## 1 Introduction  
In future decades, the number of patients with diabetes mellitus type 2 (DM2) is predicted to increase to over 693 million by 2045 [1]. DM2 will be an epidemic disease in the 21 st century, and it is currently a major cause of mortality, morbidity and global health problems in our time. DM2's relationship to the body's metabolic syndrome and fat metabolism has been well studied. Human priorities include \"quality of life\" and the \"enhanced physical activity of society\". Our results and conclusions demonstrate the importance of maintaining regular physical activity/exercise and good natural diets for DM2 patients. In the \"area of physical activity/exercise and diet\", original ideas for implementing/applying natural medicines to the clinical diabetology of DM2 would be useful. In the world of cells and tissues, blood platelets (PLTs, thrombocytes) are closely related to the pathogenesis of DM2 and micro- and macrovascular complications of the disease. Prominent theories in this field include the viscera-portal hypothesis, the ectopic fat hypothesis, and adipose tissue as an endocrine gland [2]. These theories are based on the relationship between observed energy metabolism and beta-oxidation of fats. \"Insulation resistance\" may be involved when B-oxidation prevails over glycolysis [2]. DM2 affects important hemorheological markers closely related to blood flow [3; 4]. Myogenic and endothelial factors, such as basic rheological/biorheological markers, play an essential role in human blood circulation. Diabetes mellitus type 2 can affect the hemorheological markers of erythrocytes, causing a decrease in cell deformability as well as an increase in erythrocyte aggregation and blood viscosity. Blood platelets (thrombocytes) are produced in the bone marrow and spleen as small (1-2 um in diameter), anucleate fragments from the cytoplasm of megakaryocytes. Platelets (PLTs) have a smooth surface and a discoid shape. In the peripheral blood, PLTs are involved in thrombogenesis, as confirmed by clot formation modeling both in vivo and in vitro [5]. PLTs contain and synthesize cell growth factors, chemokines, coagulation proteins, two types of secretory granules (alpha granules and \"dense\" granules), adhesion molecules, etc. [6; 7]. In response to various stimuli and/or damages, PLTs undergo morphological and functional changes, known as PLT \"activation\" [8]. Activated (procoagulant) thrombocytes play a central role in hemostasis and repairing vascular vessels [9; 10]. Procoagulant PLTs generate thrombin and develop three-dimensional fibrin matrices during hemostasis/thrombogenesis. Human platelet membrane-derived, small (\(\leq\)0.1 um) micro-particles with procoagulant effects are involved in thrombin formation and, thus, thrombotic complications (e.g., attributable to diabetes mellitus type 2 (DM2)) [11; 12]. During PLT activation, changes in PLT shape appear first, from discoid to spherical, with actin-rich philopodia (cytoplasmic extrusions) interacting, flattening, and spreading onto surfaces in the final activation phases [13; 14; 15]. The same authors characterized PLT activation stages morphometrically and nanomechanically by atomic force microscope (AFM) for diagnostic purposes. In our opinion, DM2 clinical practice should focus its efforts on bridging the gap between scientific research (as a source of updated information on DM2) and DM2 practitioners (as a source of useful information about vascular disease complications). Currently, several popular hypotheses explain the molecular pathogenesis of DM2 (the viscera-portal theory and ectopic fat) and the endocrine function performed by adipose tissue [2]. The roles of oxidative stress, mitochondrial dysfunctions, and the endoplasmic reticulum \"activation\" have been fully examined. The shift in energy metabolism--from normal glycolysis to the beta-oxidation of fats--is commonly observed. The beta-oxidation of fats plays a fundamental role in preventing over-glycolysis.