Biology- Homeostasis and Signalling molecules SAC HELPPPP!!

[sabii]

Hi everyone! I have a Biology SAC coming up on Homeostasis, negative feedback system, how blood glucose is regulated, signalling molecules, signal transduction pathway and the causes, symptoms and effect of Diabetes Type 1 & 2 (also the difference between the two).

I am having major trouble with learning the signalling molecules (hormones, neurohormones and neurotransmitters)- what exactly do they do and how does it work? What are the diiferences?

Also I am confused about the signal transduction process- how does it work?

I will REALLY APPRECIATE any help! Thank you!

[Rachet123]

Hi everyone! I have a Biology SAC coming up on Homeostasis, negative feedback system, how blood glucose is regulated, signalling molecules, signal transduction pathway and the causes, symptoms and effect of Diabetes Type 1 & 2 (also the difference between the two).

I am having major trouble with learning the signalling molecules (hormones, neurohormones and neurotransmitters)- what exactly do they do and how does it work? What are the diiferences?

Also I am confused about the signal transduction process- how does it work?

I will REALLY APPRECIATE any help! Thank you!

Homeostasis: is the maintenance of a relatively stable internal environment, within a narrow bandwidth, despite changes/fluctuations in the external environment.

Negative feedback system: in a negative feed back system the response acts in the opposite direction to the stimulus, thus generally restoring the stimulus to its optimal/original state or just below it.

How blood glucose is regulated: in the pancreas a group of cells called the Islets of Langerhans detect the the stimulus (glucose concentration in the blood) the stimulus may be excessively above normal or below normal. The Effectors, Alpha and Beta cell, also found in the pancreas then release glucagon- liver (secondary effector) is 'told' to convert glycogen into glucose- and insulin- encourages body cells to absorb more glucose thus reducing glucose concentration in the blood- accordingly. When Blood glucose levels are above normal bandwidth Alpha cells produce less glucagon and Beta cells increase production of Insulin, and so the stimulus dives to bellow the optimal bandwidth and so Alpha Cells produce more Glucagon and less insulin causing blood glucose level to go above normal- this is a prime example of a negative feed back loop in which no exact level is maintained but fluctuations occur at a close bandwidth.

Signal transduction pathway and the causes: A signal transduction is described as being a Cascade of events that detect, amplify and respond to a stimuli usually by changes in enzyme activity(e.g. Activation of an enzyme), activation of genetic material(transcription factors) or opening or closing of ion channels. In this Cascade the original signal is converted form one form to another and is amplified along the way, meaning small amounts of original signalling molecule can still cause 'large' effects. A signal transduction occurs when a ligand(signalling molecule that attaches onto a receptor) attaches onto a receptor which activates.....(don't think you need to know anything specific after this)... and  signal transduction begins. Let me know if you do want to know about what gets activated and stuff

Hormones: Is a chemical substance released by a cell, gland or organ that effect the activities of other specific target cells else where in the body or even itself, hormones are usually transported in the blood. Basically used for regulation and communication.
Steroid Hormones: lipid based and so can travel freely through the plasma membrane, yet they require a protein carrier molecule in order to travel through the blood as they are insoluble; receptors are found in the cytoplasm.


Protein and Peptide: composed of amino acids, peptide hormones contain less than 200 AA whilst protein hormones contain 200+ AA.
Amino Acid Derivatives: as the name suggests these are modified amino acids.
These two are hydrophilic hormones and so do not require any carrier molecule to travel in the blood, yet being lipophilic means that they require receptors on the cell membrane due to their inability to pass through the membrane. They also require a secondary messenger(G Protein) to carry/pass on the 'message'.


Neurotransmitters: typical neurotransmitters are released by neurones to cross the synapse and carry on a message, they do so by binding onto receptors on the next neurone. Neurotransmitters only last for fractions of a second and are broken down quite rapidly by enzymes, they also travel tiny amount(across the synaptic gap).

Neurohormone: is secreted by neurosecretory cells(typically found in the hypothalamus) and can target specific cells far away its point of release. Unlike neurotransmitters neurohormones can travel further and last longer hence the reason why they are called neurohormes; they may also act as neurotransmitters an example would be dopamine. So in a way a neurohormones is like a hormone and neurotransmitter hybrid(not a great definition)
 
Good Luck let me know if I missed anything or if I wasn't clear.

[sabii]

OMMMGGGG Thank you so much! I really really really appreciate all the time and effort you put into your response! Thank you so much!!!
That is actually very clear now! The only thing I had trouble understand was the signal transduction pathway? Could you explain it in simple terms?
Also please correct me if I'm wrong:

So the pancreas produces two hormones which are insulin and glucagon. These are responsible for controlling the blood glucose. If the blood glucose is above normal or optimal range then two things happen. The Beta cells in the pancreas produce more insulin meaning that the cells will absorbs more glucose. On the other hand alpha cells in the pancreas produce less glucagon, and the glucose moves from the blood stream into the lIver where it is stored as glycogen and thus the blood glucose level falls.

If the blood glucose level is below normal/its optimal, then the Beta cells decrease their production of insulin meaning less glucose is absorbed by cells. In contrast the alpha cells produce more glucagon, and the glycogen in the liver is converted to glucose which enters the bloodstream. As a result the blood glucose levels drop?

Also could you explain the main difference between Diabetes Type 1 and 2? And are they hypo/herglycarmia?

THANK YOU!!!!!!!!!!!!!!!!!!!!!!!

[Rachet123]

OMMMGGGG Thank you so much! I really really really appreciate all the time and effort you put into your response! Thank you so much!!!
That is actually very clear now! The only thing I had trouble understand was the signal transduction pathway? Could you explain it in simple terms?
Also please correct me if I'm wrong:

So the pancreas produces two hormones which are insulin and glucagon. These are responsible for controlling the blood glucose. If the blood glucose is above normal or optimal range then two things happen. The Beta cells in the pancreas produce more insulin meaning that the cells will absorbs more glucose. On the other hand alpha cells in the pancreas produce less glucagon, and the glucose moves from the blood stream into the lIver where it is stored as glycogen and thus the blood glucose level falls.

If the blood glucose level is below normal/its optimal, then the Beta cells decrease their production of insulin meaning less glucose is absorbed by cells. In contrast the alpha cells produce more glucagon, and the glycogen in the liver is converted to glucose which enters the bloodstream. As a result the blood glucose levels drop?

Also could you explain the main difference between Diabetes Type 1 and 2? And are they hypo/herglycarmia?

THANK YOU!!!!!!!!!!!!!!!!!!!!!!!

No worries, I'm glad to help.
Two things about your above statements, less glucagon doesn't mean that your liver will begin to absorb glucose and convert it into glycogen(you must remember that insulin does this). What is really happening is that the increase in insulin inhibits the release of glucagon by the alpha cells. Because you liver is also a body cell the insulin also affects your liver causing it to absorb glucose and convert it into glycogen. Glucagon although it targets all cells, it has a more profound effect on liver cells as they store glycogen. Glucagon stimulates you liver cells to convert glycogen into glucose and release it into the bloodstream, thus increasing blood glucose level. Ok      

Stages of Signalling:
There are three steps:
Detection of the signal
Transduction
Response

Detection occurs when the signalling molecule binds to the receptor. The receptor then undergoes a shape change,a gprotein attaches to this modified receptor and thus the G-protein(note this is for an extra cellular signal) Is activated. This activated Gprotein activates a enzyme(adenyll Cyclase) which converts ATP into Cyclic AMP, this then activates other enzymes called kinases which in turn activate other kinases(this is the signal transduction). The final activated enzyme then causes a response in the cell. From the one signalling molecule many final enzymes are produced-this is why it is said transduction amplifies the signal. [sorry I had pictures that I was going to post here but I cannot get it to work.]


Diabetes 1: Is generally genetic and inherited, meaning you are born with it. Type one diabetics are unable to produce insulting and thus unable to maintain relatively stable levels of glucose in the blood.

Diabetes 2: Is generally acquired in ones lifetime(although research has suggest some genetic weighting may be involved) due to unbalance diets and/or no physical activity. In this type of diabetes ones cells do not respond properly to the insulin released by the Beta cells in the pancreas. 

Hyper/Hypoglycaemia although not meaning 'diabetes' are words used to describe blood glucose levels. Persons with constant Hyperglycaemia generally has diabetes, hypoglycaemia may occur in those that inject insulin, too much insulin may cause too much glucose to be taken in by cells thus causing complications.

[Russ]

Your phrasing is unclear for T1; the vast majority of type 1 diabetics aren't born with it, they're born with a predisposition to it that is exacerbated by environment

[Shenz0r]

Type I diabetes is an autoimmune disease, when the beta cells in Islets of Langerhans are attacked by your immune system and thus the machinery to produce insulin is destroyed.

Type II diabetes is when the insulin receptors cannot respond to insulin appropriately, which produces no response from the target cell.

[ealam2]

Just a quick out of topic question here. Does anyone know why the body's immune system attacks its own cells for any autoimmune diseases?

[alondouek]

Essentially, autoimmune diseases stop the immune system for recognising self-cells as self. Instead, it treats the body's own cells as non-self, and then attempts to destroy them as it would any foreign body.

Briefly, autoimmune diseases affect the ability of the immune system to distinguish between self and non-self cells.

[ealam2]

Essentially, autoimmune diseases stop the immune system for recognising self-cells as self. Instead, it treats the body's own cells as non-self, and then attempts to destroy them as it would any foreign body.

Briefly, autoimmune diseases affect the ability of the immune system to distinguish between self and non-self cells.

But why and how does that happen? (Thanks for answering by the way. )

[alondouek]

I'm not sure I can answer this to the extent that some others could, but I'd posit that it would be as a result of changes to genetic sequencing.

The antibodies that our body forms to combat non-self antigens are protein-based, and therefore are produced by protein synthesis from a gene sequence. If a virus were to change a sequence (or cause a 'mutation') in such a way that the resultant protein product - the anitbodies - were not able to distinguish between self and non-self antigens, then the autoimmune system will attack the self antigens that it cannot recognise as self. There are a number of types of mutation that could potentially lead to this, but it can be generally taken as being a form of block/point deletion, addition, inversion or substitution mutation at a specific point in the gene sequence that codes for the antibodies. You'll be looking at mutations in much greater detail in Unit 4.

So that should cover the how (though there's a great deal more biochemistry involved), but as for why? Simply because of infection by some sort of pathogen, and the resulting effect of that pathogen on normal body function.

Hope that helped!

[Russ]

The real answer to "why" autoimmunity happens is well beyond the scope of VCE and you don't need to worry too much. Alondouek's answer is quite logical but probably a very minor cause (if a cause), since the genes that code for antibody production undergo normal mutation/rearrangement as part of their function. More on that at the end.

We know that, fundamentally, autoimmunity results from responding to self as non self, so we have to consider the mechanisms the body normally uses to not detect non self.

One of them is by having very specific receptors/antibodies that only respond to a non self antigen - what happens if this non self antigen resembles a self antigen? It is plausible that some pathogens have antigens that are responded to and then self molecules get caught up in the crossfire. Another part of this is cross reactivity. What if we make an antibody against one pathogen to clear it, but then that antibody accidentally gets bound by cells and triggers reactions that way?

Secondly, the body deliberately doesn't allow the production of cells that are capable of targeting self and kills off the cells that do. What happens if this process goes wrong? We would get T cells or B cells (or both) that exist within our bodies, with a specificity that allows them to attack our own cells.

Thirdly, immune cells that want to attack something, can only do so in a certain environment (known as a permissive microenvironment). This environment is basically the presence of inflammation and pathogenic antigens - thus we can only respond to things we need to respond to. These permissive molecules, however, are capable of activating any immune cell, so what if they activate the wrong ones and thus cause damage. It is also possible to have a microenvironment that is fundamentally skewed towards autoimmunity, where we produce too many cytokines that promote inflammation and damage and so forth.

Many of the mechanisms by which our bodies control our immune system require certain functioning genes, so genetic mutation and disease is another common cause of autoimmunity, but generally by one of the above mechanisms.

As an aside, on antibodies;
I forget the exact numbers, but lets say that our immune system can produce 1 billion kinds of antibody. Does that mean that within our genome, there are 1 billion different sets of genes, 1 for each of the types? The answer is no, there aren't. There are only a few genes that code for antibody production (<100) but the manner in which they work is extremely important. Not only are they randomly selected from, but they also involved certain regions of "hyper variability" that undergo deliberate mutation at an extremely high rate. This introduces an element of randomness and thus allows for more specificities to be produced. Furthermore, there are certain enzymes that are responsible for randomly changing the base sequence and length, in order to produce a truly massive amount of possibilities for antibody gene sequences.

Sorry if that was a little long or complicated, immunology is my favourite

[ealam2]

Thanks guys! I asked this lecturer a couple of months back and he said they don't really know and that they're still researching that. Yes, immunology is interesting.

[sabii]

Type I diabetes is an autoimmune disease, when the beta cells in Islets of Langerhans are attacked by your immune system and thus the machinery to produce insulin is destroyed.

Type II diabetes is when the insulin receptors cannot respond to insulin appropriately, which produces no response from the target cell.

Thank you! 

[Random_Acts_of_Kindness]

The real answer to "why" autoimmunity happens is well beyond the scope of VCE and you don't need to worry too much.

Just on the topic of things that are no longer in the scope of VCE. Everything to do with negative feedback and positive feedback and plant hormones are no longer apart of VCE anymore with the introduction of the new Study Design. I suppose it is just a result of dumbening down the course after they took out the Mid-Year Exam 

[Snorlax]

Just on the topic of things that are no longer in the scope of VCE. Everything to do with negative feedback and positive feedback and plant hormones are no longer apart of VCE anymore with the introduction of the new Study Design. I suppose it is just a result of dumbening down the course after they took out the Mid-Year Exam 

Yeah, the positive and negative feedback is just an essential though...like a lot of things fall under it in VCE...right?
Yeah, study design only mentions animal hormones and plant growth regulators.. A little confusing