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A Principles of Physiology > Metabolism & Diabetes > Flashcards

Metabolism & Diabetes Flashcards

Got a little lazy with this one and didn't transcribe all, put time stamps for what part of lecture to watch

1
Q

Absorptive state

A
  • When food is coming into the gut
  • Large quantities of carbs, fats, and amino acids entering the blood from the GI tract
  • Cells metabolize this fuel directly and store away excess
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2
Q

Post-absorptive state

A
  • When food is not coming into the gut
  • Stored energy is released and used to fuel cellular metabolism
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3
Q

In what state is insulin released?

A

Absorptive

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4
Q

Insulin

A

Causes insertion of GLUT-4 transporters into muscle at fat cell membranes and affects many enzymes in fat, muscle, and liver cells to promote storage of excess nutrients

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5
Q

The ___ nervous system regulates release of glucose from the liver

A

Autonomic

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6
Q

Flow chart

A

Lecture at 8:54

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7
Q

What triggers enzymes in the liver to break down glycogen into glucose, or use glycerol to create new glucose (or from other nutrients in flow chart)?

A

A drop in blood glucose levels

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8
Q

Flow chart breakdown

A

Neurons metabolize:
- glucose from blood
- ketones from blood (when glucose is not available)

All other cells metabolize:
- free fatty acids
- ketones from blood (when present)

Muscle can metabolize:
- stored glycogen (this produces lactate & pyruvate)

When glucose is scarce the liver releases:
-glucose into blood:
- from stored glycogen
- from gluconeogenesis from glycerol
- from gluconeogenesis from lactate & pyruvate
-ketones from metabolism of fatty acids in liver

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9
Q

What do neurons metabolize?

A
  • glucose from blood
  • ketones from blood (when glucose is not available)
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10
Q

What do muscle cells metabilize?

A

Stored glycogen (this produces lactate & pyruvate)

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11
Q

What do all other cells (other than neurons and muscle) metabolize?

A
  • free fatty acids
  • ketones from blood (when present)
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12
Q

When glucose is scarce, what does the liver release?

A

Glucose into blood:
- from stored glycogen
- from gluconeogenesis from glycerol
- from gluconeogenesis from lactate & pyruvate

Ketones from metabolism of fatty acids in liver

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13
Q

Diagram showing absorptive vs. post-absorptive state

A

16:45

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14
Q

What happens in the absorptive state?

A
  • Blood glucose, amino acids, and fatty acid levels increase due to absorption from GI tract and activity in the pathways is changed (high insulin)
  • Amino acids are built into protein, glucose is stored as glycogen, fatty acids are stored as triglycerides, and the liver builds glycogen and stops producing glucose and ketones
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15
Q

Diagram showing effects of increased plasma insulin levels (during absorptive state)

A
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16
Q

Diagram showing effects of decreased plasma insulin levels (during post-absorptive state)

A
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17
Q

What is the primary stimulus for insulin release?

A

Combination of increase in blood sugar levels and other stimuli related to the GI tract (e.g. GIP)

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18
Q

Detail on insulin diagrams

A

Watch lecture at 21 mins

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19
Q

Which cells allow glucose to go back and forth across the membrane in a way that’s independent from insulin?

A

Those that contain GLUT-2 receptors
(neurons and liver have this, so they let glucose across the membrane without insulin presence)

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20
Q

How does exercise affect glucose permeability? (important for people with diabetes)

A
  • After exercise, muscle cell membranes lose their dependence on insulin to absorb glucose
  • If you don’t have diabetes, after exercise, the sugar that comes into the blood doesn’t spike as high as it otherwise would and insulin doesn’t rise as high
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21
Q

Diagram of insulin action at the cellular level

A
  • For cells that rely on GLUT-4 transporters to get sugar to cross the membrane, insulin is the trigger for this
  • Insulin binds and triggers second-messenger systems
  • There’s exocytosis and insertion of the transporters and now glucose from the plasma can come into the body
  • If this was a muscle cell, and it was burning glucose, glucose levels would be low in the cell and glucose transport in the blood would be favored. Not having transporters in the membrane would prevent glucose from going down its gradient.
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22
Q

Glucose movement across the membrane

A
  • Depends on the concentration gradient
  • If the cell is using glucose, and blood sugar levels are high, then glucose will come into the cell where glucose levels are low
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23
Q

GLUT-2 receptors

A
  • Expressed in liver cells
  • Does not rely upon the presence of insulin to transport glucose across the membrane
  • However, the presence of sugar affects how sugar goes across the membrane by regulating levels of glucose inside the cell
  • Insulin is released when glucose levels are high
  • Glucose binds to beta cells and stimulates release of insulin into bloodstream
  • Presence of carbohydrates in the gut stimulates the release of GIP, which triggers the release of insulin into the body
  • Insulin does not affect GLUT-2 transporters. Rather, it affects intracellular biochemistry
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24
Q

Does insulin affect GLUT-2 transporters?

A

No, but it does affect intracellular biochemistry

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25
Q

What cells does glucose bind to and what does this trigger?

A

Binds to beta cells to trigger release of insulin into bloodstream

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26
Q

GLUT-2 receptors are expressed in ___ cells

A

Liver

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27
Q

What cellular/molecular changes does insulin trigger?

A
  • Inside of the cell, glucose is not being produced when there’s a lot of sugar outside that’s being absorbed through the GI tract
  • It triggers increased activity of hexokinase, which keeps intracellular glucose concentration lower than extracellular, promoting glucose uptake (this reduces the concentration of glucose inside the cell to create a gradient for glucose)
  • Increases glycogen synthesis, which converts intracellular glucose into glycogen
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28
Q

How does the autonomic NS regulate liver function?

A
  • Stimulation of symp and parasymp affects glucose release from liver:
    -Sympathetic stimulation causes glucose to be pushed into the blood, parasymp causes glucose uptake by liver
  • Leptin, a hormone released from fat cells, activates ANS and lowers release of glucose from liver
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29
Q

Type 1 diabetes

A
  • Makes up 5% of all cases
  • Destruction of beta cells
  • Autoimmunity against beta cells of pancreas
  • Controlled with insulin therapy
30
Q

Type 2 diabetes

A
  • Makes up 95% of all cases
  • Insulin resistance
  • Insufficient insulin levels
  • Receptors to insulin not as effective
  • Can be controlled by diet and exercise but may require medication and insulin therapy
31
Q

Gestational diabetes

A

Occurs in 18% of pregnancies

32
Q

Video to learn more about diabetes

A

https://www.youtube.com/watch?v=BME0639IP5g

33
Q

Symptoms of type 1 diabetes

A
  • Hyperglycemia (elevated blood sugar level)
  • Polyphagia (increased eating)
  • Polydipsia (increased drinking)
  • Glucosuria (sugar in urine)
  • Ketoacidosis and hyperkalemia (metabolic acidosis due to ketone metabolism; increased potassium levels due to release from cells)
  • Acetone on breath (one ketone, acetoacetate, converts into acetone in the blood, which is volatile in lungs)
  • Muscle and fat wasting (weight loss)
  • Hyperkalemia (increased potassium in extracellular fluid)
34
Q

Flow chart about insulin deficiency (don’t memorize, will be on exam)

A

53 mins

35
Q

Causes of type 1 diabetes

A
  • Autoimmune disease where immune system makes antibodies that attack beta cells in pancreas
  • Contributing factors include a genetic predisposition and environmental factors
  • Increased incidence of type 1 diabetes CAN NOT be explained by genetics
  • Proposed environmental factors include diet, gut microbiome, and viral infections (human enterovirus (HEV)) that contain antigens similar in structure to beta cell proteins
36
Q

Banting (MD) and Best (med student at University of Toronto - pig pancreas

A
37
Q

Mechanisms of long-term complications of diabetes (type 1 and 2)

A
38
Q

Medical treatments (combined with lifestyle changes of counting carbohydrates consumed and exercise)

A
  • Insulin therapy
  • Glucose monitoring
  • Closed-loop system
39
Q

Insulin therapy

A
  • Balance between carbohydrates consumed, exercise, and insulin taken (remember that muscles become ‘glucose sponges’ after exercise)
  • Injections of insulin (long-lasting/basal and short-lasting/bolus
  • Insulin pump - basal rate with bolus when carbs are consumed
40
Q

Glucose monitoring

A
  • Urine test (poor information, antiquated)
  • Blood glucose from finger prick (accurate but sporadic)
  • Continuous blood glucose monitoring (CBG)
    -Subcutaneous sensor measures glucose levels in extracellular fluid
    -Calibrated several times per day with blood glucose from finger prick
41
Q

Closed-loop system

A

Combines CBG monitoring with insulin pump to create ‘artificial pancreas’ functioning

42
Q

Control of feeding behavior

A
  • Long-term: calories in vs. calories out over the time course of weeks to years
  • Short-term: satiety signals that end feeding behavior at each meal. Time course is minutes
43
Q

Feeding behavior and body weight over the long term

A

1:13

44
Q

Graph showing weight over periods of starvation and forced feeding

A
45
Q

Experimental modulation of brain to change feeding behavior in animals

A
  • If you lesion one area of the hypothalamus, the animal will eat more (hyperphagia)
  • If you lesion another area, it will eat less (hypophagia)
46
Q

Leptin effects in mice

A

1:17:30

47
Q

Leptin effects in humans

A

Mutation of gene that produces leptin is rarely an issue in humans, but there are some cases

48
Q

Evidence that leptin is involved in weight regulation

A
  • Leptin is produced by fat cells (adipocytes)
  • Blood levels of leptin into the CSF of genetically obese mice causes a long-term decline in feeding
  • Some (but not all) cases of pathological obesity in humans are associated with low or absent levels of blood leptin
  • Injection of leptin reduces the weight of these patients
  • There are leptin receptors in the brain, particularly in the hypothalamus
49
Q

Lipostatic model

A
  • Too much fat in the body will activate anorectic circuit
  • Not enough fat will activate orexigenic
50
Q

Short-term control of feeding (anorectic signals)

A
  • Once feeding begins, your stomach becomes fuller, activating stretch-receptors
  • The stretch-receptors send action potentials to the nucleus of the solitary tract
  • The chemical contents of the lumen of the SI affect neurons as well, causing a visceral sensory signal
  • Also, the cells lining the GI tract release hormones into the blood that send signals to the same area of the brain, e.g. the hypothalamus, causing insulin to be released from the pancreas
  • All of these inhibit feeding behavior
51
Q

What are the two categories of satiety signals?

A

Hormones and action potentials

52
Q

Orexigenic signals

A
  • Ghrelin
  • Other factors
53
Q

Ghrelin

A
  • Highly concentrated in stomach
  • Released when stomach is empty
  • Has receptors in hypothalamus and anterior pituitary
  • Causes hyperphagia (increased eating) and obesity when injected
54
Q

Ghrelin levels in gastric bypass patients

A
55
Q

Ghrelin inhibits or excites

A
56
Q

Prader-Willi Syndrome

A
  • Most common genetic cause of obesity
  • Never feeling full, constantly hungry
  • Fasting levels of ghrelin are vastly elevated in adults with Prader-Willi Syndrome
  • Fasting levels are normal in PW children before the onset of obesity but rise with its appearance
57
Q

What are ‘satiety signals’?

A
  • Gastric and gut distention, vagal activation
  • Rise in blood levels of insulin AND glucose
  • Release of hormones that impact the hypothalamus:
    -Cholecystokinin (CCK)
    -Glucose-dependent insulinotropic polypeptide (GIP)
    -Glucagon-like peptide (GLP-1)
58
Q

Take-home lessons

A
  • The hypothalamus is a key player in behavioral and physiological systems controlling body temperature, blood pressure, blood volume, and body energy stores
  • Body weight is a controlled variable. It regulates feeding behavior in the long term through feedback mechanisms that measure body fat, among other things. Genetic factors play a large role in this
  • Short-term feeding behavior is governed by physiological (ghrelin, CCK, etc.) as well as hedonic factors (taste, smell, and environmental cues)
59
Q

Bariatric surgery

A
60
Q

Incretins (GIP and GLP-1)

A
61
Q

GLP-1 genetics and pharmacology

A
  • GLP-1 comes from proglucagon gene, the same gene as glucagon
  • GLP-1 half-life in blood is minutes because of enzymatic breakdown from DPP-4 (enzyme in blood)
62
Q

The incretin effect is diminished in people with type 2 diabetes

A
  • Insulin release on the y-axis
  • Black line is what happens when carbs are introduced into the GI tract- big release of insulin
  • Blue line shows injection of glucose- blunted release of insulin
  • In people with type-2 diabetes, insulin release is blunted - cause and effect of elevated blood sugar levels
63
Q

Physiological vs. pharmacological actions of GLP-1

A

52 mins

64
Q

The metabolic actions of GLP-1 in different organs and cell types (focus on pancreas, brain, and stomach)

A
  • GLP-1 stimulates beta cells to increase insulin secretion
  • It also increases the biosynthetic pathway of secretion
  • It decreases apoptosis - population of beta cells is maintained at a higher level
  • Decreases glucagon secretion
65
Q

Beta cells in type 1 diabetes

A

Beta cells are removed much faster than they’re produced and the volume is very low, if anything

66
Q

Beta cells in type 2 diabetes

A

Modulated

67
Q

GLP-1 decreases ___ secretion

A

Glucagon

68
Q

Timeline of GLP-1 discovery and clinical development (don’t need to memorize)

A
69
Q
A
70
Q
A
71
Q

What is gluconeogenesis?

A

The synthesis of glycogen or glucose from non-sugar precursors such as glycerin, lactic acid, and amino acids.

A Principles of Physiology (25 decks)

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