Immunohistochemical identification and assessment of the location of leptin, visfatin and chemerin in the liver of men with different body mass index.

BACKGROUND: Adipokines such as leptin, visfatin and chemerin play a pivotal role not only in the pathogenesis of excessive weight gain but also impact on hepatic metabolism. However, alterations in the production of these peptides in the liver of overweight individuals have not been fully elucidated yet. The aim of the study was to evaluate changes in leptin, visfatin and chemerin biosynthesis in the liver of men with different BMI. METHODS: Fourteen adult men without symptoms from the digestive system were recruited. Research material consisted of liver samples. Study participants were divided into two groups: lean (BMI ≤ 25 kg/m2) and overweight subjects (BMI > 25 kg/m2). Paraffin liver sections were processed by immunohistochemistry for detection of leptin, visfatin and chemerin. Hepatic expression of leptin, visfatin and chemerin genes was determined by qRT-PCR method. RESULTS: Increased immunoreactivity for leptin and chemerin, and decreased immunoreaction for visfatin were observed in the liver of overweight men in comparison to lean subjects. Overweight subjects with hepatic steatosis displayed increased immunoreactivity for leptin and weaker immunoreaction against visfatin and chemerin in the liver, compared to individuals with normal organ structure. Expression of leptin and chemerin was enhanced in the liver of overweight individuals, with the highest expression observed in subjects with hepatic steatosis. Conversely, expression of visfatin in the male liver was decreased in overweight subjects and those with and liver steatosis. CONCLUSIONS: The present study proves that the expression of leptin, visfatin and chemerin in the male liver is altered in overweight individuals. Our report also indicates the potential importance of these peptides in hepatic steatosis associated with overweight.

Altered cannabinoid receptor expression in pancreatic islets in experimental model of uraemia.

BACKGROUND: Uraemia leads to a number of metabolic and hormonal disorders including defective carbohydrate metabolism. Endocannabinoids exert their effect on insulin and glucagon secretion via activation of specific receptors named CB1 and CB2. For this reason and the absence of reports on location and immunoreactivity of CB1, CB2 receptors compared to immunoreactivity of insulin- and glucagon-secreting cells in experimental uraemia, the author decided to investigate this issue. The aim of the present study was the immunohistochemical localisation and evaluation of cannabinoid receptors (CB1, CB2), insulin and glucagon in the pancreatic islets of uraemic rats. MATERIALS AND METHODS: Fragments of the rat's pancreas were collected 28 days after surgical resection of one kidney and removal of 70% of the other kidney cortex. Paraffin-embedded sections were stained with haematoxylin-eosin and immunohistochemical reactions were performed with the use of a specific antibody against CB1-, CB2-receptors, insulin and glucagon. RESULTS: It was revealed the decreased immunoreactivity of the CB1 receptor and higher intensity of the immunohistochemical reaction against CB2 receptor as compared to the value in the control animals. Significantly higher immunoreactivity of glucagon-positive cells and weaker immunoreactivity of insulin-positive cells were observed in pancreatic islets of uraemic rats. CONCLUSIONS: The obtained results indicate the involvement of cannabinoid receptors in the pathomechanism of carbohydrate metabolism disorders, associated with abnormal secretion of hormones by the α and ß cells in uraemia.