Liver disturbances in obesity and diabetes mellitus.
Abnormal liver tests, right upper quadrant pain and hepatomegaly occurring in an obese or in a diabetic patient may point to the presence of fat or of glycogen accumulation in the liver parenchymal cells. Marked hepatomegaly due to cytoplasmic glycogen deposition is mainly found in poorly controlled insulin-dependent diabetic patients. If accompanied by cushingoid features, growth retardation and by delayed puberty, a diagnosis of Mauriac syndrome can be made. Hyperglycaemia, insulin administration and increased concentrations of the counterregulatory hormone cortisol may all play a role in the glycogen deposition by their concerted actions on the glycogen phosphorylase and synthase enzymes, promoting the accumulation of glycogen. Hypercortisolism may be responsible for growth retardation and delayed puberty in Mauriac patients. Regression of hepatomegaly and of the associated clinical characteristics may be obtained by a better metabolic control due to the administration of long-acting insulin and the change from single to twice daily injections. Fatty liver is rare in insulin-dependent diabetic patients and is indicative of a poor diabetic control. This process is quickly reversible by adequate insulin treatment. Steatosis is frequently found in maturity-onset diabetics and in obese patients. The pathogenetic mechanisms leading to the accumulation of triglycerides and of fatty acids in the hepatocytes can easily be understood from the normal cycling of fatty acids between the adiopose tissue and the liver. Histologic features of nonalcoholic steatohepatitis can also be found in obese and in diabetic patients. Steatohepatitis may rarely evolve into cirrhosis. In general, there is no correlation between the degree of the biochemical alterations and the severity of the histological findings.(ABSTRACT TRUNCATED AT 250 WORDS)
Van Steenbergen
W
W
Department of Internal Medicine, University Hospital Gasthuisberg, Leuven, Belgium.
Lanckmans
S
S
D048909:Diabetes Complications; D003920:Diabetes Mellitus / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D005227:Fatty Acids / Q000378:metabolism; D005234:Fatty Liver / Q000209:etiology* / Q000473:pathology; D006003:Glycogen / Q000378:metabolism; D006801:Humans; D008099:Liver / Q000378:metabolism; D009765:Obesity / Q000150:complications* / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D014280:Triglycerides / Q000378:metabolism
D005227:Fatty Acids; D014280:Triglycerides; D006003:Glycogen