title: Pancreatic D-cells in aging and intraislet effects of pancreatic somatostatin.
abstract: In old organisms pancreatic D-cells are not changed in number. During the aging in mentioned cells takes place the intensification of secretory and extrusive functions, which are more prominent in old organisms than in young ones. Peripherally situated D-cells are vascularly ineffective within the pancreatic islet and do not suppress locally B- and A-cells. D-cells' major target tissue may be pancreatic acinar cells. Functionally activated D-cells in old organisms may play the main role in the development of involutive processes in exocrine pancreas and in its atrophy. Stagnation of the secretory granules in pancreatic A- and B-cells in old ages could not be caused by influence of paracrine effect of somatostatin. The given process could be considered as a result of reduction of energopotentials and suppression of signal ways for initiation of insulin and glucagon secretion. Respectively, extrusion impediment of secretory granules resulted in their stagnation could be explained by suppression of exocytosis as an energy- and signal-dependent process. We suppose that cytotopographic and microvascular peculiarities of pancreatic islets in human beings and rodents is a reflection of intensification of insulin apparatus and is directed to loose the B-cells from the local (microvascular or paracrine) influences (effects of D- or A-cells). The mentioned is of high physiological importance (especially in the process of aging) for the organisms of above-presented taxonomic groups due to rich amount of carbohydrates in their food ration. The above-mentioned fact gains the special importance in human beings, where evolutionary "solitary" (represented by single B-cells) insulin apparatus is faced with evolutionary "rooted" strong and diverse contrainsulin apparatus, leading to development of diabetes mellitus (type 2) in late ages.
authors.affiliation: Tbilisi State Medical University, Laboratory of Clinical Skills, Direction of Cytopathology, Klaipeda University, Health Sciences Faculty, Lithuania.
authors.forename: D G
authors.initials: DG
authors.lastname: Kasradze
authors.forename: R V
authors.initials: RV
authors.lastname: Beriashvili
authors.forename: M G
authors.initials: MG
authors.lastname: Kasradze
authors.forename: A G
authors.initials: AG
authors.lastname: Tavartkiladze
authors.forename: P A
authors.initials: PA
authors.lastname: Nozade
mesh_terms: D000375:Aging / Q000502:physiology*; D000818:Animals; D048429:Cell Size; D004721:Endoplasmic Reticulum / Q000648:ultrastructure; D006056:Golgi Apparatus / Q000648:ultrastructure; D008297:Male; D008928:Mitochondria / Q000648:ultrastructure; D010179:Pancreas / Q000648:ultrastructure*; D051381:Rats; D022142:Secretory Vesicles / Q000648:ultrastructure; D013004:Somatostatin / Q000502:physiology*; D019864:Somatostatin-Secreting Cells / Q000502:physiology* / Q000648:ultrastructure*
chemical_list: D013004:Somatostatin