Including exhaustion of different compensatory and adaptive mechanisms and systemic metabolic changes. This makes the clinical course of MS hardly predictable in individual patients. Therefore, it is not surprising that we could not find a high statistically significant correlation of titers of Abs to DNA and RAs of abzymes with all parameters measured, since each patient can be characterized by an individual combination of genetic, environmental, chronic, inflammatory, autoimmune, demyelinating, neurodegenerative and other factors. Overall, all data obtained demonstrate that the DNase activity is an intrinsic property of IgGs deriving from CSF and sera of MS patients. These IgGs are polyclonal and may consist of extremely different repertoires of DNase subfractions in the case of CSF and sera. We have shown previously that the appearance of abzymes specifically hydrolyzing DNA is among the earliest and clear signs of autoimmune reactions in a number of autoimmune diseases when titres of Abs to DNA or other auto-antigens have not yet increased significantly and correspond to their ranges for healthy donors. Therefore, detection of DNase Abs in the sera and CSF of peoples can be considered as an additional index for early diagnostic of this pathology. Bile acids are important endocrine molecules, initiating signalling by the nuclear farnesoid X receptor and Gprotein coupled receptor, TGR5. Bile acid signalling exerts diverse influence over glucose, lipid and energy homeostasis, functions additional to the classical role of bile acids in lipid solubilisation and absorption in the intestine. In the L-cells of the intestinal epithelium, TGR5 activation by bile acids stimulates the release of gut hormones such as glucagonlike peptide-1, resulting in improved glucose homeostasis. In plasma, bile acid concentrations rise rapidly in response to glucose ingestion, which likely underpins many of the mechanisms by which bile acids play a role in regulation of the body’s response to food intake. In pancreatic b-cells TGR5 and FXR activation enhances insulin secretion,whilst in the liver, FXR activation may inhibit gluconeogenesis, whilst increasing glycogen synthesis and improving hepatic insulin sensitivity, although a role for FXR in gluconeogenesis remains controversial. Glucose itself stimulates expression of cholesterol 7ahydroxylase, which catalyses the rate-limiting step in bile acid production. Many diabetes-associated changes in bile acid metabolism have been reported; these include altered synthetic rate, pool size and composition of bile acid species. Lowering of the bile acid pool size using a synthetic FXR agonist reduces energy expenditure and induces obesity and diabetes in mice. Moreover, bile acid sequestrant therapy improves glycaemic control in type 2 diabetes, in addition to its lipid-lowering action. Obesity increases the risk of type 2 diabetes mellitus.