation
  • Adipose: Increased lipolysis, uncoupling of mitochondrial oxidative phosphorylation
  • Pancreas: Suppression of insulin synthesis, increased glucagon secretion

Metabolism II (9 decks)

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