Diabetes and Endocrinology Research Center
In recent years, obesity and related diseases such as cardiovascular disease and diabetes have emerged as significant challenges for public health. While extensive research has been conducted on the genetic causes of these diseases, the role of environmental factors in the development of obesity and diabetes is still less understood. The Diabetes and Endocrinology Research Center at the Endocrine Institute was established with the aim of promoting comprehensive research in the fields of obesity, insulin resistance, and diabetes.
Our research group focuses on the pathophysiology of obesity and diabetes processes in their various aspects. The main research areas in the laboratory are:
The impact of food preservatives on metabolism: both environmental and nutritional factors have been observed to influence the transmission process of endocrine signals. These substances can function as either activators or inhibitors for specific receptors within a diverse range of biological systems. Our laboratory recently identified a commonly used preservative in the food industry, which has distinct metabolic effects. Our study revealed that this substance triggers an elevation in glucose production in the liver, along with alterations in glucagon and insulin levels. Chronic exposure to this substance caused weight gain and the development of insulin resistance in murine models. We are currently working on translating the preclinical results to humans through a series of randomized controlled studies. In addition, using in-vitro and in-vivo animal models, we aim to evaluate the effects of micronutrients in the modern diet on the development of obesity and diabetes.
The cellular mechanism that connects overnutrition to the onset of chronic inflammation, insulin resistance, and diabetes: Prior studies have unequivocally demonstrated that chronic inflammation and cellular stress are fundamental characteristics of obesity and the related metabolic syndrome. This inflammatory response is distinct and appears to be responsive to cellular signals, differing from the conventional inflammatory response. In recent years, numerous findings have accumulated concerning the molecular mechanisms that underlie the development of inflammatory reactions and stress responses, and their intricate relationship with the maintenance of metabolic homeostasis. The research in the laboratory focuses on controlling inflammatory and stress states in relevant metabolic tissues, such as liver and adipose tissue. We explore intercellular communication via gap junctions and the signalling mechanism between cells in response to stress conditions, like tissue inflammation, and the potential role of such communication in mediating insulin resistance and metabolic disorders.
Gap junctions are one of the most common forms of intercellular communication in cellular organisms. This is made possible by the creation of channels between the plasma membranes of adjacent cells, allowing the passage of ions, signaling molecules, and metabolites. These channels are formed by coupling between two connexons of adjacent cells. Each hemichannel is composed of six subunits called connexins (Cx). Different connexins create channels with varying permeability, determining the type and specificity of the intercellular communication they mediate. Mice and human genomes have 20 and 21 genes encoding connexins, respectively. The connexin 43 (Cx43) gene encodes a protein weighing 43 kilodaltons. It is a widely expressed protein with important regulatory and developmental roles in many tissues.
The objective of our study is to understand the potential role of Cx43 in adipose tissue under conditions of obesity and insulin resistance. We explore the role of Cx43 in mediating intercellular communication under stressed conditions of the endoplasmic reticulum in adipose tissue, using advanced methods combining murine models, in vivo imaging, as well as intercellular communication assays in in vitro systems.
In addition to the basic research of understanding the mechanisms leading to insulin resistance and diabetes, we also engage in clinical studies that evaluate new risk factors and possible therapeutic approaches for these conditions. We are engaged in several research studies investigating the potential role of the adipokine FABP4 (fatty acid binding protein 4) secreted from adipocytes (fat cells) as an antagonist of insulin activity in hypoglycemic conditions and as a potential contributor to the development of gestational diabetes.
