Sovremennye aspekty patogenezasakharnogo diabeta 1 tipa

Pathogenesis of Type 1 Diabetes Mellitus and Rodent Experimental Models

“…More than 192 methods that can be used to prevent T1DM in NOD mice have been reported [ 36 - 38 ]. Prevention of diabetes is relatively simple in mice, but it is extremely complicated in humans [ 5 ]. One of the causes may be that greater importance is attached to the similarity of T1DM in NOD mice and humans than to the differences [ 39 ].…”

“…The peak of hyperglycemia occurs on day 2 or 3, followed by a short period of euglycemia. This is associated with the potential ability of β-cells to enter mitosis under the influence of a high glucose concentration [ 5 ]. Activation of β-cell proliferation is believed to occur on the 3 rd day of diabetes [ 63 ].…”

“…Adverse environmental factors (especially those acting during early ontogeny) that cause a stress response through a high level of glucocorticoids and changes in the neuroendocrine regulation of the pancreatic islet function can lead to endocrine imprinting associated with significant rearrangement of the intracellular systems of β-cell function regulation [ 63 ]. In adult animals that have undergone stress in the prenatal period, glucose-stimulated insulin secretion and glucose tolerance are impaired and the sensitivity of β-cells to the toxic effect of STZ is significantly increased [ 5 ].…”

“…Initially, the genetics of T1DM were considered to be relatively simple. The presence of certain alleles of the HLA system genes was believed to lead to an almost complete dominance of the disease [ 5 ].…”