M3 L4 Flashcards

(79 cards)

1
Q

What happens to glucose availability during fasting? what will decrease bc of this?

A

Glucose levels drop due to lack of dietary intake.

Insulin will decrease

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2
Q

What does insulin inhibit?

A

inhibits processes that raise blood glucose or break down energy stores

  • lypolysis
  • glycogenesis (producing glucose)
  • glycogenolysis (glycogen into glucose)
  • ketogenesis
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3
Q

What is lipolysis?

A

The process of breaking down triglycerides into FFAs and glycerol.

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4
Q

What causes the body to shift metabolism during overnight fasting?

A

A drop in blood glucose due to no food intake for several hours.

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5
Q

Which hormones change in response to fasting?

A

Insulin decreases, glucagon increases.

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6
Q

What metabolic pathway does the liver activate during fasting to maintain glucose levels?

A

Gluconeogenesis

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7
Q

Why do muscle and other tissues switch to fatty acids for energy during fasting?

A

To spare glucose for the brain and red blood cells.

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8
Q

what does glucagon do?

A

increases gluconeogensis and lipolysis

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9
Q

what does insulin do?

A

it increases glucose uptake

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10
Q

What happens if you can make glycogen but cant break it down?

A

you get fasting hypoglycemia — even if glycolysis inside cells still works.

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11
Q

What are two factors that increase blood glucose?

A
  • glucose absorption from digestive tract
  • hepatic glucose production (via glycogenolysis or gluconeogensis)
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12
Q

what is glycogenolysis

A

breaking down glycogen into glucose to be used for energy

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13
Q

What are two factors that decrease blood glucose?

A
  • transport of glucose into cells (for storage or utilization of energy production like for ATP)
  • urinary excretion of glucose
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14
Q

What is the role of glycerol, sterols, and fatty acids in the liver regarding lipid transport?

A

Glycerol combines with sterols and fatty acids to form lipid droplets in liver cells, which are then used to synthesize VLDLs that transport fats (triglycerides and cholesterol) through the bloodstream to other tissue

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15
Q

what happens when glucose enters the liver via GLUT2?

A

used to make glycogen, nucleotides, glycerol, and lipids.

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16
Q

Diff between GLUT2 and GLUT4 for their KMs??

A
  • GLUT2 lets glucose move in and out freely based on concentration because it has a high Km (low affinity), so it only needs to act when glucose levels are high.
  • GLUT4 has a low Km (high affinity), so it works well even when glucose is low. BUT here’s the key: GLUT4 is insulin-dependent.
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17
Q

Where is GLUT4 found?

A

mainly in muscle and fat (adipose) tissues

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18
Q

Where is GLUT2 found?

A

found in the liver, pancreas, and kidney

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19
Q

What does it mean that GLUT 4 is insulin dependent?

A
  • When insulin is present (like after you eat), it signals muscle and fat cells to bring GLUT4 transporters to the cell surface.
  • GLUT4 then helps those cells take up glucose from the blood efficiently for energy use or storage.
  • Without insulin, GLUT4 stays inside the cell, so glucose uptake in muscle/fat is limited.
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20
Q

Is GLUT2 insulin dependent?

A

No, GLUT2 is not affected by insulin.

GLUT2 is a passive glucose transporter and its presence on the membrane is constant and does not change with insulin levels.

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21
Q

What is Type 1 diabetes?

A

it is an autoimmune disease of Beta cells in the pancreas

so the pancreas cant make insulin

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22
Q

What does insulin normally do?

A

Stimulates glucose uptake into tissue cells (like muscle and fat).

Stimulates glycogen formation in the liver (stores glucose as glycogen).

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23
Q

Type 1 Diabetes: what happens when the pancreas cant make insulin?

A
  • Glucose can’t enter cells.
  • Liver can’t convert glucose to glycogen.
  • Blood sugar remains high (chronic hyperglycemia).
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24
Q

What happens to blood sugar levels in Type 1 Diabetes?

A

They rise (hyperglycemia), because glucose can’t enter cells or be stored in the liver

  • this is bc no insulin means no key to unlock the lock which is the cell so glucose stay in blood
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25
Why does the liver make more glucose in Type 1 Diabetes?
Because insulin usually suppresses glucose production; without insulin, gluconeogenesis continues unchecked. * also it thinks we aren't getting glucose bc it isn't being let in
26
What are Insulin granules and what do?
storage vesicles in pancreatic beta cells that hold insulin and release it into the bloodstream when blood glucose is high.
27
What happens when calcium enters the beta cell?
It triggers exocytosis of insulin granules
28
What is the final signal for insulin secretion?
An influx of calcium into the beta cell
29
Why is calcium essential for insulin release?
It causes insulin granules to fuse with the cell membrane and release insulin into the blood
30
What is type 2 diabetes?
insulin resistance develops (the insulin receptors to be specific) and the cells fail to respond to insulin * could lead to an excess of insulin bc its there but it just cant work with the receptor
31
Glucose Stimulation of Insulin Release What transporter allows glucose to enter pancreatic β-cells?
GLUT2 (a low-affinity, high-Km glucose transporter)
32
Glucose Stimulation of Insulin Release What happens to glucose once it enters the β-cell (via GLUT2 receptors)?
It is oxidized through glycolysis and the TCA cycle to produce ATP
33
Glucose Stimulation of Insulin Release What effect does increased ATP have on potassium channels?
It closes ATP-sensitive K⁺ channels on the β-cell membrane
34
Glucose Stimulation of Insulin Release What happens when potassium channels close?
The membrane depolarizes due to potassium buildup inside the cell which triggers the opening of voltage gated Ca+ channels
35
Glucose Stimulation of Insulin Release What is the role of calcium in insulin secretion?
Calcium influx triggers insulin granules to fuse with the membrane
36
Glucose Stimulation of Insulin Release What happens after insulin granules fuse with the membrane?
Insulin is released into the bloodstream via exocytosis
37
Glucose Stimulation of Insulin Release Why is GLUT2 important in this process?
It allows the β-cell to "sense" high blood glucose and start the insulin release pathway
38
What are these 4 diagrams showing?
explains how insulin controls glucose uptake in muscle and adipose (fat) tissue by regulating the location of GLUT4, the glucose transporter. * Muscle tissue (top half) * Adipose (fat) tissue (bottom half)
39
What is GLUT4
A glucose transporter found in muscle and fat cells. It helps import glucose into cells, but only appears on the cell surface in response to insulin.
40
What is the insulin receptor
A protein on the cell surface that binds insulin and triggers signals that cause GLUT4 to move to the membrane.
41
Fasted state
A condition when no food has been eaten recently, so blood glucose and insulin are low.
42
Fed state
A condition after eating, when blood glucose is high and the pancreas releases insulin.
43
Describe what is happening here
This is the fasted state which means there is no glucose, so there is no insulin. the insulin receptor is empty which means the GLUT4 receptor stays in the cell. * little glucose uptake occurs
44
Describe what is happening here
This is the fed state so there is glucose that needs to go inside the cell. This glucose activates the insulin to bind to the receptor which causes GLUT4 to move to the membrane and take muscle in to store as glycogen.
45
Describe what is happening here
This is the fasted state so there's no need for insulin and so GLUT4 stays inside the fat cell * no glucose uptake bc it must save for brain when in low energy state
46
Describe what is happening here
This is the fed state where insulin binds to the receptor and GLUT4 moves to the surface. The fat cells will take in glucose to store as fat (triglycerides)
47
what is Exocytosis
the process called when vesicles fuse with the membrane to insert GLUT4
48
What is the sequence of events starting from insulin binding?
Insulin binds → signal cascade → GLUT4 exocytosis → glucose entry
49
What hormone decreases after a carbohydrate meal?
Glucagon
50
What is the counterregulatory response?
This is a response to hypoglycemia is the body’s defense system that prevents blood glucose from dropping too low by releasing hormones that raise blood sugar.
51
What is the term for hormones like glucagon that oppose insulin?
Counterregulatory hormones.
52
Explain what is happening here:
Glycogen binds and activates a GPCR which activates adenylyl cyclase. Then ATP converts cAMP and then cAMP activates PKA
53
What happens once PKA is activated?
cAMP stimulates PKA which targets several proteins: - inhibition of glycogen synthase - activation of glycogen phosphorylase (so we go from glycogen to glucose) - activates the transcription factor CREB and promotes gluconeogenesis
54
Where do pyruvate and lactate come from?
glycolysis and muscle activity
55
where does Lactate come from (what does it get converted back to later)
muscle (via the Cori cycle), and is converted back to pyruvate in the liver.
56
What happens with excess lipolysis
could have accumulation of lipids in the liver which can lead to ketoacidosis
57
What can stress stimulate the release of?
release of catecholamines (Norepinephrine and Epinephrine) and glucocorticoids (cortisol).
58
how can stress cause hyperglycemia?
Stress can upregulate glucose production in liver
59
Glucocorticoud receptor: * where found * what activated by * what do
found in the liver activated by cortisol GR stimulates expression of gluconeogenic genes.
60
Adrenergic receptors * where expressed * what do
expressed in the liver and stimulate glycogenolysis
61
what is the cori cycle
A cycle that transfers lactate from muscle to liver, where it is converted to glucose and sent back to muscle. * metabolic pathway that occurs during anaerobic conditions (like exercise).
62
Why is lactate produced in muscles?
Because oxygen is limited, so pyruvate is converted to lactate to regenerate NAD⁺.
63
What happens to lactate after it leaves the muscle?
It travels through the bloodstream to the liver.
64
What does the liver do with lactate in the Cori Cycle?
Converts it back to pyruvate, then to glucose via gluconeogenesis.
65
How is the glucose produced in the liver used?
It’s sent back to the muscle for energy.
66
Explain the four steps of the Cori Cycle
1) start in the muscle - glucose is broken down through Glycolysis to make ATP --> produces pyruvate --> converted to lactate 2) build up of lactate leads to lactate being taken up by liver. in there, it is converted back to pyruvate then glucose via gluconeogenesis 3) new glucose goes back to muscles to be used 4) cycle continues
67
Why can the Cori Cycle lead to hypoglycemia?
Because the liver uses lots of ATP for gluconeogenesis, and glucose is burned quickly by muscles.
68
Why does turning OFF the Cori Cycle help maintain normal blood sugar?
Muscles use oxygen efficiently, so less lactate is produced, reducing the liver’s glucose-making burden.
69
What is gluconeogenesis?
The process of making new glucose from non-carbohydrate sources like lactate or amino acids.
70
Microvascular complications of diabetes: Eye
High blood glucose and high blood pressure can damage eye blood vessels, causing retinopathy, cataracts and glaucoma
71
Microvascular complications of diabetes: Kidney
High blood pressure damages smal blood vessels and excess blood glucose overworks the kidneys, resulting ni nephropathy.
72
Microvascular complications of diabetes: Neuropathy
Hyperglycemia damages nerves ni the peripheral nervous system. This may result in pain and/or numbness. Feet wounds may go undetected, get infected and lead to gangrene.
73
Macrovascular complications of diabetes: Brain
Increased risk of stroke and cerebrovascular disease, including transient ischemic attack, cognitive impairment, etc.
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Macrovascular complications of diabetes: Heart
High blood pressure and insulin resistance increase risk of coronary heart disease
75
Macrovascular complications of diabetes: Extremities
Peripheral vascular disease results from narrowing of blood vessels increasing the risk for reduced or lack of blood flow ni legs. Feet wounds are likely to heal slowly contributing to gangrene and other complications.
76
Where are all glucose and amino acids and most mineral salts and water reabsorbed in the nephron?
Proximal Convoluted Tubule (PCT)
77
What is the main function of the Loop of Henle?
Reabsorbs some water and helps concentrate urine
78
Which part of the nephron reabsorbs some mineral salts by active transport?
Distal Convoluted Tubule (DCT)
79