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
glycogenesis
glycogenolysis
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.