Showing posts with label diabetes and liver. Show all posts
Showing posts with label diabetes and liver. Show all posts

Diabetes and liver.. Maintain a normal level of sugar in the blood. Cracking glycogen stored in the liver and increase the production of glucose from amino acids and glycerol

The regulator of liver glucose in Hepatic glucostat blood In addition to other vital functions. The liver maintains normal level of sugar in the blood. Vijrj sugar from the liver in case of shortage of sugar in the blood while increasing the flow of sugar from the blood to the liver in the case of the high level of sugar in the blood. And undergo liver in the performance of this function to the impact of a group of hormones:
  • 1 - insulin and leads to the following effects:
  • A - increase glycogen synthesis (animal starch) in the liver than glucose. The increase of glucose stored in the form of glycogen in the liver to be used when it is needed.
  • B - reducing sugar manufacturing of amino acids in the liver Gluconeogenesis 0
  • 2 - glucagon leads to: increased production of sugar from liver cells by increasing break glycogen stored in the liver Glycogenolysis And increase glucose synthesis of amino acids Gluconeogenesis Thereby increasing the level of sugar in the blood.
  • 3 - adrenaline and noradrenaline, and cortisol, and growth hormone: and lead to increased glucose out of the liver as well.
Thus, the level of sugar in the blood at any given moment is a kind of balance between the amount of glucose entering the blood, and the amount leaving the blood to the muscle cells and other organs in the body. After digesting carbohydrates turns 5% of the glucose into glycogen and 30-40% of it turns to fat trilogy. While the remaining amount is used by the muscles and other tissues. During fasting (in Ramadan, for example) are broken down glycogen stored in the liver, and increased production of glucose from amino acids and glycerol in the liver to maintain the level of sugar in the blood.

The impact of diabetes on the liver.. Enlargement of the liver size. Fatty hepatitis. Viral hepatitis. Cirrhosis

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.
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