title: Modifications in the TXA(2) and PGI(2) plasma levels and some other biochemical parameters during the initiation and development of non-insulin-dependent diabetes mellitus (NIDDM) syndrome in the rabbit.
abstract: Having developed a non-insulin-dependent diabetes mellitus (NIDDM) syndrome model in the rabbit using Wirsung duct ligation, it appeared interesting to use it to study the relationship between glycemia and the plasma levels of TXA(2)and PGI(2), and of some other biochemical parameters such as cholesterol, triglycerides, alkaline phosphatase and transaminases. A comparative study was carried out in the sham-operated rabbits (controls, C) and those having their pancreatic duct ligatured (NIDDM, D) at 15, 30, 40, 50 and 60 days post-ligation. On the 40th days, whereas in the controls, glycemia was 1.17 +/- 0.04 g.l(-1), it reached a maximum of 4.62 +/- 0.76 g.l(-1)(25.40 mM) in the NIDDMs. No significant modification was observed either in cholesterolemia or in triglyceridemia in either group. The GOT and GPT were highly increased, from 11.50 +/- 4.00 IU. l(-1)and 27.00 +/- 1.50 IU.l(-1)(C) to 37.50 +/- 5.64 IU.l(-1)(P<0. 001) and 58.50 +/- 7.50 IU.l(-1)(D) (P<0.001) in the NIDDM group, suggesting that hyperglycemia occurred simultaneously with the degeneration of the pancreatic tissue. In parallel, in D rabbits, the plasma levels of TXB(2)and 6 keto PGF(1alpha)were augmented to 68.22 +/- 6.20 pg.ml(-1)versus 22.49 +/- 5.74 pg.ml(-1)(C) (P<0.001), and 127.11 +/- 14.39 pg.ml(-1)versus 48.65 +/- 4.51 pg.ml(-1)(C) (P<0. 001) respectively. Statistical studies showed a significant correlation (P<0.05 and <0.02) between glycemia and the biosynthesis of eicosanoids under study. Moreover, 25 mM was found to be the threshold level of glucose excess essential to increase the TXA(2)and PGI(2)biosynthesis significantly. This supports the results obtained by other authors studying the action of glucose on phospholipase activity and consequent eicosanoid production.
authors.affiliation: Laboratoire de Pharmacologie de la Régulation, Université P. Sabatier 38, Toulouse, France.
authors.forename: B
authors.initials: B
authors.lastname: Lasserre
authors.forename: C
authors.initials: C
authors.lastname: Navarro-Delmasure
authors.forename: A
authors.initials: A
authors.lastname: Pham Huu Chanh
authors.forename: J
authors.initials: J
authors.lastname: Catala
authors.forename: E
authors.initials: E
authors.lastname: Hollande
mesh_terms: D015121:6-Ketoprostaglandin F1 alpha / Q000097:blood; D000469:Alkaline Phosphatase / Q000097:blood; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D001798:Blood Proteins / Q000378:metabolism; D002784:Cholesterol / Q000097:blood; D003921:Diabetes Mellitus, Experimental / Q000097:blood*; D003924:Diabetes Mellitus, Type 2 / Q000209:etiology; D004195:Disease Models, Animal; D011464:Epoprostenol / Q000096:biosynthesis / Q000097:blood*; D006943:Hyperglycemia / Q000097:blood; D008026:Ligation; D010183:Pancreatic Ducts / Q000601:surgery; D010975:Platelet Aggregation Inhibitors / Q000097:blood; D011817:Rabbits; D013928:Thromboxane A2 / Q000096:biosynthesis / Q000097:blood*; D013929:Thromboxane B2 / Q000097:blood; D013997:Time Factors; D000637:Transaminases / Q000097:blood
chemical_list: D001786:Blood Glucose; D001798:Blood Proteins; D010975:Platelet Aggregation Inhibitors; D013929:Thromboxane B2; D013928:Thromboxane A2; D015121:6-Ketoprostaglandin F1 alpha; D002784:Cholesterol; D011464:Epoprostenol; D000637:Transaminases; D000469:Alkaline Phosphatase