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ROLE OF BONE MARROW HEMATOPOIESIS IN THE ONSET OF INFLAMMATION IN MICE WITH MELANOCORTIN OBESITY (TYPE 2 DIABETES)


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Abstract

Hematopoietic stem cells (HSCs) directly and immediately respond to inflammatory signals by activation of proliferation, differentiation and migration, therefore early hematopoietic progenitors become involved in the pathogenesis of inflammatory diseases. The inflammatory nature of D2T is characterized by a number of immune mechanisms. In humans, among other forms of monolocus obesity, melanocortin-dependent obesity is the most common form. Animal model for studying melanocortin-dependent obesity is mouse strain with heterozygous mutation yellow at the agouti locus (Ay/a mice). Due to this mutation melanocortin receptors activity is constitutively reduced, Ay/a mice are prone to the development of obesity and DT2 at certain age. In present study we investigated bone marrow hematopoiesis during development of obesity and DT2 in Ay/a mice at age 10 weeks (no obesity), 15 weeks (moderate obesity), and 30 weeks (manifestation of obesity and DT2). At 30 weeks, in Ay/a mice the number of early (CFU-GEMM) progenitors was increased, which may occur due to enhanced proliferative activity and delayed mobilization of HSC. At 10 weeks, in Ay/a mice the number of erythroid (BFU-E + CFU-E) and granulocyte-macrophage (CFU-GM) colonies was increased, compared to control mice. It may suggest that block of erythroid differentiation and alterations in inflammatory status in Ay/a mice occur much earlier than obesity and DT2 develop.


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