title: [The content of individual fatty acids and numbers of double bonds, insulin, C-peptide and unesterified fatty acids in blood plasma in testing tolerance to glucose].
abstract: The glucose tolerance test demonstrates that content of unesterified fatty acids in blood plasma decreases up to three times and the content of oleic and linoleic acids is more decreased in the pool of fatty acids lipids. Out of resistance to insulin, hormone secretion increases up to three times. The decreasing of level of individual fatty acids occurs in a larger extent. Under resistance to insulin secretion of insulin is increasing up to eight times. The decreasing of level of each fatty acid is less expressed. The effect of insulin reflects decreasing of content of double bonds in blood plasma. The number of double bonds characterizes the degree of unsaturation of fatty acids in lipids of blood plasma. The higher number of double bonds is in the pool of unesterified fatty acids the more active is the effect of insulin. The hyper-secretion of insulin is directly proportional to content of palmitic fatty acid in lipids of blood plasma on fasting. According the phylogenetic theory of general pathology, the effect of insulin on metabolism of glucose is mediated by fatty acids. The insulin is blocking lipolysis in insulin-depended subcutaneous adipocytes and decreases content of unesterified fatty acids in blood plasma. The insulin is depriving all cells of possibility to absorb unesterified fatty acids and "forces" them to absorb glucose increasing hereby number of GLUT4 on cell membrane. The resistance to insulin is manifested in high concentration of unesterfied fatty acids, hyperinsulinemia, hyperalbuminemia and increasing of concentration of C-reactive protein-monomer. The resistance to insulin is groundlessly referred to as a symptom of diabetes mellitus type II. The resistance to insulin is only a functional disorder lasting for years. It can be successfully arrested. The diabetes mellitus is developed against the background of resistance to insulin only after long-term hyper-secretion of insulin and under emaciation and death of β-cells. The diabetes mellitus type I and not type II is an undesirable outcome of resistance to insulin.
authors.forename: V N
authors.initials: VN
authors.lastname: Titov
authors.forename: N N
authors.initials: NN
authors.lastname: Sazhina
authors.forename: A V
authors.initials: AV
authors.lastname: Aripovskiĭ
authors.forename: N M
authors.initials: NM
authors.lastname: Evteeva
authors.forename: É M
authors.initials: ÉM
authors.lastname: Tkhagalizhokova
authors.forename: R M
authors.initials: RM
authors.lastname: Parkhimovich
mesh_terms: D002096:C-Peptide / Q000097:blood*; D003922:Diabetes Mellitus, Type 1 / Q000097:blood*; D003924:Diabetes Mellitus, Type 2 / Q000097:blood*; D005231:Fatty Acids, Unsaturated / Q000097:blood*; D005260:Female; D005951:Glucose Tolerance Test; D006801:Humans; D007328:Insulin / Q000097:blood*; D007333:Insulin Resistance; D008297:Male
chemical_list: D002096:C-Peptide; D005231:Fatty Acids, Unsaturated; D007328:Insulin