In terms of development of evolutionary biomedicine using invertebrate animals as models for study of molecular grounds of various human diseases, for the first time the
streptozocin (ST) model of
insulin-dependent diabetes in the mollusc Anodonta cygnea has been developed. This model is based on the following authors' data: (1) redetection of
insulin-related
peptides (IRP) in mollusk tissues: (2) discovery of the
adenylyl cyclase signal mechanism (ACSM) of action of
insulin and other
peptides of the
insulin superfamily in tissues of mammals, human, and mollusc. A. cygnea; (3) concept of molecular defects in hormonal signal systems as causes of
endocrine diseases. Studies on the ST model have revealed in mollusc smooth muscle on the background of
hyperglycemia at the 2nd, 4th, and 8th day after the ST administration a decrease of the ACSM response to activating action of
insulin,
IGF-1, and
relaxin. These functional disturbances were the most pronounced at the 2nd day of development and rather less marked at the 4th and 8th day. Analysis of data on effect of hormonal and non-hormonal (NaF, GIDP, and
forskolin) ACSM activators has shown that the causes of impair of signal-transducing function of this mechanism are (1) a
hyperglycemia-induced increase of the basal AC activity and as a consequence--a decrease of the
enzyme catalytic potentials in response to
hormone; (2) a decrease of functions of Gs-
protein and of its coupling with AC. Besides, administration of ST produced in the mollusc muscles an attenuation of regulation by
insulin of carbohydrate metabolism
enzyme (glucose-6-phosphate dehydrogenase, glycogensynthase). The pattern of disturbances in the studied parameters in the mollusc is very similar to that revealed by the authors in rat and human muscle tissues in
type 1 diabetes.