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Metabolism > Lecture 7.1: Endocrine System and Pancreatic Hormones > Flashcards

Lecture 7.1: Endocrine System and Pancreatic Hormones Flashcards

1
Q

Control System

A

Controls variables (e.g. blood glucose, body temperature) by maintaining them at an optimal level

Control System:
• Receptor
• Control centre
• Effector

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2
Q

Control System Requirements

A

• Must be able to monitor the controlled variable
— Receptor (Sensor) e.g. thermoreceptors

• Must be able to compare actual value with what it should be
— Control centre e.g. hypothalamus

• Must be able to change the controlled variable
— Effector e.g. sweat glands

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3
Q

Feedback

A

Stimulus to Receptor/Sensor
Receptor/Sensor to Control
Control to Effector
Effector to Stimulus

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4
Q

Feedback: Control System

A

The control system must use the effector to change the controlled variable until the receptor (sensor) indicates it has reached the set point determined by
the control centre

Can change the controlled value by changing the set point

The set point can vary over a 24hr light/dark cycle (circadian rhythm)

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5
Q

Negative Feedback

A

• Most common
• The effect of the response to stimulus is to decrease its effect
• The effector is switched off when value reaches set point

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6
Q

Positive Feedback

A

The effect of the response to stimulus is to increase its effect

The effector is not switched off and the control system quickly goes out of control leading to catastrophic change

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7
Q

Examples of positive feedback in the body

A

• Blood clotting cascade
• Ovulation
• Lactation

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8
Q

What are Hormones?

A

Hormones are chemical signals produced in endocrine glands that travel in the bloodstream to affect other tissues

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9
Q

Features of Hormones

A

• Travel to all parts of the body in 30 seconds
• Can have different effects in different places
• The effect that hormone has on target cell depends on its concentration in
the blood stream
• Good for coordinated multiple responses

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10
Q

Hormone Secretion - Endocrine Glands: Head and Neck

A

• Pituitary gland – anterior and posterior parts
• Thyroid glands
• Parathyroid glands

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11
Q

Hormone Secretion - Endocrine Glands: Abdomen

A

• Adrenal glands – cortex and medulla
• Pancreas
• Kidney
• Gut

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12
Q

Hormone Secretion - Endocrine Glands: Pelvis

A

• Gonads (Ovaries, Testes)
• Uterus
• Placenta

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13
Q

Classification of Hormones (4)

A

• Peptide/Polypeptide hormones (around 20)
• Glycoprotein hormones (4)
• Amino acid derivatives (3 major)
• Steroid hormones (around 10)

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14
Q

What does Hormone Structure define?

A

• Made
• Transported in the blood
• Interacting with cell receptors
• Inactivated

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15
Q

Peptide/Polypeptide Hormones

A

Nearly all single chain peptides, varying in chain length

— Thyrotropin-releasing hormone (TRH) - 3 amino acids
— Glucagon- 21 amino acids
— Insulin - 51 aminoacids
— Growth hormone (GH) - 191 amino acids

Some organised in closely related families (e.g. gut hormones)

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16
Q

Glycoprotein Hormones

A

All have two polypeptide chains with carbohydrate side chains (α and β chains)

— Thyroid stimulating hormone (TSH)
— Follicle stimulating hormone (FSH)
— Luteinizing hormone (LH)
— Human chorionic gonadotrophin (HCG)

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17
Q

Peptide/Polypeptide and Glycoprotein Hormones Similarities

A

Hydrophilic

Synthesised as larger precursor molecules called pro-hormones (or pre-pro-hormones) and stored in vesicles before release

Cleaved to active hormone and released from vesicles

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18
Q

Amino Acid Derivatives

A

All of them are derived from tyrosine

Adrenaline

Thyroid hormones:
— Tetra-iodothyronine (thyroxine), T4
— Tri-iodothyronine, T3

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19
Q

Adrenaline

A

Hydrophilic

Stored in vesicles in adrenal medulla (chromaffin cells)

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20
Q

Thyroid Hormones

A

Stored extra-cellularly in follicles in thyroid gland as colloid

Hydrophobic

21
Q

Steroid Hormones

A

• Derived from cholesterol
• Not stored by cells but synthesised on demand from cholesterol esters
• Hydrophobic

22
Q

Control of the Hormonal Secretion

A

The endocrine cells are stimulated chemically (mainly by another hormone) to release hormones

Often related in some way to hormone action

Produces negative feedback control which tends to keep hormone concentration in blood at controlled level

23
Q

Calcium Homeostasis

A

Parathyroid hormone (PTH) secretion is stimulated when blood calcium levels fall

PTH acts on bone and kidney to make calcium levels rise which reduces its secretion

24
Q

Most Common Control of Hormonal Secretion

A

Many hormones are controlled by other hormones (tropic hormones)

E.g. Secreted by anterior pituitary gland e.g. TSH, ACTH (adrenocorticotropic hormone)

Connection of pituitary gland to brain allows brain to influence the endocrine
system

25
Q

Hormones Transport in the Blood: Soluble in Simple Solution

A

Few hormones soluble enough to travel in simple solution such as:

• Peptide/Polypeptide and glycoprotein hormones
• Adrenaline (amino acid derivative hormone)

26
Q

Hormones Transport in the Blood: Must bind to proteins

A

• Often specific
• Steroids
• Thyroid hormones (amino acid derivative hormone)

27
Q

Inactivation of Hormones

A

Inactivation may occur in target tissues, but also in other tissues, especially in the liver

Peptides/Polypeptides are degraded to amino acids

Steroids and amino-acid derivatives have small changes in structure or are recycled/excreted

28
Q

Pancreas

A

An organ of digestive and endocrine systems

Anatomically divided into: head, body and tail

Histologically/Functionally divided into: Endocrine (2%, e.g.insulin, glucagon) and Exocrine (98%, e.g.digestive enzymes)

29
Q

Functions of Pancreas: Exocrine

A

Produces digestive enzymes (amylases, lipases, proteases etc.)

Alkaline secretions drain into pancreatic duct, then into duodenum

30
Q

Functions of Pancreas: Endocrine

A

Produces polypeptide hormones:
• Insulin and glucagon- regulate blood glucose
• Somatostatin- inhibits islet secretions
• Pancreatic polypeptide, ghrelin and amylinregulate appetite

31
Q

Insulin and Glucagon Control Glucose

A

α-cells:

• Blood glucose needs to be tightly controlled
• Insulin lowers blood glucose levels
• Glucagon raises blood glucose levels

β-cells:

Insulin sensitive: adipose, skeletal muscle, liver

32
Q

Insulin: Actions and Metabolic Effects

A

• Stimulated by feeding
• Affects metabolism of carbohydrates, lipids and proteins
• Increases protein synthesis
• Promotes energy storage (anabolic), reducing blood glucose

33
Q

Insulin: Target Tissues

A

• Skeletal muscle
• Liver
• Adipose tissue
• Glycogenic (liver, muscle)
• Anti-gluconeogenic (liver)
• Anti-lipolytic (adipose tissue) and anti-ketogenic (liver)

34
Q

Glucagon Actions and Metabolic Effects

A

• Stimulated by fasting
• Affects metabolism of carbohydrates and lipids
• Mobilises energy stores (catabolic), increasing blood glucose

35
Q

Glucagon: Target Tissues

A

• Liver
• Adipose tissue
• Glycogenolytic (liver)
• Gluconeogenic (liver)
• Lipolytic (adipose tissue) and ketogenic (liver)

36
Q

What is between Preproinsulin and Insulin?

A

Preproinsulin to Proinsulin to Insulin

37
Q

Mature Form of Insulin

A

Insulin consists of two polypeptide chains connected by two disulphide bridges between cysteines

The third disulphide bond is in chain A

3 disulphide bridges: rigid structure

38
Q

Insulin Secretion

A

Mature secretory vesicles move along microtubules towards the plasma
membrane of β-cell (margination)

Upon stimulation of β-cell by glucose, calcium enters the cell:
• Vesicle membranes fuse with plasma membrane
• Calcium induces contraction of microfilaments leading to release of insulin
and peptide C from vesicles by exocytosis

39
Q

Glucose Stimulated Insulin Secretion

A

• Glucose transported into β-cell by facilitated diffusion (GLUT2)
• Glucose is utilised providing ATP which closes K+ channels
• Increased intracellular K+ levels lead to membrane depolarisation
• Influx of extracellular Ca2+
• ↑ Intracellular Ca2+ triggers release of insulin from secretory vesicles

40
Q

What can be used to treat Type 2 Diabetes?

A

Insulin secretagogues such as sulphonylureas (SUR) are used to treat Type 2 Diabetes

41
Q

How does Insulin Exert its Action through Insulin Receptors?

A

Insulin receptor (tyrosine kinase receptor) on target cell

Transmembrane dimer:
• Two identical monomers
• Each monomer has one α- and one β-subunit, connected by single disulphide
bonds

42
Q

α-subunit and β-subunit of Insulin Receptor

A

α-subunit is extracellular and insulin binding

β-subunit is intracellular (Spans the plasma membrane has activity of tyrosine kinase)

43
Q

Activation of the Insulin Receptor

A

Following insulin binding to receptor on target cell:
• α-subunits move towards each other, wrap the insulin
• β-subunits move towards each other & pull insulin into cell (internalisation)
• β-subunits become an active tyrosine kinase
• Tyrosine residues undergo autophosphorylation
• Active tyrosine kinase phosphorylates tyrosine residues in other protein
• Activation of signalling pathways and metabolic effects

44
Q

How is Glucose uptake via Insulin regulated?

A

1) Insulin binds to receptor
2) Signal cascade
3) This causes exocytosis of GLUT4
4) This permits glucose entry

45
Q

Glucagon Synthesis in a-cells

A

• Synthesised as large precursor: pre-proglucagon
• Cleaved to glucagon- a single polypeptide chain (29 a.a.)
• No di-sulfide bridges: flexible structure

Synthesised in and excreted from a-cells:
• Synthesised in RER, transported to Golgi and packaged in secretory
granules
• Secretory granules move to cell surface by margination and release
contents into blood by exocytosis

46
Q

Glucagon Exerts its Action through Glucagon Receptor

A

• Glucagon binds to G-protein coupled receptor (GPCR)

• α-subunit activates adenylate cyclase which leads to production of cAMP

• cAMP activates PKA leading to signalling cascade and metabolic effects

47
Q

Clinical Signs of Abnormal Insulin Levels

A

• High levels result in hypoglycaemia
• Low levels result in hyperglycaemia (diabetes mellitus)
• Insulin resistance results in hyperglycaemia and hyperinsulinaemia

48
Q

Clinical Signs of Abnormal Glucagon Levels

A

• High levels worsen diabetes
• Low levels may contribute to hypoglycaemia

Metabolism (16 decks)

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