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Disturbance in carbohydrate metabolism and glycogen disturbance


Glucose is not identifiable histologically in tissues but glycogen, however, can be identifiable. It can be demonstrable by periodic acid-Schiff (PAS) or by Best´s carmine.


In normal situation liver cells (hepatocytes) contain glycogen within the cytoplasm. The nuclei of hepatocytes frequently contain high glycogen content as well. It gives them peculiar clear and glassy appearence. Thís is likely to be found in cases of diabetes mellitus. Otherwise its significance in the absence of diabetes is unknown.


Variations of glycogen from its normal amount and distribution form an important feature of certain diseases. For example diabetes mellitus and glycogen storage diseases.


Diabetes mellitus:

Type I - autoimmune lymphocytic insulitis, insulin dependent diabetes

Type II - peripheral organs and tissues exhibit insulin resistency (usualy conected with obesity), non-insulin dependent diabetes

In a presence of glycosuria, the epitelial cells of lower proximal convoluted tubules and Henle´s loops shows vacuolation (small or larger masses of glycogen)


Complications of diabetes:


diabetic macroangiopathy - caused by aterosclerosis

diabetic microangiopathy - altered structure of basement membrane by glycosylation of proteins (retinopathy, glomerulosclerosis)


Nodular diabetic glomerulosclerosis

diabetic cataract - osmotic vacuolar degeneration of the lens epitelium

diabetic liver - secondary glycogenesis and fatty degeneration (obesity)

diabetis neuropathy - myelin degeneration (late complication)

susceptibility to infections - furunculosis and candida mycosis


Glycogen storage diseases - glycogenoses:


Rare genetic defect of glycogen metabolism. It results in abnormal accumulation of glycogen in cetain organs. Occurs in infancy.


Type I - Gierke´s disease: defect of glucose-6-phosphatase in kidneys and liver, leading to their enlargement.

Glycogenosis of the liver

Type II - Pompe disease: generalized lysosomal glycogenosis with muscle weakness with compensatory hypertrophy of these muscles(heart, skletal muscles, tonque).

Type III- Forbes disease: defect in amylo-1,6-glucosidase, causin cardiomegaly, hepatomegaly and muscles weakness.