Adiponectin expression and metabolic markers in obesity and Type 2 diabetes.

BACKGROUND: Adiponectin has emerged over the last decade as a key adipokine linking obesity, insulin resistance, and Type 2 diabetes. However, the molecular mechanisms controlling adiponectin expression in adipose tissue are not fully elucidated. Furthermore, increasing evidence indicates that peroxisome proliferator-activated receptor- γ (PPAR-γ) plays an important, and beneficial, role in modulating adiponectin expression. AIM: The aim of the present study was to assess the separate role of obesity and Type 2 diabetes in the relationship between endogenous PPAR-γ signaling and adiponectin expression in subcutaneous adipose tissue. SUBJECTS AND METHODS: Enzyme-linked immuno sor bent assay and real time quantitative PCR analysis were carried out in overweight, obese, and/or diabetic Tunisian patients who underwent an abdominal surgery. RESULTS: These results collectively indicate that circulating levels of adiponectin were decreased in all overweight, obese, and/or diabetic (p<0.001). However, the subcutaneous mRNA expression of adiponectin was reduced only in diabetics (p<0.01) but presents some discrepancies in obese individuals. Moreover, mRNA levels of adiponectin were positively correlated with levels of mRNA encoding PPARγ and its heterodimeric partner retinoid X receptor-α (RXR-α), in both obese and diabetic patients. CONCLUSION: 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.

A benign cystic mass of the pancreas mimicking a malignant lesion.

Herein, we highlight the diagnostic challenges of cystic pancreatic tumours, and report a case of chronic pancreatitis caused by a cystic tumour, which consisted in a canal dilatation--and not a pseudocyst. The case thus demonstrates a rare association between a cystic form of chronic pancreatitis and adrenal adenoma. We report the case of a 46-year-old patient with no particular past medical history who presented with long lasting symptoms consisting in an abdominal pain and deterioration in general health. Imaging findings (ultrasound, CT-scan, MRI) showed a 3-cm cystic lesion of the tail of the pancreas associated with a 3-cm adrenal mass. Because of the suspicion of a malignant disease, surgical treatment was performed. Pathological findings consisted in fibrotic chronic pancreatitis with canal dilatation and an adrenal adenoma. Pancreatic cystic lesions are rare tumours. Despite of the multiplicity of imaging techniques, differential techniques lack sensitivity and specificity. Final diagnosis must be based on pathological features.

[Right paraduodenal hernia: a rare cause of intestinal obstruction]. / Hernie paraduodénale droite: une cause rare d'occlusion intestinale.

A 17 year old male was admitted emergently with acute small bowel obstruction. An urgent laparotomy revealed a loop of gangreous ileum herniated through a right paraduodenal hernia. The compromised bowel was resected and a primary anastomosis was performed. This case report allows us to discuss the diagnostic and therapeutic features of this rare condition.

[Beta 2-microglobulin amyloidosis presenting as intestinal perforation in a haemodialysis patient]. / Amyloïdose de type beta2-microglobuline révélée par une perforation intestinale chez une hémodialysée chronique.

Long term haemodialysis patient is subject to several complications such as generalised amyloidosis which is the result of deposits of beta2-microglobulin not depurated by haemodialysis. Digestive location causes ischemic accidents such as ulcer, infarctus, digestive haemorrhage, pseudo-obstruction and perforation manifested by a surgical emergency. Our observation is the 6th case of intestinal perforation caused by amyloidosis deposit reported in the literature.