Abstract:
Obesity has reached epidemic proportions globally. Obesity is accompanied by co-morbidities affecting multiple peripheral tissues. Obesity associated non-alcoholic fatty liver disease (NAFLD) is the leading cause of chronic liver disease in the US. The molecular mechanisms underlying the development and the progression of NAFLD, however, remain poorly understood. Stomach is an important endocrine organ that produces a number of bioactive peptides with important roles in the metabolism of energy. Stomach is located in the vicinity of the liver, but so far it has been largely neglected as an organ with potentially important role in obesity and associated NAFLD. This study provides the evidence for the contribution of the stomach-specific expression changes in a number of molecules previously implicated in inflammation and energy homeostasis to the pathogenesis of obesity-associated NAFLD.
White adipose tissue (WAT) represents the majority of adipose tissue in humans, is the main fat storage organ. In contrast, brown adipose tissue (BAT) has a unique ability to spend energy through producing heat in mitochondrial "uncoupling". The facultative nature of BAT activity and its distribution within WAT depots complicate the detection of BAT in adult humans. In this study, the expression of genes involved in transcriptional regulation of brown adipocyte-specific UCP1 gene and BAT differentiation was assessed as quantitative indicator of BAT activity in adipose of adult humans.
