control of blood glucose concentration

the role of adrenaline by

• attaching to receptors on the surfaces of target cells

• activating enzymes involved in the conversion to glycogen to glucose

glycogenolysis

hydrolysis of glycogen into glucose in liver and muscles

gluconeogenesis

creation of new glucose from amino acids and glycerol

glycogenesis

creation of glycogen

hormones

steroid hormones
- e.g. oestrogen
- lipid soluble
- diffuse across phospholipid bilayer of cell surface membrane and enter cell

peptide hormones
- e.g. adrenaline
- water soluble
- can’t diffuse across phospholipid bilayer of cell surface membrane
- use the second messenger model

secondary messenger model

the hormone is the 1st messenger (e.g. adrenaline)

binds to specific complementary receptor on target cell (hormone-receptor complex)

this activates an intracellular enzyme (adenylate cyclase)

which produces the second messenger cyclic AMP (cAMP) from ATP

this causes a series of reactions that result in the activation of a protein kinase that activates another enzyme

which converts glycogen to glucose (glycogenolysis)

steroid hormone (??)

- enters cell and binds with an internal receptor molecule
- hormone-receptor complex enters nucleus and acts as a “transcription factor”
- this switches particular genes on and causes the production of a protein

pancreas

organ found under stomach which monitors blood glucose concentration

what happens when blood glucose level gets too high?

dehydration: lowers WP of blood causing water to leave cells by osmosis

detected by beta cells in Islets of Langerhans in Pancreas

hormone: insulin secreted

increased cellular respiration rate

increased rate of glucose absorption → cells, esp muscle (opens glucose transport proteins)

increased glucose conversion → glycogen

glycogenesis → enzymes are activated

increased glucose conversion → fat (enzymes are activated)

what happens when blood glucose level gets too low?

cells can’t respire: e.g. brain cells, glucose required to release energy from respiration

detected by alpha cells in Islets of Langerhans in Pancreas

hormone: glucagon secreted

in liver cells: glycogen → glucose (glycogenolysis), amino acids and glycerol → glucose (gluconeogenesis)

adrenaline

- secreted from adrenal gland
- increases blood glucose
- peptide hormone
- glycogenolysis enzymes activated
- inhibits glycogenesis enzymes
- activates liver enzyme: glycogen → glucose
- inhibiting enzyme: glucose → glycogen

glucagon

- alpha-cells in islets of Langerhans in pancreas
- increases blood glucose
- peptide hormone
- glycogenolysis enzymes activated
- gluconeogenesis stimulated

- attaches to receptors on the surface of target cells
- activates enzymes involved in the conversion of glycogen to glucose
- activates enzymes involved in the conversion of glycerol and amino acids into glucose

insulin

- beta-cells in islets of Langerhans in pancreas
- decreases blood glucose
- peptide hormone
- glycogenesis enzymes activated
- glucose absorption increases
- respiratory rate increased
- glucose → fat

type I diabetes

• insulin dependent

• pancreas doesn’t make enough insulin

• starts in childhood

• maybe due to an autoimmune response which attacks beta cells

• develops quickly and obvious symptoms

type II diabetes

insulin independent

body cells not responsive to insulin / insufficient insulin supply from pancreas

starts later in life (e.g. over 40)

can be caused in adolescents by poor diet

develops slowly and less severe symptoms (which can go unnoticed)

treatment for type I diabetes

• controlled by insulin injections (2-4 times a day)

• which are matched to glucose intake so blood glucose levels are monitored which biosensors

treatment for type II diabetes

by regulating carbohydrates in diet and matching to exercise

can be supplemented by insulin injections

OR using drugs which stimulate insulin production

and other drugs which slow the rate at which the body absorbs glucose from the intestine

what factors bring on earlier onset of type II diabetes?

• obesity

• diet high in sugar

• being of Asian or Afro Caribbean descent

• family history

Explain why a change in the amino acid sequence of insulin prevents insulin binding to its receptor.

1. Changes tertiary structure

2. No longer complementary to receptor