glucose

Keeping blood glucose stable.

Everything links back to:

  • homeostasis

  • hormones

  • liver function

  • pancreas function

  • negative feedback

That’s the whole lecture.


WHY GLUCOSE IS IMPORTANT

Main role

Glucose is:

  • the main fuel for respiration

  • used to make ATP


IMPORTANT POINT

Brain cells rely heavily on:

  • glucose

So blood glucose must stay relatively constant.


NORMAL BLOOD GLUCOSE

Typical concentration:

5\ mmol/L


WHY GLUCOSE MUST BE REGULATED

Low blood glucose (hypoglycaemia)

Too little energy available.

Especially dangerous for:

  • brain function


High blood glucose (hyperglycaemia)

Causes:

  • osmotic imbalance

  • water movement problems

  • tissue damage


HOMEOSTASIS

Definition

Maintaining a stable internal environment.

Blood glucose control is a classic example.


HORMONAL VS NERVOUS COORDINATION

Hormonal

Nervous

Hormones

Nerve impulses

Blood transport

Neurones

Slower

Very rapid

Long-lasting

Short-lived

Widespread

Localised


HORMONES

Definition

Chemical messengers released by endocrine glands into blood.

Only target cells respond because they have:

  • specific receptors


HOW HORMONES WORK

Hormone binds receptor →

intracellular signalling activated →

cell response occurs


SECOND MESSENGERS

Some hormones work using:

  • second messenger systems

Example:

  • adrenaline using cAMP


MAIN ORGANS INVOLVED

MOST IMPORTANT:

  • pancreas

  • liver


THE LIVER

Functions in glucose regulation

  1. glycogenesis

  2. glycogenolysis

  3. gluconeogenesis


GLYCOGENESIS

Definition

Formation of glycogen from glucose.

Storage process.


GLYCOGENOLYSIS

Definition

Breakdown of glycogen into glucose.

Raises blood glucose.


GLUCONEOGENESIS

Definition

Making glucose from NON-carbohydrate sources.

Examples:

  • amino acids

  • glycerol


GLYCOGEN

Definition

Storage form of glucose.

Stored mainly in:

  • liver

  • muscle


IMPORTANT FACT

Liver stores about:

  • 75–100 g glycogen

Enough for:

  • ~12 hours blood glucose maintenance


THE PANCREAS

Contains:

  • Islets of Langerhans

These produce hormones.


α-CELLS

Produce:

Glucagon


β-CELLS

Produce:

Insulin


BLOOD GLUCOSE SOURCES

  • diet

  • glycogenolysis

  • gluconeogenesis


NEGATIVE FEEDBACK

MOST IMPORTANT CONCEPT.

Change detected →

response reverses change →

returns variable toward normal


WHEN BLOOD GLUCOSE FALLS

1. α-cells detect low glucose


2. Glucagon released


3. Liver activated

Main effects:

  • glycogenolysis

  • gluconeogenesis


4. Glucose released into blood

Blood glucose rises.


5. Glucagon secretion decreases

Negative feedback restored.


WHEN BLOOD GLUCOSE RISES

1. β-cells detect high glucose


2. Insulin released


3. Insulin binds receptors

Target tissues:

  • liver

  • muscle

  • adipose tissue


INSULIN EFFECTS

Increased glucose uptake

Especially:

  • muscle cells


Increased glycogenesis

Stores glucose as glycogen.


Increased fat synthesis


Increased respiration

Cells use more glucose.


HOW INSULIN INCREASES GLUCOSE UPTAKE

Insulin:

  • increases glucose transporter activity

  • increases transporter insertion into membrane

Allows more glucose entry by:

Facilitated\ diffusion


RESULT OF INSULIN

Blood glucose falls.

Then:

  • insulin secretion decreases

Negative feedback restored.


INSULIN VS GLUCAGON

VERY IMPORTANT COMPARISON.

Insulin

Glucagon

Lowers glucose

Raises glucose

β-cells

α-cells

Glycogenesis

Glycogenolysis

Glucose uptake ↑

Glucose release ↑


ADRENALINE

Also increases blood glucose.

Released during:

  • stress

  • excitement

  • fight-or-flight


ADRENALINE EFFECTS

Acts via:

  • second messengers (cAMP)

Stimulates:

  • glycogenolysis

Result:

  • increased blood glucose


DIABETES MELLITUS

Definition

Inability to regulate blood glucose properly.


TYPE I DIABETES

Cause

Little/no insulin production.

Usually due to:

  • autoimmune destruction of β-cells


FEATURES

  • childhood onset

  • develops rapidly

  • insulin dependent


SYMPTOMS

  • hyperglycaemia

  • glucose in urine

  • excessive urination

  • thirst

  • hunger

  • weight loss

  • blurred vision

  • tiredness


TYPE II DIABETES

MOST COMMON.

Cause

Reduced response to insulin:

  • insulin resistance

Sometimes reduced insulin secretion too.


FEATURES

  • usually later onset

  • associated with obesity

  • develops slowly


IMPORTANT POINT

Cells become less responsive because:

  • insulin receptors/signalling impaired


Type I

Type II

No insulin production

Insulin resistance

Usually young onset

Usually older onset

Rapid onset

Slow onset

Requires insulin injections

Often lifestyle/drug managed


DIABETES TREATMENT

Type I

  • insulin injections

  • glucose monitoring


Type II

  • diet control

  • exercise

  • metformin

  • drugs improving insulin sensitivity

  • drugs increasing insulin secretion


METFORMIN

Important drug.

Functions:

  • decreases liver glucose production

  • improves insulin sensitivity


MOST IMPORTANT EXAM CONTENT

Prioritise:

  • homeostasis

  • negative feedback

  • glycogenesis

  • glycogenolysis

  • gluconeogenesis

  • liver role

  • pancreas role

  • α vs β cells

  • insulin vs glucagon

  • insulin mechanism

  • facilitated diffusion

  • adrenaline

  • Type I vs Type II diabetes


ENTIRE TOPIC IN ONE FLOW

Blood glucose changes →

pancreas detects change →

α-cells or β-cells release hormones →

liver + tissues respond →

glucose storage/release altered →

blood glucose returns toward normal →

negative feedback reduces hormone release.