The important component of obesity pathogenesis is inflammatory activation of innate immune cells within adipose tissue and in other body locations. Both the course of obesity and innate immune reactivity are characterized by sex-associated differences. The aim of the work was a comparative investigation of metabolic profiles of phagocytes from different locations in male and female rats with MSG-induced obesity. The administration of monosodium glutamate (MSG) caused obesity, with sex-associated differences, that was more severe in male rats. Obesity was associated with pro-inflammatory activation of CD14+ phagocytes from adipose tissue in female, but not in male rats, which was demonstrated by decreased phagocytosis activity along with increased ROS generation. Phagocytes from the peritoneal cavity and peripheral blood of obese female rats exhibited neutral metabolic profile, whereas those cells from obese male rats displayed a pro-inflammatory metabolic profile. Thus, the manifestation of obesity-induced inflammation was characterized by different patterns of metabolic profile of phagocytes in male and female rats. Identified immune cell characteristics expand our knowledge of obesity immunobiology and may help to develop more effective preventive and therapeutic interventions for obese patients of different sexes.

No abstract

We had characterized low-, medium- and high-molecular protein fractions of hepatocytes under development of glutamate-induced obesity and correction of nanocrystalline cerium dioxide and pioglitazone. Protein fractions were separated by electrophoresis using a 10 % Laemmli SDS-PAGE sodium dodecyl sulfate. Protein hepatocytes change under glutamate-induced obesity: high-protein reduced, and low-protein increased. Changes in hepatocyte proteins are consistent with previously established changes in protein content of hepatocytes under the influence HCD rich in fats and carbohydrates. We had noticed similar changes in protein of hepatocytes under correction cerium dioxide, but compared with glutamate-induced obesity, low proteins were lower. Pioglitazone didn't show a positive effect on hepatocyte proteins that may be associated with short-term administration.

Nonalcoholic fatty liver disease (NAFLD) or steatohepatosis has recently become widespread, but its pathogenesis has not been thoroughly understood for today. Most scientists have appropriated a central role in the mechanisms of its development to mitochondria and so-called "mitochondrial dysfunction," which is observed in most animal models and in most patients. The aim of this work was to determine phospholipid composition of inner mitochondrial membrane of rat hepatocytes under diet-induced and glutamate-induced steatohepatosis, as well as to compare the data about developing steatohepatosis of different types. Obtained data indicate the disruption of normal functional state of the inner mitochondrial membrane under the conditions of diet-induced and glutamate-induced steatohepatosis. Amount of oxidized forms of the major phospholipids including cardiolipin, indicates the increasing oxidative stress under the conditions of both steatohepatosis types.