I’ve lived with my lumps now for over 20 years. I had 2 bouts of surgery to remove some when I was younger, but just ‘live with them’ nowadays (I have about 50 of them, most very small). Every couple of years (about now) I dip into seeing what’s new, and hopeful of a cure / treatment.
Thing is though, I've never 'really' understood what a lipoma is. The best I can find is "a benign tumour composed of adipose tissue". Adipose tissue (aka body fat at the lower level) is something that most people will have seen in media/tv surgery documentaries. From my surgery experience (youtube is good also)’ lipomas look completely different to the surrounding fat cells - mis-shapen pink blobs, not resembling the adipose fat at all.
I realise a lipoma is generally encapsulated, I'm guessing therefore that what I saw of my lipomas was effectively a 'sac' like membrane containing standard adipose fat cells? Parking the obvious question of why and how my body decides to do this (which I think is unknown?), I’m left wondering more about the lifecycle of a lipoma and what possible means there are to break the cycle / sac to allow for correct metabolism of the fat cells (treatment wise not curatively as I suspect this has a massive linkage genetically speaking).
I’m in danger of rambling on with questions, so I’ll stop at this point. Perhaps someone could jump in and help my pea brain and tell me/us if I’m on the right path of understanding, and that it is the membrane / sac that appears to present the problem and then a possible opportunity for treatment (I very much like the post made by Laura Roslin and with injectable xiaflex / collagenase, I looked up the application of this with Dupuytren's / hooked fingers, and was amazed at the results).
- Lipoma Guru
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- Number of lipomas: 61-100
- Location: Finland
I'm sorry you had difficulties with replying. There's currently only one restricted thread concerning the Pomaway results. Few have been locked but all others should be open to everyone, even for those who have not registered. Btw, I just created a test user and all seemed to work fine for me. The "Post reply" buttons are found at the top and at the bottom of each thread.
About your first post... You asked some good questions! And the simple answer (which I like to call the "go away there's nothing to see here" answer) is that lipomas are made of matured fat cells.
But why do they appear? Because of the gene mutation? Why there are different mutations in the cells then? And why does the mutation happen in the first place? Was it inherited? Sometimes it looks like it was and sometimes it doesn't.
Oh boy, I wish I could answer to your questions but I can only make assumptions.
You may want to read the What Is Lipoma thread for some inspiration.
PS. Let's try to continue the discussion in the existing thread. I will leave this open for now if for some odd reason you are still having problems in replying to other threads. Thanks!
To be honest though, I read the existing post you refer to as mainly questions with speculative thoughts & theories regarding liopma and the how's and why's.
I'm looking to better understand exactly what a lipoma is made up of and how it differs from the surrounding fat cells within the subcutaneous layer of the adipose tissue. For me, and my pea brain, it is only then that I believe I can comprehend and decipher the myiad of possible treatments, and perhaps even develop my own thoughts with this regard.
This is where the questions begin. It's well documented that the subcutaneous layer (hypodermis) it'self is made up mainly of fat cells(adipose cells) and loose connective tissue(fibroblasts). I read that this layer also contains a third cell type called macrophages, my initial understanding of these cells reads interestingly with regards their stimulant and repair qualities.
So, it seems a lipoma is indeed made up internally at least of regular/mature fat cells. I'm guessing that someone has opened up / dissected a lipoma, not just to confirm it's cancerous capability, but to document and understand exactly what it's made up of? (I haven’t been able to find this info). Moving on. It is the sac/membrane that poses the biggest query for me. If we can answer what this is, then we can consider how to best break, reduce or avoid/rid it.
Can someone please confirm my understandings so far. I would be very grateful if someone could also push this post further to enable my/our better understanding.
Many thanks, Sparky.
- Lipoma Guru
- Posts: 1172
- Joined: Tue Mar 29, 2011 8:01 am
- Number of lipomas: 61-100
- Location: Finland
CYTOPATHOLOGY OF SKIN AND SUBCUTANEOUS MASSES
From here you may found something of interest, like the enlargened vacuoles in lipomas.
I have spent considerable time researching the lipoma pathology but there are not many such studies available. It almost feels like the medical community is not interested because they have already made up their minds about these growths and believe no further investigation is needed.
Now, please continue in the existing thread. I will close this one for now.
My reasons for starting this post are to explore, discuss, learn and better understand what a exactly makes up a lipoma and how it differentiates with the surrounding fatty layer / skin tissues of our bodies. Why, because I don’t know (there seems to be very little detailed information generally available); a detailed understanding of what lipoma are is essential for me to assess the myriad of claims, treatments and cures.
The first point to make is that my question “what exactly is a lipoma” relates somewhat generically to all lipoma, but as there are many forms/types, I’d like to focus my efforts on lipoma formed within the subcutaneous skin layer (very common).
The second point to make is that like most of us on this forum/board, I am not from a medical back ground, I simply have a strong mind for knowledge, treatments and ultimately a cure for my lipoma. To be honest, I’m not sure how much information I myself can bring to this post, but I do intend to spend some time researching and will post back as/when I can. My hope is that someone/people here may have more knowledge to share that will help develop or even directly answer the question.
That said, Matt makes a good point in his initial post back to me “go away there's nothing to see here". I understand this point, and I guess is a likely reason why there is so little out there, but I simply cannot accept a lipoma is that indifferent to it’s surrounding fatty subcutaneous tissues. To this end, I am particularly interested in the differences of the adipose materials, as well as what, how and why do many lipoma develop an encapsulation (sac, membrane, capsule).
Anyone like to add anything at this point?
First off, it has been difficult to find any meaningful information or details of a factual nature with regards the specific pathology and make up of lipoma vs surrounding adipose. Mostly, lipoma are discussed more generally as tumours having much the same pathology as adipose, but are often observed with a varying appearance size/thickness encapsulation made of fibrous connective tissue (membrane, sac, capsule).
Ok, so this much we know. Digging deeper though, whilst presenting very medically technical (ouch my brain hurts!), there are some case reports that I have found that provide some meaningful fact as well as some suggestive conclusions as to what a lipoma is and how it differs from standard adipose.
The following two links are to 'abstracts' of case studies asking such questions:
http://www.ncbi.nlm.nih.gov/pubmed/1261213 This small but interesting study investigates two very important enzymes used to gain access to, and control fat stores within our bodies (comparitively lipoma vs adipose).
http://www.ncbi.nlm.nih.gov/pubmed/6482388 This larger study associates strongly with the first study, again detailing these two enzymes as clear, important differences.
The two enzymes discussed are Lipoprotein Lipase (LPL) and Hormone Sensitive Lipase (HSL). Both of the reports from the studies show that LPL activity as being 'much' higher within lipoma adipose (15 to 40 times higher) than was found in non-lipoma adipose. It was also found that HSL activity was lower (study didnt quantify).
These two enzymes play an important role within our bodies in the release of energy stored in adipose (lipolysis).
The second report makes an interesting point "It is likely that the high lipoprotein lipase activity of lipoma contributes to the growth of the tumour"
From Wiki - "Lipoprotein lipase (LPL) is a water soluble enzyme that hydrolyzes triglycerides in lipoproteins, such as those found in chylomicrons and very low-density lipoproteins (VLDL), into two free fatty acids"
In other words, LPL takes a lead role in the fat storage process. What activates LPL? Well, in adipocytes (fat cells), insulin is mainly responsible. Insulin both activates LPL and also blocks lipolysis by inhibiting the release of glucagon.
Hormone-sensitive lipase (HSL) is activated when the body needs to mobilize energy stores. HSL hydrolyzes the triglyceride (fatty acid within the adipocyte) into free fatty acids and glycerol where they can then be re-esterified and released back into general circulation.
Ok, so I just brought a few things together there. I did it becuase the report mentions some significant differences in these enzymes to that of normal adipose fat. It concludes by providing evidence of LPL as being very much higher, with HSL lower in lipoma cells against standard adipose. My brain works very cause & effect..... I'm interested to learn how and why that state occurred, and what can done to correct it. It's thinking: high LPL activity = lots of energy input = lots of fat, but without much HSL things are out of control and the tumour / lipoma is a result? I guess I'm trying to work out some of the details behind the report conclusion "It is likely that the high lipoprotein lipase activity of lipoma contributes to the growth of the tumour".
This much I can understand, does anyone know any more about the Lipogenesis (fat storage) and Lipolysis (fat mobilization) to take this further and push me forward or pull me back.
So, as a lipoma sufferer, it appears that the normal cycle of lipogenesis (fat storage) and lipolysis (fat mobilization) is happening correctly for most of my adipose, but for some reason, LPL is not being regulated within some of my adipocytes (fat cells). It's almost like some adipocytes are 'stuck' in lipogenesis - uncontrolled situation, LPL is high and presumably more triglycerides (free fatty acids) are being allowed stay/pack into my cells creating a mass / tumour.
What should be regulating LPL and allowing correct lipolysis? Well, during the lipolysis process with insulin levels lowering, Hormone-sensitive lipase (HSL) should be activated. But we know that HSL levels found in lipoma are lower than normal adipose, could it be that this lowering is significant enough to cause uncontrolled LPL and thus perpetuate lipogenesis?
If so, what activates and regulates HSL? This is where it gets a bit 'heavy' for me right now, but I'll have a go. It appears that something called Perilipin A may be very significant. From wiki - "phosphorylated perilipin A" is the primary HSL activation..... Phosphorylated means there is an addition phosphate to the perilipin A. BUT perilipin on it's own "perilipin acts as a protective coating from the body’s natural lipases, such as hormone-sensitive lipase" - wiki. Is it possible then that Perilipin is somehow not becomming phosphated in activating HSL which in turn is not regulating LPL which in turn is not allowing correct lipolysis?
From Wiki: Perilipin is a protein that coats lipid droplets in adipocytes, the fat-storing cells in adipose tissue. Perilipin acts as a protective coating from the body’s natural lipases, such as hormone-sensitive lipase, which break triglycerides into glycerol and free fatty acids for use in metabolism, a process called lipolysis.
Perilipin A, phosphated:
PMID: 17878492: Perilipin restricts the access of cytosolic lipases to lipid droplets and thus promotes triacylglycerol storage. In times of energy deficit, perilipin is phosphorylated by Protein kinase A (PKA) and facilitates maximal lipolysis by hormone-sensitive lipase and adipose triglyceride lipase. A model is discussed whereby perilipin serves as a dynamic scaffold to coordinate the access of enzymes to the lipid droplet in a manner that is responsive to the metabolic status of the adipocyte
So Perilipin is a protien that also has an active part in regulating lipogenesis (fat storage) and lipolysis (fat mobilization). It does this by 'shielding' exposure of HSL to the lipids/adipocyte/fat cell.
Could it be that Perilipin isn't being phosphated by PKA in my lipoma tumours, limiting HSL access etc...? Need to know more about the PKA process.....
During this research process I'm asking myself 'whatever is going on in creating my lipoma, why is it occurring in only some locations?' I cannot begin to answer that question unil I fully understand the process chain of events that have led to that overiding pathological position of extremely evivated LPL in lipoma.
If you have any input to this folks, I'd be very pleased for your thoughts.
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