Biology (9610) | Hormones and the control of blood glucose concentration

Welcome to Control: Hormones and Blood Glucose!

Hello future Biologists! This chapter is all about how your body performs one of its most critical balancing acts: keeping the amount of sugar (glucose) in your blood perfectly stable. This process, called homeostasis, is essential for survival.
Think of it like setting the temperature in your house. If it gets too hot or too cold, sensors detect the change and turn on the heating or cooling system to bring it back to the set point. In your body, hormones like insulin and glucagon are the control systems that manage your "sugar temperature."

Don't worry if this seems tricky at first; we will break down the roles of the key organs and hormones step-by-step!

Key Takeaway: Why Control Blood Glucose?

Maintaining a stable blood glucose concentration (BGC) is vital for two main reasons, as outlined in the syllabus:

1. Energy Transfer: Glucose is the primary fuel for cell respiration (the process that makes ATP). If BGC is too low, cells, especially brain cells, don't get enough energy and stop functioning correctly.
2. Water Potential (Osmosis): If BGC is too high, it lowers the water potential of the blood. This causes water to move out of the cells and into the blood via osmosis, leading to cell shrinkage and damage. If BGC is consistently high (as in untreated diabetes), water is also lost in the urine, leading to dehydration.

1. The Central Role of the Liver

The liver is the main organ responsible for storing and releasing glucose, acting as the body’s glucose buffer. It achieves this by controlling three key processes involving glucose and its storage form, glycogen.

The Three "Glyco" Processes: Know Your Terms!

These terms often confuse students, but they have clear meanings based on their suffixes:

• -genesis means creation or making.
• -olysis means splitting or breaking down.
• gluco- means glucose.

The liver carries out three key roles:

1. Glycogenesis (Glucose → Glycogen):
   The creation of glycogen.
   When blood glucose levels are high (e.g., after a meal), the liver converts excess glucose molecules into the storage polysaccharide glycogen. This makes the BGC fall.
2. Glycogenolysis (Glycogen → Glucose):
   The splitting of glycogen.
   When blood glucose levels are low (e.g., during fasting), the liver breaks down stored glycogen back into glucose molecules, which are then released into the blood. This makes the BGC rise.
3. Gluconeogenesis (Non-Carbohydrate → Glucose):
   The creation of new glucose.
   When glycogen stores are depleted and blood glucose is very low (e.g., prolonged fasting), the liver makes new glucose from non-carbohydrate sources, specifically glycerol (from lipids) and amino acids (from proteins). This process is crucial for long-term BGC maintenance.

2. The Hormones: Insulin, Glucagon, and Adrenaline

The key hormones controlling BGC are produced in specialised cells within the Pancreas, found in structures called the Islets of Langerhans.

• Alpha cells produce Glucagon (raises BGC).
• Beta cells produce Insulin (lowers BGC).

2.1. The Role of Insulin (The Lowering Hormone)

Insulin is a protein hormone released by the Beta cells when blood glucose concentration is too high. Its primary targets are liver, muscle, and fat cells.

Insulin acts by three key mechanisms:

1. Attaching to Receptors: Insulin binds to specific protein receptors located on the surface membranes of its target cells (e.g., liver and muscle cells).
2. Increasing Glucose Uptake: This binding triggers a response that causes target cells to insert more channel proteins (specifically, glucose carrier proteins) into their surface membranes. This dramatically increases the permeability of the cell membrane to glucose, allowing rapid uptake from the blood.
3. Activating Glycogenesis: Insulin activates enzymes (like glucokinase) involved in the conversion of glucose to glycogen (Glycogenesis) within liver and muscle cells, thereby removing glucose from the blood for storage.

2.2. The Role of Glucagon (The Raising Hormone)

Glucagon is a protein hormone released by the Alpha cells when blood glucose concentration is too low. Its primary target is the liver.

Glucagon acts by:

1. Attaching to Receptors: Glucagon binds to specific receptors on the surface membranes of liver cells.
2. Activating Glycogenolysis: It activates enzymes involved in the conversion of glycogen to glucose (Glycogenolysis).
3. Activating Gluconeogenesis: It activates enzymes involved in the conversion of non-carbohydrates (glycerol and amino acids) to glucose (Gluconeogenesis).

2.3. The Role of Adrenaline (The Emergency Hormone)

Adrenaline (or Epinephrine) is a stress hormone released by the adrenal glands during exercise, danger, or excitement. Its purpose is to rapidly mobilise energy stores.

Adrenaline acts very similarly to glucagon on the liver:

• It attaches to receptors on the surface of target cells (especially liver cells).
• It activates enzymes involved in the rapid conversion of glycogen to glucose (Glycogenolysis).

Did you know? Glucagon and Adrenaline often work together during stress or extreme fasting, ensuring the body has enough fuel for the fight-or-flight response.

3. How Protein Hormones Work: The Second Messenger Model

Glucagon and Adrenaline are protein hormones (meaning they are made of amino acids). Because they are large and water-soluble, they cannot simply diffuse across the lipid bilayer of the cell membrane to influence the cell directly.

They use an indirect method called the Second Messenger Model:

Imagine the hormone (the "first messenger") is knocking on a locked door. The cell can't let it in, so it sends a message (the "second messenger") to the inside factory to start working.

Step-by-Step Process (Adrenaline and Glucagon Action):

1. Binding (First Messenger): The hormone (Adrenaline or Glucagon) binds to a specific complementary receptor protein located on the outside surface of the target cell membrane (e.g., liver cell).
2. Activation of Adenyl Cyclase: The binding of the hormone causes the receptor to change shape on the inside of the cell. This change activates a membrane-bound enzyme called adenyl cyclase.
3. Production of cAMP (Second Messenger): Activated adenyl cyclase converts ATP inside the cytoplasm into a signalling molecule called cyclic AMP (cAMP). cAMP is the second messenger.
4. Enzyme Cascade: cAMP activates inactive enzymes inside the cell, starting a cascade. Specifically, cAMP activates an enzyme called protein kinase.
5. Final Effect: Activated protein kinase then activates the enzymes responsible for glycogenolysis (the breakdown of glycogen to glucose). This process is highly amplified, meaning one hormone molecule can lead to the release of millions of glucose molecules.

Key Takeaway: The second messenger model allows a small external signal (hormone) to produce a massive, fast response inside the cell without ever entering the cell itself.

4. Diabetes Mellitus: When Control Fails

Diabetes Mellitus is a condition characterised by an inability to control blood glucose concentration, resulting in chronically high BGC (hyperglycaemia).

4.1. Symptoms Explained

The classic symptoms of diabetes (thirst, frequent urination, fatigue) can be explained directly using your knowledge of BGC control:

• Excessive Urination & Thirst (Polyuria and Polydipsia): Very high BGC lowers the water potential of the blood filtrate entering the kidneys. Not all glucose can be reabsorbed, so it remains in the urine. This glucose draws water out of the body by osmosis, leading to dehydration, which triggers thirst.
• Fatigue: Glucose cannot move efficiently into muscle and body cells (either due to lack of insulin or resistance to it). Cells must break down fats and proteins for energy instead, leading to muscle weakness and tiredness.

4.2. Type 1 Diabetes

Type 1 is usually caused by an autoimmune response where the body's immune system mistakenly attacks and destroys the Beta cells in the Islets of Langerhans.

• Cause: Absolute deficiency of insulin production.
• Risk Factors: Primarily genetic predisposition; onset is usually in childhood or young adulthood.
• Control: Requires external insulin (injections or pump) to manage BGC, alongside strict monitoring of diet and exercise.

4.3. Type 2 Diabetes

Type 2 is far more common and occurs when the body either does not produce enough insulin, or the target cells (especially liver and muscle) do not respond correctly to the insulin that is present. This is known as insulin resistance.

• Cause: Insulin resistance and impaired insulin production.
• Risk Factors: Obesity, poor diet, lack of exercise, age, and genetics.
• Control: Initially controlled by manipulating diet (reducing simple carbohydrate intake) and increasing exercise. Medication may be used to improve cell sensitivity to insulin or stimulate insulin production. Eventually, some patients may require insulin injections.

4.4. Overview: Negative Feedback Control

The control of blood glucose is a classic example of negative feedback. This mechanism ensures that any change away from the optimal level (the set point) is quickly counteracted to restore stability.

Summary of Negative Feedback in BGC Control:

1. BGC Rises (e.g., after eating carbohydrates):
• Detected by Beta cells in the pancreas.
• Insulin released.
• Liver and muscle cells increase glucose uptake and perform Glycogenesis.
• BGC falls back to the set point.

2. BGC Falls (e.g., during exercise or fasting):
• Detected by Alpha cells in the pancreas.
• Glucagon (and Adrenaline) released.
• Liver performs Glycogenolysis and Gluconeogenesis.
• BGC rises back to the set point.