ABSTRACT
Objective To investigate the therapeutic effect of astragalus injection onβcells apoptosis of type 1 diabetes mice. Methods 32 mice were randomly divided into a control group, a diabetes group, a small dose group and a large dose group of astraglus. Except the control group, mice in the other 3 groups received intraperitoneal injection of STZ in order to induce diabetic mellitus. Then one week after injection of STZ, mice in the small dose group and the large dose group of astraglus were given 30, 60 g/(kg?d) doses of astragalus injection, while the other 2 groups were injected into an equal volume saline for 4 weeks. Serum NO, inducible nitric oxide synthase (iNOS) and insulin levels were detected by enzyme linked immunosorbent assay method, and apoptosis was measured by using a TUNEL assay. Results Compared with the diabetes group, the serum NO (25.81 ± 2.09μmol/L, 18.84 ± 3.95μmol/L vs. 30.34 ± 2.53μmol/L) and iNOS (21.38 ± 4.48μmol/L, 17.00 ± 3.05μmol/L vs. 26.62 ± 2.48μmol/L) levels were significantly reduced in the small dose group and the large dose group of astragalus (P0.05). Conclusion Astragalus injection can reduce the iNOS activity and NO production, but can not effectively decreasingβcells apoptosis.
ABSTRACT
Objective To investigate the interference effects of orexin A on cell proliferation of the insulin?secreting beta?cell line(INS?1 cells) through the orexin receptor 1(OX1R)and the AKT/PKB signaling pathway. Methods INS?1 cells were exposed to different concentrations of orexin A in vitro,and treated with OX1R antagonist(SB334867),PI3K antagonist(wortmannin),or AKT antagonist(PF?04691502). The INS?1 cell proliferation and apoptosis,insulin secretion,OX1R protein activity and AKT phosphorylation level were determined. Results Orexin A(10-10 to 10-6 mol/L)stimulated the proliferation and activation of INS?1 cells,prevented apoptpsis,and increased insulin secretion. Additionally,AKT phosphorylation was stimulated by orexin A(10-10 to 10-6 mol/L). The OX1R antagonist SB334867(10-6 mol/L),the PI3K antagonist wortmannin (10-8 mol/L)and the AKT antagonist PF?04691502(10-6 mol/L)weakened the effects of orexin A. Conclusion Orexin A activated the AKT sig?naling pathway through the mediation of orexin A?OX1R,and promoted cell proliferation in INS?1 cells.
ABSTRACT
Objective To investigate the insulin resistance and the changes of pancreaticβ-cell function in order to improve the clinical diagnosis and therapy .Methods 99 cases of pregnant women in the late ministers were randomly selected for the study and divided into three groups(normal glucose tolerance group ,impaired glucose tolerance group ,and gestational diabetes group) .The in-sulin resistance and isletβ-cell function of the three groups were evaluated by HOMA model and its related indicators .Results The blood pressure and blood lipid level was not significant different among the three groups(P>0 .05) .Pairwise comparisons of glu-cose infusion rate ,the first phase insulin secretion ,the second phase insulin secretion ,fasting glucose ,fasting insulin ,HOM A-IR , and HOMA-βwere made among the three groups ,and there were difference with statistical significance(P<0 .05) .Conclusion The situation of insulin resistance and the dysfunction of pancreaticβ-cell in trimester pregnant women would become bad associated with the abnormal glucose tolerance .
ABSTRACT
Insulin is a hormone produced by isletβcells, which plays an important role in regulating cell division, cell differentiation, cell growth and regulating blood glucose levels.Decreased insulin and isletβcell dysfunction are vital fundamental characteristics of diabetes.There are many transcription factors involved in the development and maintaining of isletβcells.This review focuses on the transcription factors aboutβcell development.
ABSTRACT
[ ABSTRACT] Diabetes is characterized by an absolute or relative deficiency inβ-cell mass, which cannot be re-versed with existing therapeutic strategies.The restoration of the endogenous islet β-cells can stabilize the level of blood glucose.The isletβ-cells can be obtained from the directional differentiation of stem cells, but the process is complex and has the risk of teratomas generation.Cell direct reprogramming, one terminal differentiated cell can transdifferentiate into another kind of terminal differentiated cell, which is other than directional differentiation from stem cells.Direct reprogram-ming gives rise to the generation of isletβ-cells from one terminal differentiated cell, may be preferable for diabetes therapy because of its unique advantage.