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Phy Sci 111B > M1 L6 > Flashcards

M1 L6 Flashcards

1
Q

what is the Islets of Langerhans

A

specialized cells found in the pancreas. They play a critical role in regulating blood sugar levels

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2
Q

What do beta cells produce?

A

insulin

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3
Q

what do alpha cells produce?

A

glucagon

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4
Q

What activates beta cells?

A

high blood glucose - they make insulin

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5
Q

What activates alpha cells?

A

low blood glucose - they make glucagon

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6
Q

If blood glucose is high - which cell is inhibited and which is activated

A

alpha cell inhibited (make glucagon)

beta cell activated (make insulin)

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7
Q

If blood glucose is low - which cell is inhibited and which is activated

A

alpha cell activated (make glucagon)

beta cell inhibited (make insulin)

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8
Q

What can increase blood glucose?

A

1) glucose absorption from digestive tract

2) liver glucose production - subject to hormonal regulation

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9
Q

What can decrease blood glucose?

A

1) urinary excretion of glucose at abnormal levels

2) transport of glucose into cells for energy production or storage - subject to hormonal regulation

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10
Q

What is Glycogenolysis
* effect on blood glucose?

A

mobilizing glucose from glycogen

glucose monomers are removed from glycogen branches via phosphorolysis

  • this increases blood glucose
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11
Q

What is Gluconeogenesis
* effect on blood glucose?

A

synthesis of new glucose via liver

it is the conversion of two pyruvate molecules into glucose
* this increases blood glucose

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12
Q

What is Glycogenesis
* effect on blood glucose?

A

storing glucose as glycogen

Stored in many organs, primarily liver (and skeletal muscle)
* this decreases blood glucose

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13
Q

What happens in the liver between meals or during short fasts when no new nutrients are being absorbed?

A

Glycogenolysis occurs, breaking down glycogen stored in the liver to maintain blood glucose levels. This depletes liver glycogen stores over time.

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14
Q

What is glycolysis
* effect on blood glucose?

A

glucose splits into 2 pyruvate molecules
* this decreases blood glucose

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15
Q

Where is glucose coming from?

A

Digestion: sugar from ur food

Glycogenolysis: liver mobilizes glucose stored as glycogen

Gluconeogenesis: liver turns to alternate sources (fat and muscles)

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16
Q

What is the inactive precursor of a peptide called?

A

pre-pro peptide

  • 2 steps of processing to become peptide
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17
Q

Whats propeptide? like proglucagon

A

its one step of processing away from being what it needs to be

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18
Q

How does glucose get into cells?

A

Sodium-glucose transporters (SGLTs)

Facultative glucose transporters (GLUTs)

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19
Q

Sodium-glucose transporters (SGLTs)
* dependence on energy?
* where common?

A
  • energy dependent
  • common in kidney and intestines
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20
Q

Facultative glucose transporters (GLUTs)
*dependence on energy?
* what do?

A
  • Energy independent
  • Allow transport across membrane along concentration gradient
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21
Q

How do glucose transporters work in both directions?

A

GLUTs can transport glucose into or out of the cell, depending on the gradient.

  • After a meal: glucose moves into cells (blood glucose is high).
  • During fasting: liver cells may release glucose out into the blood.
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22
Q

Glucose stimulation of insulin secretion steps:

1) How does glucose enter the pancreatic beta cell?

A

Via facilitated diffusion through the GLUT2 transporter.

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23
Q

Glucose stimulation of insulin secretion steps:

2) What happens to glucose once inside the beta cell?

A

It is phosphorylated to glucose-6-phosphate, which helps maintain the glucose gradient.

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24
Q

Glucose stimulation of insulin secretion steps:

3) How is ATP generated in the beta cell?

A

By the oxidation of glucose-6-phosphate through cellular respiration.

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25
Glucose stimulation of insulin secretion steps: 4) What effect does ATP have on K⁺ channels in the beta cell?
ATP closes ATP-sensitive K⁺ channels, preventing K⁺ from leaving the cell.
26
Glucose stimulation of insulin secretion steps: 5) What happens when K⁺ builds up in the cell?
It causes membrane depolarization (less negative inside the cell).
27
Glucose stimulation of insulin secretion steps: 6) What does depolarization of the beta cell membrane do?
It opens voltage-gated Ca²⁺ channels.
28
Glucose stimulation of insulin secretion steps: 7) What happens after Ca²⁺ channels open?
Calcium enters the beta cell.
29
Glucose stimulation of insulin secretion steps: 8) What does calcium do once inside the beta cell?
It triggers exocytosis of insulin-containing vesicles.
30
Glucose stimulation of insulin secretion steps: 9) What is the final result of this cascade in the beta cell?
Insulin is secreted into the bloodstream.
31
Insulin effect on * glucose uptae * glycogenesis * glycogenolysis * gluconeogensis
* INC glucose uptae * INC glycogenesis * DEC glycogenolysis * DEC gluconeogensis
32
Glucagon effect on: * glycogenesis * glycogenolysis * gluconeogensis
* DEC glycogenesis * INC glycogenolysis * INC gluconeogensis
33
What are the growth hormone axis hormones
GHRH: Growth Hormone Releasing Hormone SST aka GHIH: Somatostatin, Growth Hormone Inhibiting Hormone GH: Growth Hormone IGFs: Insulin-like Growth Factors
34
Whats somatostatin
Somatostatin inhibits the release of several other hormones.
35
What are IGFs * where made?
Insulin-like Growth Factors * in liver
36
what is glucose sparing?
when we use other forms of glucose and prioritize it for the brain
37
What two hormones from the hypothalamus regulate growth hormone secretion?
GHRH (Growth Hormone–Releasing Hormone) – stimulates GH release GHIH (Somatostatin) – inhibits GH release
38
What are the metabolic (direct) effects of growth hormone? * fat breakdown: * glucose uptake * glucose output
↑ Fat breakdown - lipolysis (↑ blood fatty acids which preserves glucose for brain) ↓ Glucose uptake by muscles (less glucose in muscles - more for brain) ↑ Glucose output by liver (keeps glucose levels high via gluconeogenesis) * These actions support glucose sparing
39
What kind of feedback does IGF-1 exert on the hypothalamus and pituitary?
Negative feedback – inhibits GH release by: Stimulating somatostatin (GHIH) Inhibiting GHRH
40
What does growth hormone do to prioritize glucose for the brain?
It reduces glucose use in muscles and increases glucose production in the liver — a form of glucose sparing.
41
What are the growth-promoting actions of IGF-1?
↑ Protein synthesis (↓ blood conc of amino acids bc theyre being used to make proteins) ↑ Cell division ↑ Bone growth
42
Where are the neurons that regulate growth hormone (GH) release located?
in the hypothalamus, including the arcuate
43
What do somatotropes do?
They are cells in the anterior pituitary that produce growth hormone
44
What stimulates somatotropes to release GH?
GHRH from the hypothalamus.
45
What inhibits somatotropes from releasing GH?
Somatostatin (SST) from the hypothalamus.
46
How does growth hormone (GH) induce IGF-1 production?
GH binds to the growth hormone receptor (GHR) on liver cells, activating intracellular signaling pathways. These pathways lead to gene expression changes, especially upregulation of IGF-1. The repeated, pulsatile GH signals help maintain proper timing and levels of IGF-1 production.
47
Why does GH signaling occur in repeated pulses?
Growth hormone is released in pulses, especially during sleep or stress. Repeated binding of GH to its receptor triggers recurring activation of signaling pathways, leading to sustained or cyclical IGF-1 production depending on the body's needs.
48
Why does IGF-1 have a more sustained regulatory effect compared to GH?
Because IGF-1 has a longer half-life (12 hours vs. 20–30 minutes for GH)
49
Explain the Short-loop feedback in the hypothalamus
GH (from the pituitary) feeds back to the hypothalamus to regulate its own production by influencing GHRH and somatostatin levels
50
Explain the Long-loop feedback in the hypothalamus
feedback loop occurs when IGF-1 inhibits GH and GHRH release * IGF-1 has a longer half-life so it can sustain feedback control more effectively.
51
Explain the ultra short-loop feedback in the hypothalamus * ex
feedback occurs within the gland that secretes the hormone, like the pituitary * regulates itself - somatotrophes can make GH and sense it to modulate its release
52
What are the 2 major growth spurts
Postnatal growth spurt and pubertal growth spurt
53
Which condition can occur in the pre-pubertal growth spurt
giantism
54
Which condition can occur in the pre-post pubertal growth spurt
acromegaly
55
What is a burst of growth in teen years associated with?
an inc in IGF-1 production
56
What do chondrocytes do in bone growth?
They drive endochondral ossification, leading to linear growth (bone lengthening).
57
How does GH/IGF-1 affect osteoclasts?
Stimulates bone resorption (breaking down bone).
58
How does GH/IGF-1 affect osteoblasts?
Promotes bone formation and increases Bone Mineral Density (BMD).
59
What is the result of increased activity in both osteoclasts and osteoblasts?
Increased bone turnover and ultimately higher BMD.
60
What is acromegaly and how does it occur
* prominent bones of jaw, cheek, brow * exces GH --> excess effects on bones
61
What is gigantism and how does it occur
Gigantism is a rare condition where a person grows abnormally tall due to excessive growth hormone (GH) during childhood before the growth plates in the bones close.
62
Diff between gigantism and acromegaly?
Timing is key * If this excess GH happens before puberty, bones can still lengthen → result: extreme height (gigantism) * If it happens after growth plates close, it leads to acromegaly instead (growth of hands, feet, jaw—but not height).
63
What happens to glucose during a prolonged fast? * what else is used for energy instead
During a prolonged fast, the body has limited glucose available from food. Since the brain relies heavily on glucose for energy, the body shifts its metabolism to save glucose for the brain. It uses fatty acids instead for energy

Phy Sci 111B (6 decks)

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