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Background: Diabetes mellitus is an endocrine disorder characterized by a state of hyperglycemia. It is caused by defect in the insulin secretion, insulin action or even both. Long-term complications of diabetes are many as nephropathy, retinopathy and neuropathy. Diabetes mellitus is considered the most common cause of renal failure worldwide. Diabetes results in many histological changes in the kidney. Most cell types of the kidney as podocytes, tubular cells and mesangial cells affect in diabetes.The most characteristic change in diabetic nephropathy (DN) is glomerular alteration as glomerular expansion and thickened glomerular basement membrane.Many alterations of the respiratory functions aredetected in diabetic patients. Several characteristic histological changes had been described in the lung of diabetic animals. Diabetic lung is characterized with increased connective tissue at the expense of alveolar air spaces.This review focuses on histological changes on the kidney and lung of diabetic animal model. Conclusion: Kidney and lung are target organs for diabetes. DN is one of common chronic complications of diabetes. DN is the most common indication for renal replacement therapy worldwide. Several histopathological changes were reported in lung of diabetic animals. It is essential to provide novel therapeutic strategies that could prevent complication of diabetes on kidney and lung.

Liver sinusoids are lined by fenestrated endothelial cells surrounded by perisinusoidal cells, Kupffer cells, and pit cells, as well as large granular lymphocytes. The functional ability of the liver cells can be substantially modified by exposure to toxins. In the current work, we assessed the histopathological and ultrastructural effects of a time-course exposure to aflatoxin B1 (AFB1) on the hepatic structures of rats. A total of 30 adult female Wistar rats were randomly divided into three groups: a control group, a group orally administered 250 µg/kg body weight/day of AFB1 for 5 days/week over 4 weeks, and a group that received the same AFB1 treatment but over 8 weeks. Histopathological and ultrastructural examinations of hepatocytes revealed massive vacuolar degeneration and signs of necrosis. Furthermore, the rat liver of the treated group exhibited damage to the sinusoidal endothelium, invasion of the space of Disse with hyperactive Kupffer cells, and some immune cells, as well as Ito cells overloaded with lipids. In addition, damaged telocytes were observed. Taken together, our results indicate that AFB1 induces irreversible adverse effects on the livers of rats.