Pancreas anatomy and physiology Flashcards
(55 cards)
1
Q
Which is the larger component of the pancreas - exocrine or endocrine component?
A
Exocrine = larger component
2
Q
What is the function of the exocrine pancreas?
A
- Secrete digestive enzymes in response to gastrointestinal hormones e.g. CCK
- Secrete bicarbonate to neutralise acid produced in the stomach (this is in response to secretin produced by intestinal cells)
3
Q
What do trypsin and carboxypeptidase act on?
A
Peptides and proteins
4
Q
What does lipase act on?
A
Triglycerides
5
Q
What does amylase act on?
A
Starch
6
Q
What does phospholipase act on?
A
Phospholipid
7
Q
What does ribonuclease act on?
A
RNA
8
Q
What does deoxyribonuclease act on?
A
DNA
9
Q
Where are endocrine cells concentrated in the pancreas?
A
In the Islets of Langerhans
10
Q
What 3 types of cells are found in the Islets of Langerhans?
A
Alpha, beta and delta cells
11
Q
What hormone is produced by alpha cells?
A
Glucagon
12
Q
What hormone is produced by beta cells?
A
Insulin
13
Q
What hormone is produced by delta cells?
A
Somatostatin
14
Q
Where is somatostatin produced?
A
- Delta islet cells
- Periventricular nucleus of the hypothalmus
- Stomach
- Intestine
15
Q
What is the effect of somatostatin?
A
It has a paracrine function, suppressing the secretion of insulin and glucagon.
16
Q
Describe the synthesis of insulin
A
- Insulin = peptide hormone
- First synthesised as a preprohormone → then converted to a prohormone (proinsulin)
- There is an intracytoplasmic pool of proinsulin
17
Q
What is the significance of C-peptide in insulin secretion?
A
- Secretion of insulin requires removal of C-peptide from proinsulin
- C-peptide = connecting peptide released in equal amounts to insulin; it is biologically inactive and removed from the body at a much slower rate
18
Q
Describe the structure of insulin
A
Insulin consists of 2 polypeptide chains: alpha and beta amino acid chains connected by two disulphide bonds
19
Q
What is the plasma half-life of insulin?
A
5-8 mins
20
Q
Describe the kinetics of insulin
A
Secreted by beta islet cells of pancreas → enters veins → portal system → insulin acts upon liver first → insulin enters general circulation
21
Q
Where and how is insulin degraded?
A
- Liver or kidney
- This occurs via cleavage of 2 disulphide bonds within target cells after receptor binding
22
Q
How is insulin secretion regulated?
A
- Nutrients: glucose and amino acid levels
- GI hormones: incretins such as gastric inhibitory peptide (GIP) and glucagon-like peptide (GLP-1)
- Autonomic nervous system: parasympathetic nervous system stimulates, sympathetic nervous system inhibits
23
Q
How does the parasympathetic nervous system stimulate insulin secretion?
A
- Via the vagus nerve
- The vagus nerve increases GI motility and digestion
- There is higher insulin secretion after feeding
24
Q
How does the sympathetic nervous system inhibit insulin secretion?
A
- Direct innervation via sympathetic neurones
- Indirect response via adrenaline
- The stress response produces hyperglycaemia
Note: both insulin secretion and action are inhibited.
25
True/false: it is not a specific level of insulin or glucagon in the body that determines the actions in the body.
True: it is not a specific level of insulin/glucagon that determines the actions in the body; it’s the ratio between the two which leads us to anabolism vs. catabolism
26
This diagram describes the events in the beta cell that lead to insulin secretion. Fill in the blanks.
27
Describe how events in the intestinal tract affect insulin secretion
* GIP and GLP-1 are released by small intestinal cells. Their release stimulates insulin secretion.
* GIP and GLP-1 are increased when food reaches the intestine. This causes insulin secretion in advance of nutrient absorption.
28
Describe the 2 phases of insulin release that occurs in humans and some animals
* First phase: release of intracytoplasmic pool of proinsulin
* Second phase: insulin secretion resulting from new protein synthesis
29
True/false: the release of insulin from beta cells occurs through the process of potassium-mediated exocytosis.
**False.**
The release of insulin from beta cells occurs through the process of _calcium-mediated_ exocytosis.
30
Give some examples of glucose transporters
GLUT-1
GLUT-2
GLUT-4
31
Which of the following glucose transporters (GLUT1, GLUT2, GLUT4) are insulin dependent vs independent?
* GLUT1 and GLUT2 = insulin independent
* GLUT4 = insulin dependent
32
True/false: insulin is a water soluble peptide hormone.
What receptors would it therefore bind to/would it move straight into the cell?
True: insulin is a water soluble peptide hormone.
It binds to insulin receptors on the plasma membranes. The density of receptors is one determinant of insulin sensitivity.
33
The binding of insulin to insulin receptors on the plasma membrane activates what signal transduction pathway?
It activates the **tyrosine kinase** signal transduction pathway.
34
Which of the glucose transporters allows glucose to enter cells in a concentration-dependent manner, working independently of insulin?
**GLUT2**
is a type of glucose transporter that allows glucose to enter cells in a concentration-dependent manner. It provides **facilitated, insulin-independent glucose transport**.
35
Where are GLUT1 transporters found?
* CNS
* RBCs
They supply the basic energy requirements of the cells here.
36
Where are GLUT2 transporters found?
* Liver
* Islet glucose sensor
37
Where are GLUT4 transporters found?
* Muscle
* Fat
38
Describe the action of insulin on muscle (where carbohydrates are concerned)
* Insulin promotes uptake of glucose via GLUT4 into muscle
* Insulin increases glycogen synthase activity, stimulating glycogenesis
39
Describe the action of insulin on energy metabolism in the liver (with respect to carbohydrates)
* There is no GLUT4 in the liver. Glucose uptake occurs via **GLUT2**
* **Insulin inactivates glycogen phosphorylase** → inhibit glycogenolysis
* **Insulin increases glycogen synthase activity** → stimulates glycogenesis
* **Insulin promotes** the conversion of glucose into fats = **de novo lipogenesis**
* **Insulin inhibits gluconeogenesis** (glucose creation from breakdown of stores)
40
Describe the action of insulin on energy metabolism in the brain
* There is no GLUT4 in the brain. Glucose uptake occurs via the **insulin independent GLUT1 transporter**
* The exception to this is satiety and appetite centres, where insulin is required for glucose uptake
* Without insulin (i.e. diabetes mellitus) appetite increases
41
Describe the effect of insulin on fat metabolism
* **Insulin inhibits hormone-sensitive lipase (HSL)** so thus decreases lipolysis
* **Insulin stimulates de novo lipogenesis;** excess glucose increases TCA cycle intermediates (e.g. citrate) and malonyl CoA (fat precursor) is formed
* **Insulin increases delivery of fat to tissues**
42
Describe the effect of insulin on protein metabolism
* **Insulin increases amino acid uptake by tissues**
* **Insulin increases the rate of transcription and translation**
* **Insulin inhibits catabolic of proteins**
* **Insulin depresses the rate of gluconeogenesis in the liver** by inhibiting enzymes and by lowering the supply of amino acids from tissues e.g. muscle
43
Which of these statements is false?
* Glucagon is a peptide hormone secreted by the alpha islet cells
* Glucagon is synthesised as preproglucagon which is rapidly converted to glucagon
* Glucagon has a short plasma half-life of 8-9 mins
✅ Glucagon is a peptide hormone secreted by the alpha islet cells
✅ Glucagon is synthesised as preproglucagon which is rapidly converted to glucagon
❌ Glucagon has a short plasma half-life of 8-9 mins → glucagon's half life is 5-6 mins
44
True/false: glucagon is generally an anabolic hormone.
**False**.
Glucagon is generally a catabolic hormone and its primary site of action is the liver.
45
Where is the primary site of action of glucagon? Where is it metabolised?
Primary site of action = liver
Metabolised in liver and kidneys
46
What is the function of glucagon?
* To maintain blood glucose levels between meals (in the inter-prandial period)
* It is activated during negative energy balance
* It stimulates glycogenolysis and gluconeogenesis
47
What factors inhibit glucagon secretion?
* **Glucagon secretion is inhibited by high blood glucose levels**
48
What factors stimulate glucagon secretion?
* **Glucagon secretion is stimulated by high amino acid levels**
* This occurs after a protein-rich meal
* This means glucagon promotes gluconeogenesis
* This is “protective” after a protein-rich meal, otherwise, insulin stimulated by the amino acids of a protein meal would cause low blood glucose
49
Which of the following hormones cause gluconeogenesis?
Insulin
Glucagon
Cortisol
Epinephrine
**Glucagon and cortisol**
Glucagon - glucose levels are low between meals. We need more glucose so must make some.
Cortisol - we are stressed. Cortisol is a glucocorticoid. We must increase the availability of glucose to the brain and thus may need to make some more. Cortisol acts on liver, muscle, adipose tissue and pancreas to achieve this.
50
Which of the following hormones increase glucose uptake into cells?
Insulin
Glucagon
Cortisol
Epinephrine
Insulin
51
Which of the following hormones promote glycogenolysis?
Insulin
Glucagon
Cortisol
Epinephrine
**Glucagon and epinephrine**
Glucagon - glucose is low between meals. Let's release some from glycogen.
Epinephrine - we're scared. Let's release some glucose from glycogen ASAP.
52
Which of the following hormones increases protein synthesis? Which inhibits it?
Insulin
Glucagon
Cortisol
Epinephrine
**Insulin increases protein synthesis.**
**Cortisol inhibits protein synthesis.** This is presumably to free up amino acids for gluconeogenesis/provision of energy.
53
# Fill in the blanks.
54
Which type of glucose transporter is shown here? Where is this transporter found?
GLUT4 = insulin dependent glucose transporter found in muscle and fat.
55
What cell is shown here? What is the significance of the glucose transporter type?
Beta islet cell.
GLUT2 transporter = faciliatated insulin-independent glucose transporter. Allows glucose to enter the islet “glucose sensor” in a concentration-dependent manner, therefore influencing insulin secretion.
