The impact of diabetes on the liver
We all know the risks that unbalanced diabetes poses, especially for the heart, the arteries, and the reins of those who have it. There is also evidence that good control of diabetes can limit these risks, even avoiding them if things are done well early on. On the other hand, the liver is not one of these classic targets of chronic hyperglycaemia, on the contrary, it plays a major role in the regulation of glucose flows allowing good glycemic regulation in non-diabetic subjects.
Admittedly, the liver can be damaged by toxins (hepatitis B and C viruses) or products that it is responsible for eliminating. The best known example is that of alcohol (a substance naturally purified by the liver), but whose excessive consumption can lead to progressive damage to the liver.
which goes through successive stages:
- steatosis (fatty degeneration of liver cells).
- steatohepatitis (appearance of chronic inflammation and oxidative stress).
- cirrhosis (definitive fibrous transformation of liver cells).
- liver cancer.
The same lesions can occur in the event of metabolic aggression and in particular of massive accumulation in the liver of free fatty acids known to be hepatotoxic. The factors favoring this accumulation are obesity and especially excess abdominal fat, insulin resistance, hypertriglyceridemia, but also chronic hyperglycemia, all situations encountered in type 2 diabetes (T2D). This accumulation leads to non-alcoholic steatohepatitis (NASH = Non Alcoholic Steato-Hepatitis), which can also be evaluated if it is not corrected towards fibrosis, more exceptionally towards cancer.
Today T2D is the 3rd cause of serious liver damage, and in particular in the USA for liver transplants. The diagnosis of NASH is based on the ultrasound appearance of the liver and biological abnormalities, in particular an increase in transaminases (ASAT and especially ALAT). On the other hand, only the liver biopsy puncture makes it possible to measure the degree of fibrosis, and therefore to estimate the risk of progression towards cirrhosis.
The treatment of this liver damage will be all the more effective if it is addressed to an early stage of NASH, with as little fibrosis as possible. Two elements are essential, namely:
weight reduction, which must be at least 7% of the initial weight, ideally 10%, as part of the dietary hygiene recommended for any obese type 2 diabetic;
glycemic balance.
Some drugs have demonstrated some effectiveness in reducing NASH, in particular metformin, pioglitazone (glitazone withdrawn from the market in France) and liraglutide (analogue of GLP1), without it being possible yet to offer their routine use. Today, hepatic monitoring becomes just as important in obese type 2 diabetics as that of the heart, arteries and kidneys and the hepatologist must be consulted in the event of persistent abnormalities.
