Homeostasis Flashcards
Homeostasis
● Maintenance of a stable internal environment within restricted limits
● By physiological control systems (normally involve negative feedback)
Importance of maintaining stable core temp
● If temperature is too high:
○ Hydrogen bonds in tertiary structure of enzymes break
○ Enzymes denature; active sites change shape and substrates can’t bind
○ So fewer enzyme-substrate complexes
● If temperature is too low:
○ Not enough kinetic energy so fewer enzyme-substrate complexes
Too low bgc
Hypoglycaemia
● Not enough glucose (respiratory substrate) for respiration
● So less ATP produced
● Active transport etc. can’t happen → cell death
Too high bgc
Hyperglycaemia
● Water potential of blood decreases
● Water lost from tissue to blood via osmosis
● Kidneys can’t absorb all glucose → more water
lost in urine causing dehydration
Negative feedback in homeostasis
- Receptors detect change from optimum
- Effectors respond to counteract change
- Returning levels to optimum / normal
Explain the importance of conditions being controlled by separate mechanisms involving negative feedback
Departures in different directions from the original state can all be controlled / reversed
● Giving a greater degree of control (over changes in internal environment
Describe positive feedback
- Receptors detect change from normal
- Effectors respond to amplify change
- Producing a greater deviation from normal
What influences bgc
● Consumption of carbohydrates → glucose absorbed into blood
● Rate of respiration of glucose eg. increases during exercise due to muscle contraction
Glycogenesis
Converts glucose to glycogen
Glycogenolysis
Glycogen to glucose
Gluconegenesis
Amino acids or glycerol to glucose
Explain the action of insulin in decreasing blood glucose concentration
Beta cells in islets of Langerhans in pancreas detect blood glucose concentration is too high → secrete insulin:
● Attaches to specific receptors on cell surface membranes of target cells eg. liver / muscles
1. This causes more glucose channel proteins to join cell surface membrane
○ Increasing permeability to glucose
○ So more glucose can enter cell by facilitated diffusion
2. This also activates enzymes involved in conversion of glucose to glycogen (glycogenesis)
○ Lowering glucose concentration in cells, creating a concentration gradient
○ So glucose enters cell by facilitated diffusion
Explain the action of glucagon in increasing blood glucose concentration
Alpha cells in islets of Langerhans in pancreas detect blood glucose concentration is too low → secrete glucagon
● Attaches to specific receptors on cell surface membranes of target cells eg. liver
1. Activates enzymes involved in hydrolysis of glycogen to glucose (glycogenolysis)
2. Activates enzymes involved in conversion of glycerol / amino acids to glucose (gluconeogenesis)
● This establishes a concentration gradient → glucose enters blood by facilitated diffusion
Explain the role of adrenaline in increasing blood glucose concentration
Fear / stress / exercise → adrenal glands secrete adrenaline:
● Attaches to specific receptors on cell surface membranes of target cells eg. liver
● Activates enzymes involved in hydrolysis of glycogen to glucose (glycogenolysis)
● This establishes a concentration gradient → glucose enters blood by facilitated diffusion
Describe the second messenger model of adrenaline and glucagon action
Adrenaline / glucagon (‘first messengers’) attach to specific receptors on cell membrane which:
- Activates enzyme adenylate cyclase (changes shape)
- Which converts many ATP to many cyclic AMP (cAMP)
- cAMP acts as the second messenger → activates protein kinase enzymes
- Protein kinases activate enzymes to break down glycogen to glucose
Adv of 2nd messenger model
● Amplifies signal from hormone
● As each hormone can stimulate production of many molecules of second messenger (cAMP)
● Which can in turn activate many enzymes for rapid increase in glucose
Type 1
Key point = β cells in islets of langerhans in pancreas produce insufficient insulin
● Normally develops in childhood due to an autoimmune response destroying β cells of Islets of Langerhans
Type 2
Key point = receptor (faulty) loses responsiveness / sensitivity to insulin (but insulin still produced)
● So fewer glucose transport proteins → less uptake of glucose → less conversion of glucose to glycogen
● Risk factor = obesity
How can type 1 be controlled
● Injections of insulin (as pancreas doesn’t produce enough)
● Blood glucose concentration monitored with biosensors; dose of insulin matched to glucose intake
● Eat regularly and control carbohydrate intake eg. those that are broken down / absorbed slower
○ To avoid sudden rise in glucose
Why can’t insulin be taken as a tablet
Insulin is a protein
● Would be hydrolysed by endopeptidases / exopeptidases
How can type 2 be controlled
● Not normally treated with insulin injections (as pancreas still produces it) but may use drugs which target insulin receptors to increase their sensitivity
○ To increase glucose uptake by cells / tissues
● Reduce sugar intake (carbohydrates) / low glycaemic index → less absorbed
● Reduce fat intake → less glycerol converted to glucose
● More (regular) exercise → uses glucose / fats by increasing respiration
● Lose weight → increased sensitivity of receptors to insulin
