Regulation of blood glucose

Question 1

blood glucose levels

Answer 1

– Normal fasting blood glucose levels are between 3.9–5.4 mmol/L.
– Normal blood glucose levels two hours after starting a meal are between
6-10 mmol/L.
– Hypoglycaemia – glucose levels < 4.0 mmol/L
– Hyperglycaemia – fasting glucose levels > 7.0 mmol/L

Question 2

Factors that cause an increase in blood glucose levels (Fasting):

Answer 2

– Absorption from intestine
– glycogen breakdown –> glucose
– gluconeogenesis
– Hyperglycaemic hormones : glucagon, steroids, GH, thyroid hormones etc

Question 3

Factors that cause decrease of glucose in the blood are (Fed):

Answer 3

– Utilization by tissues for energy
– glucose –> glycogen synthesis
– Storage of glucose –> fat
– Hypoglycaemic hormone - Insulin

Question 4

when glucose levels are too low, how to increase the blood glucose conc

Answer 4

– Glucagon is released
–> Liver produces glucose
–> Stimulates glycogenolysis (first response)

(glycogenolysis is first response because its an immediate source of glucose while gluconeogeneis takes time to convert non carb sources into glucose)

followed by gluconeogenesis
(sustained response)

Adipose tissue
–> glucose uptake and oxidation is decreased
–> Lipolysis begins

Muscle
–-> changes fuel source
== Oxidise fatty acids and ketone bodies instead of glucose for production of energy.

Question 5

when glucose levels are too high, how to lower the blood glucose conc

Answer 5

– Absorptive (post-prandial) state
Insulin is released
–-> Stimulates glycolysis (used as fuel source for ATP synthesis)

Adipose tissue:
- increase glucose uptake
- == Stimulate lipogenesis (make fat) and glucose oxidation
- decrease lipolysis

Skeletal muscle
- increase glucose uptake

Liver
- increase glucose uptake
- increase glycogenesis
– Decrease Gluconeogenesis

Question 6

insulin secretion

Answer 6

occurs in pancreatic beta cells
1. GLUT 2 on surface of beta cells and expressed at all times
2. glucose enters cell through GLUT 2
3. glucokinase converts glucose = G6P
4. Glycolysis occurs and produces ATP
5. the ATP/ADP ratio increase inhibits the ATP sensitive potassium channel
6. closing the K+ channels = depolarisation of membrane = voltage gated calcium channels to open
7. Ca2+ enters the cell and causes the exocytosis of insulin vesicles
=== insulin is released

Question 7

insulin synthesis

Answer 7

insulin synthesis is continous:
1) preproinsulin gene (INS) = transcribed into preproinsulin mRNA : within the nucleus of the beta cells.
2) preproinsulin mRNA undergoes translation = produce preproinsulin
3) preproinsulin enters the ER = becomes proinsulin
4) proinsulin enters the trans-Golgi network and packaged into vesicles
5) processed into mature insulin

during glucose-regulated insulin secretion = the influx of calcium triggers the exocytosis of insulin granules, releasing mature insulin into the bloodstream.

Question 8

Incretins

Answer 8

potentiate glucose induced insulin secretion
in beta-cells
–> increases insulin production

Question 9

how insulin regulates blood glucose

Answer 9

1) insulin binds to surface receptors of target cells
2) tyrosine kinase is activated
3) GLUT 4 transporters moved to plasma membrane
4) glucose absorbed :
a. metabolism via glycolysis = ATP + pyruvate = via lipolysis = lipids
b. storage via glycogenesis = glycogen

Question 10

Response of Islet Cells to Low Glucose

Answer 10

beta cells, K atp sensitive channels continue to pump K+ so no depolarisation = mature insulin vesicles remain in cell :)

alpha cells, same mechanism, ATP ratio increases, K+ ATP sensitive channels close, depolarisation, voltage gated calcium channels open, Ca2+ floods in and glucagon vesicles are released.

Question 11

type 1 vs type 2 diabetes

Answer 11

both characterised by hyperglycemia

type 1 diabetes :
an autoimmune disorder
–> attacks and destroys the insulin-producing beta cells in the pancreas.
–> Little to no insulin is produced by the pancreas = no insulin secretion

type 2 diabetes:
where cells do not respond effectively to insulin, AND the pancreas may not produce enough insulin.
= insulin secretion PLUS insulin resistance

obesity is a major risk factor to the development of type 2 diabetes:
80% people may have insulin resistance but can compensate by producing more insulin
20% = genetic predisposition = beta cells are overworked –> insulin secretion decreases

Question 12

explain consequences of hypoglycemia

Answer 12

symptoms : shakiness, dizziness, irritability, sweating, and mood swings.

• The brain relies heavily on glucose = blood glucose drops too low = ** Impaired Brain Function**
  –> leads to compromised motor skills and coordination = Potential for Accidents

low blood sugar = releasing adrenaline (epinephrine) to try stimulate the liver to release stored glucose
–> adrenaline leads to anxiety, rapid heartbeat, and sweating.

Question 13

explain effects of hyperglycemia

Answer 13

formation of AGEs
= damage of various cells and tissues throughout the body e.g. blood vessels, nerves, and organs.

retinopathy (eye damage) : vision loss
nephropathy (kidney damage) : kidney failure
neuropathy (nerve damage) : sensory disturbances
cardiovascular diseases : heart attacks and strokes.
Impaired Immune Function (damaged immune cells)
increased urine product (body’s attempt to reduce blood glucose levels) = dehydration