AQA Biology: 3.6.4.2 Control of blood glucose concentration

factors influencing blood glucose concentration

- diet
- glycogenolysis
- gluconeogenesis

glycogenesis

the conversion of glucose into glycogen

glycogenolysis

breakdown of glycogen to glucose

gluconeogenesis

production of glucose from sources other than carbohydrates e.g. glycerol, amino acids

role of liver in regulating blood sugar

where glycogenesis, glycogenolysis and gluconeogenesis take place

why is hypoglycaemia bad

no glucose = limited respiration = limited atp prod = basic functions stop

execess lactate -> changes in pH -> enzymes denature

why is hyperglycaemia bad

glucose = soluble -> reduces wp -> changes osmotic balance -> water moves out of cells into bloodstream -> kidney, eyes, liver first affected

how does the pancreas act as an exocrine gland

secretes alkaline digestive juices into duodenum via pancreatic duct

how does the pancreas act as an endocrine gland

contains endocrine cells in Islets of Langerhans

Islets of Langerhans

- oval collection of cells scattered through pancreas
- 1-2 mil in human pancreas
- darker red than surrounding tissue (rich blood supply)
- blood drains into hepatic portal vein going directly to liver

α cells

- larger
- secrete glucagon
- contain receptors that detect hypoglycaemia

β cells

- smaller
- secrete insulin
- contain receptors that detect hyperglycaemia

the action of insulin

1. receptors on β cells detect hyperglycaemia and secrete insulin into blood plasma
2. insulin molecules bind specifically to glycoprotein receptors on cell surface membranes of body cells, bringing about:
a. a change in the tertiary structure of glucose transport carrier proteins, causing them to change shape and open, letting more glucose into the cells by FD
b. vesicles fuse with cell surface membrane, providing protein to make more glucose transport carriers
c. activation of enzymes that convert glucose to glycogen and fat

in which ways is the blood concentration of glucose lowered?

- by increasing the rate of absoprtion of glucose into cells
- by increasing the respiratory rate of cells so they use up more glucose
- by increasing the rate of glycogenesis in liver + muscle cells
- by increasing the rate of conversion of glucose -> fat

the action of glucagon

1. α cells detect hypoglycaemia and respond by secreting glucaogn directly into blood plasma. glucagons actions include:
a. attaching to specific protein receptors on cell surface membrane of liver cells
b. activating enzymes that convert glycogen to glucose
c. activating enzymes involved in gluconeogenesis

the second messenger model of adrenaline and glucagon action

1. adrenaline approaches transmembrane protein on liver cell
2. adrenaline fuses to receptor causing it to change shape and release a subunit
3. subunit migrates to adenylate cyclase on inside of membrane
4. adenylate cyclase undergoes shape change and becomes activated
5. activated adenylate cyclase converts ATP into secondary messenger cyclic AMP
6. cAMP changes shape of + activates enzyme protein kinase
7. activated protein kinase activates phosphorylase
8. phosphorylase breaks glycosidic bonds in glycogen
9. glucose leaves cell via facilitated transport

type I diabetes cause

insulin-producing β cells in Islets of Langerhan destroyed, usually onsets during childhood-young adulthood

cause uncertain, both genetic and env. factors

control of type I diabetes

daily insulin replacement

symptoms of type I diabetes

increased urination
tiredness
weight loss
increased thirst
hunger
dry skin
blurred vision

cause of type II diabetes

body produces reduced amounts of insulin/stops responding to own insulin

exact mechanism unclear; insulin receptor tertiary structure may change shape, quantity of receptors may reduce, cascade of chemical reactions triggered by insulin may be impaired

risk factors for type II diabetes

age
obesity
lack of exercise
genetics

control of type II diabetes

dietary modification
exercise
drugs to control glucose absorption in gut