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Cellular resistance to insulin caused by reduced glucose transport and metabolism is a primary defect leading to the development of metabolic disease. While the etiology of insulin resistance is multifactorial, reduced insulin action is associated with impaired activity of the glucose transporter GLUT4 in insulin-sensitive tissues. Yet, the role of adipose tissue GLUT4 deregulation in the pathogenesis of insulin resistance, obesity, and diabetes is still unclear. In this study, we assessed the relative GLUT4 level in human subcutaneous adipose tissue from obese, diabetic, and diabetic obese versus control subjects, using a real-time PCR method. GLUT4 mRNA levels were considerably decreased among type 2 diabetic patients compared with those of the controls (P < 0.01), whereas no such difference was found between obese and normal-weight controls. Multiple linear regressions analysis in both diabetic non-obese and diabetic obese groups showed a negative correlation between GLUT4 mRNA expression and both markers of obesity or insulin resistance (P < 0.01). However, in obese group, GLUT4 was inversely associated only with HOMA-IR (P < 0.01). Our findings showed that adipose GLUT4 gene expression changes were more related to insulin resistance and type 2 diabetes rather than to obesity.

Our data strongly support that the changes of thyroid hormones may be influenced by adiposity and its metabolic consequences, such as insulin resistance. This relationship can be explained by a cross talk between adipose tissue release and thyroid function. Nevertheless, metformin treatment seems to affect thyroid function in diabetic patients by maintaining plasma thyrotropin levels to subnormal levels.

Our study on Tunisian patients shows impaired regulation of circulating and mRNA adiponectin levels dependent of metabolic disorders in obesity and Type 2 diabetes. The data suggest that subcutaneous adipose tissue may play an important role in modulating adiponectin expression in diabetes and obesity. Moreover, adiponectin mRNA could be potentially regulated by endogenous PPARγ/RXRα-dependent pathways.

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Inflammatory Pseudotumor (IPT) forms a group of etiologically, histologically, and biologically heterogeneous tumefactive lesions that are histologically characterized by prominent inflammatory infiltrates. It has been described in various organs including the lungs, bladder, liver, spleen, heart, and others. It may mimic a malignant tumor clinically and radiologically. Splenic IPT are most frequently detected incidentally. We report a case of 38-year-old women admitted for recurrent abdominal pain. Physical examination was unremarkable. Contrast enhanced CT showed a well hypodense, circumscribed lesion, measuring 5 × 3.5 cm. A differential diagnosis of lymphoma, teratomas, angioma or angiosarcoma was considered. The patient underwent splenectomy. Histologically, the tumor consisted of an inflammatory infiltrate composed predominantly of diffusely lymphoplasmocytic cells and stromal fibroblasts. Epstein-Barr virus was detected on in situ hybridization exclusively in the epitheloid and spindles cells. The optimal management of this tumor and eventually in asymptomatic patients is still controversial. IPT of the spleen should be remembered when evaluating single or multiple nodules in spleens. The clinical and pathological features of previously reported cases are reviewed in this paper.

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Introduction: Hydatid cyst is a zoonosis caused by Echinococcus granulosus. It may affect any organ and tissue in the body, in particular the liver and Lung. Musculoskeletal or soft tissue hydatidosis accounts for about 0.5 -5% of all echinococcal infections in endemic areas, and is almost secondary to the hepatic or pulmonary disease.