Today I had a zoom session with the NHS Diabetes Prevention Programme, my last bloods score was 48 (on the diabetic metric), I have pre diabetes and I am right on the boundary for the full type 2 scenario.
In this zoom session they talked about blood pressure (mine is actually rather low not high) and my cholesterol average total, perfect ratio of good to bad etc.
I asked the trainer who is not a Doctor could my liver issues have anything to do with my pre diabetic status and he said if the liver was compromised it would not be able to store unused glucose efficiently, which would push it into the bloodstream.
This is the first time anyone has explained this to me, perhaps others are already aware. This would seem a very plausible scenario.
So the deal is you have liver issues, congratulations now welcome to the wonderful world of Type 2 Diabetes!
My only way of dealing with this new knowledge is to up the exercise (my lovely, eternally patient wife has me on an excellent 'liver' diet). Exercise should help soak up the glucose and reduce the fat on the liver.
I spent and hour and half at 'walking' football (everyone runs do not tell the FA!) this morning, so hopefully that helped reduce some glucose.
Speaking of fat on the liver I was called at 8.00am this morning for an US scan this afternoon, I do seem to have really put the spooks up my GP practice (see my other thread I posted) or perhaps more positively they do care!
The US scan was done by a really excellent technician, I quoted back to him about my portal being 17mm which it is and is normal. There was no coarseness on the surface of my liver thankfully but there was 'sparing of fat' on the liver, apparently this is a piece of fat at the top of the liver near the gallbladder, it is a bit like the rind on a slice of bacon.
The fact you can actually see the fat on the scan on the liver is horrifying and a further motivation for lifestyle change. That kind of brutal truth motivates.
Interestingly my GP did send me off for a US scan when I originally presented with symptoms all those years ago. At that scan the technician said my liver was a 'good size'. When I asked him about fat on the liver, he said no fat on the liver but there is fat close to it. This sounded at the time like a relatively clean bill of health.
Of course I needed more exercise but that was to do with my general health not specifically my liver.
Could the fat I have now really have accumulated after this scan or did the technician simply not understand what he was looking for and seeing?
It looks like you need to be lucky in the people you get to see in the NHS, some are excellent like my current 'stand in' GP (and partner of the practice) who organised a scan and blood tests immediately as well as the excellent US scan technician I had today. Some others well..
The technician today actually said to me that the surface of my liver was smooth 'like a baby's bottom' and looked nothing like the cirrhotic ones he had seen, that comment made feel so reassured perhaps foolishly!
Perhaps there is still hope, we shall see.
Off on a short UK break next week with my wife (I am retired), lots of walking along the coast in the winter sunshine, relaxing and eating well.
Best wishes to you all of you whatever you and yours circumstances are and wherever you live!
regards
iro1
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Iro1
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I found this information when my cirrhotic hubby was told he was borderline diabetic.
Hepatogenous Diabetes
Patients with liver cirrhosis develop frequently disturbances of glucose metabolism e. g. glucose intolerance or hepatogenous diabetes which are caused by the hepatocellular functional loss and insulin resistance due to chronic liver disease.
Until now there are no recommendations comparable to guidelines on the diagnosis of and therapy for hepatogenic diabetes. Regarding basic treatment a sufficient daily energy and protein supply should be guaranteed since the majority of patients with liver cirrhosis are malnourished. The risk of hypoglycaemia must be considered carefully under pharmacological treatment of hepatogenous diabetes. Biguanide and PPAR gamma agonists are contraindicated due to side effects in liver cirrhosis. Suitable oral antidiabetics are glinides and short-acting sulfonylureas. If a sufficient diabetes adjustment does not succeed by oral antidiabetics a prandial insulin therapy using short-acting insulins or rapid-acting insulin analogues should be applied. Optimisation of diabetic metabolic conditions is not only important to avoid typical diabetic late complications but also cirrhosis-associated complications, e. g., gastrointestinal bleeding, hepatic encephalopathy or the occurrence of hepatocellular carcinoma.
• Hepatogenous diabetes, which develops in cirrhotic individuals as a consequence of loss of liver function, is not considered as a unique clinical entity separated from type 2 diabetes occurring in chronic liver disease before cirrhosis onset.
• Recent evidence suggests that liver dysfunction per se exerts a detrimental effect on β‐cells, independently of the degree of glucose tolerance.
• Hepatogenous diabetes usually present with normal fasting plasma glucose and haemoglobin A 1c levels, thus requiring an oral glucose tolerance test for diagnosis.
• Differentiating hepatogenous diabetes from classical type 2 diabetes may be relevant for both prognostic and therapeutic purposes.
HiThank you for your informative response, I do not feel hyperglycemic but it is certainly something too look out for.
I do not think I am malnourished either so I will keep clinging to the hope that I am suffering from a fatty liver not full blown cirrhosis for the moment
Good news one -In this zoom session they talked about blood pressure (mine is actually rather low not high)
Good news two -The US scan was done by a really excellent technician,
Good news three -I quoted back to him about my portal being 17mm which it is and is normal.
Good news four -There was no coarseness on the surface of my liver thankfully.
Good news five - if a bit old - At that scan the technician said my liver was a 'good size'.
Good news six - if a bit old - When I asked him about fat on the liver, he said no fat on the liver but there is fat close to it. This sounded at the time like a relatively clean bill of health.
Good news seven - The technician today actually said to me that the surface of my liver was smooth 'like a baby's bottom'
Good news eight - Liver looked nothing like the cirrhotic ones he had seen.
Your conclusion - Perhaps there is still hope, we shall see.
My conclusion - (I am not a doctor, this is not a diagnosis but my guess)
There is nothing left to see, you are fine. Happy new year and all the best!
Hi, once I was diagnosed with NASH my gastro consultant bet me I would become diabetic and sure enough next time I had bloods done I was, very low numbers and diet controlled. Diabeties dose go hand in hand with NAFLD, I'm on a Facebook group for type 2 diabetics and nearly every day some one says they have been told they have a fatty liver.Hilary
NASH stands for Non Alcoholic Steato Hepatitis - it is the more aggressive form of non alcohol related fatty liver and it's where the liver is both fatty and inflamed (hepatitis purely means inflamed liver). NASH can progress quite quickly towards fibrosis and scarring.
Thank you that makes sense I must have NASH as I have fibrosis no medical professional has ever used the term in relation to me. So looks like I can expect to have type 2 soon I remember when I swam a lot the diabetic metric went down to 43. I will be taking it up but the open water type
I’ve responded to this type of question several times now. I should point out that I’m not medically qualified in any way, but have researched and have learnt a lot over the years. This has helped me to talk with some very knowledgeable people. Some of what I am writing about here is being taken from an email received from Dr Patricia Lalor back in 2020, Dr Lalor is a senior lecturer and senior investigator at the Centre for Liver Research and NIHR Biomedical Research Unit, Institute of Biomedical Research, at the Medical School, University of Birmingham.
So, this reply may seem a little technical to some, but I hope it will make some sense in the end.
We all have a rather special gene in our bodies called the CRTC2 gene, which is also known as the “Switch Gene”. This protein can be found in many cells including immune cells, heart and placenta and some studies suggest it in liver cells too. Also down-regulated in some cancers. This gene helps to monitor the amount of glucose in the blood.
The way I like to describe this gene is a bit like having a three positioned switch.
If the switch is in say, position 1. Then everything is performing normally, The liver is turning sugars into glucose and the glucose is being turned into glycogen. So, there you are walking down the road to the bus stop. All of a sudden you see the bus coming and you start running. The CRTC2 gene notices that the muscles now need more fuel and so the switch gene moves to position 2. This instructs the liver to dump more glucose into the blood system.
After you’ve caught the bus, and sit down, the CRTC2 gene realises there’s enough glucose in the body and the demand for more fuel is over, and it returns to position 1 again. A message is sent to the pancreas and this releases insulin. (Insulin is believed to be the instruction to the liver to stop dumping glucose).
Now, if a person was to have a cirrhotic liver, then this insulin instruction can’t always get through to the liver, and so the liver keeps on pumping out yet more glucose. This means that the liver has now become insulin resistant.
The magical thing about this CRTC2 gene is when we are having REM sleep. Here it moves into position 3. Here the body switches from glucose to fat burning mainly in response to two key hormones – insulin and glucagon – that are produced by the pancreas. Once we wake up. The switch gene returns to position 1 again and we start a new day.
I’m now going to copy an extract of Dr Patricia Lalor’s email which hopefully might clarify things more.
“In a post-transplant patient – here the medications used to prevent rejection can alter the way hepatocytes handle sugars and drive overproduction and release of glucose into the blood. Also, patients with diabetic risks before transplant are more likely to experience it after transplant.
The gene you found is interesting – the protein does indeed act as a switch to produce more sugar in fasting situations and is down-regulated when abundant sugar is present. Levels change in type 2 diabetes and this makes the hyperglycemia worse. What's most interesting is that the signals that act through this molecule are linked to a protein called calcineurin which is activated and causes the liver to make more sugar. The calcineurin levels increase in insulin-resistant states. CRCT2 is found in many cells including immune cells, heart and placenta and some studies suggest it in liver cells too. Also down-regulated in some cancers”.
However, calcineurin is also in immune cells and is linked to growth and functional responses. So some anti-rejection medications used after transplant, target calcineurin to dampen down anti-graft immune responses. Tacrolimus and cyclosporine are calcineurin inhibitors. Thus you can see how there might be a connection between anti-rejection medication and the function of CRCT2. As you say however it's quite a new area of research and it takes a while for new advances to make it into the clinic.
I hope this helps and that you and others find this interesting. I use the 1,2,3 position analogy to make is easier to try and understand, but in real life it's far more complicated than that.
What might also help to understand all this is nice video. This guy Dr John Campbell is becoming rather popular. He's put together about eight videos covering the liver. Which he talks in plain easy to understand English. This particular video is entitled, "Liver Function 3, Carbohydrate storage and metabolism", it explains rather nicely about sugars, and how the liver processes them.
I have to agree with kensimmmons, you are getting overwhelmingly great news and you still are allowing your anxiety to make you think you have cirrhosis (or temporary cirrhosis). Your exercise and healthy eating makes that possibility less likely than winning the lottery without buying a ticket
Physically you are winning, but in the battle of who is in charge in your mind, you are playing second fiddle to anxiety.
There can only be one boss. At the moment, anxiety is in charge of you, and, only you can take back control from anxiety.
I needed help because I had not realised my anxiety had become my number one problem, it was convincing me every twinge was a life threatening. (it is very devious that way, misdirection).
Now I can supress my anxiety, and, when I'm given good news, I take it on board and get on with enjoying life rather than just participating in life.
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