目的:探讨早期短期应用胰岛素泵强化治疗新诊断2型糖尿病对胰岛B细胞功能及血糖达标时间的影响。方法:选取本院2012年8月-2014年8月就诊的50例新诊断2型糖尿病患者,按照随机数字表法将其分为观察组和对照组,每组25例。对照组采用胰岛素...目的:探讨早期短期应用胰岛素泵强化治疗新诊断2型糖尿病对胰岛B细胞功能及血糖达标时间的影响。方法:选取本院2012年8月-2014年8月就诊的50例新诊断2型糖尿病患者,按照随机数字表法将其分为观察组和对照组,每组25例。对照组采用胰岛素笔多次注射胰岛素治疗(于患者三餐前皮下注射优泌林R加22时皮下注射优泌林N),观察组采用美国美敦力胰岛素泵持续皮下输注胰岛素(基础量加餐前大剂量),治疗2周后,观察并比较两组患者治疗前后空腹血糖、餐后2 h血糖、空腹C肽以及血糖达标时间。以C肽水平评估胰岛B细胞功能情况。结果:两组患者治疗后的空腹血糖(FPG)、餐后2 h血糖(2 h PG)均明显低于治疗前,空腹C肽均明显高于治疗前,差异均有统计学意义(P<0.05)。而两组患者治疗后的FPG、2 h PG比较差异均无统计学意义(P>0.05),观察组治疗后的空腹C肽明显高于对照组,差异有统计学意义(P<0.05)。观察组患者的血糖达标时间(156.44±13.20)h明显短于对照组的(204.96±19.06)h,差异有统计学意义(t=-10.462,P<0.05)。结论:胰岛素泵连续皮下输注能够明显改善新诊断2型糖尿病患者胰岛B细胞分泌功能,并能使血糖平稳及更快达标,值得临床推广。展开更多
BACKGROUND Type 2 diabetes(T2 D) is characterized by insufficient insulin secretion caused by defective pancreatic β-cell function or insulin resistance,resulting in an increase in blood glucose.However,the mechanism...BACKGROUND Type 2 diabetes(T2 D) is characterized by insufficient insulin secretion caused by defective pancreatic β-cell function or insulin resistance,resulting in an increase in blood glucose.However,the mechanism involved in this lack of insulin secretion is unclear.The level of vascular endothelial growth factor B(VEGF-B) is significantly increased in T2 D patients.The inactivation of VEGF-B could restore insulin sensitivity in db/db mice by reducing fatty acid accumulation.It is speculated that VEGF-B is related to pancreatic β-cell dysfunction and is an important factor affecting β-cell secretion of insulin.As an in vitro model of normal pancreatic β-cells,the MIN6 cell line can be used to analyze the mechanism of insulin secretion and related biological effects.AIM To study the role of VEGF-B in the insulin secretion signaling pathway in MIN6 cells and explore the effect of VEGF-B on blood glucose regulation.METHODS The MIN6 mouse pancreatic islet β-cell line was used as the model system.By administering exogenous VEGF-B protein or knocking down VEGF-B expression in MIN6 cells,we examined the effects of VEGF-B on insulin secretion,Ca2+ and cyclic adenosine monophosphate(cAMP) levels,and the insulin secretion signaling pathway.RESULTS Exogenous VEGF-B inhibited the secretion of insulin and simultaneously reduced the levels of Ca2+ and cAMP in MIN6 cells.Exogenous VEGF-B also reduced the expression of phospholipase C gamma 1(PLCγ1),phosphatidylinositol 3-kinase(PI3 K),serine/threonine kinase(AKT),and other proteins in the insulin secretion pathway.Upon knockdown of VEGF-B,MIN6 cells exhibited increased insulin secretion and Ca2+ and cAMP levels and upregulated expression of PLCγ1,PI3 K,AKT,and other proteins.CONCLUSION VEGF-B can regulate insulin secretion by modulating the levels of Ca2+ and cAMP.VEGF-B involvement in insulin secretion is related to the expression of PLCγ1,PI3 K,AKT,and other signaling proteins.These results provide theoretical support and an experimental basis for the study of VEGF-B in the pathogenesis of T2 D.展开更多
文摘目的:探讨早期短期应用胰岛素泵强化治疗新诊断2型糖尿病对胰岛B细胞功能及血糖达标时间的影响。方法:选取本院2012年8月-2014年8月就诊的50例新诊断2型糖尿病患者,按照随机数字表法将其分为观察组和对照组,每组25例。对照组采用胰岛素笔多次注射胰岛素治疗(于患者三餐前皮下注射优泌林R加22时皮下注射优泌林N),观察组采用美国美敦力胰岛素泵持续皮下输注胰岛素(基础量加餐前大剂量),治疗2周后,观察并比较两组患者治疗前后空腹血糖、餐后2 h血糖、空腹C肽以及血糖达标时间。以C肽水平评估胰岛B细胞功能情况。结果:两组患者治疗后的空腹血糖(FPG)、餐后2 h血糖(2 h PG)均明显低于治疗前,空腹C肽均明显高于治疗前,差异均有统计学意义(P<0.05)。而两组患者治疗后的FPG、2 h PG比较差异均无统计学意义(P>0.05),观察组治疗后的空腹C肽明显高于对照组,差异有统计学意义(P<0.05)。观察组患者的血糖达标时间(156.44±13.20)h明显短于对照组的(204.96±19.06)h,差异有统计学意义(t=-10.462,P<0.05)。结论:胰岛素泵连续皮下输注能够明显改善新诊断2型糖尿病患者胰岛B细胞分泌功能,并能使血糖平稳及更快达标,值得临床推广。
基金Supported by National Natural Science Foundation of China,No.31771284National Natural Science Foundation of China Youth Project,No.31702024+1 种基金Major Basic Research Project of Shandong Provincial Natural Science Foundation,No.ZR2019ZD27Shandong Province Higher Educational Science and Technology Plan Project,No.J17KA258。
文摘BACKGROUND Type 2 diabetes(T2 D) is characterized by insufficient insulin secretion caused by defective pancreatic β-cell function or insulin resistance,resulting in an increase in blood glucose.However,the mechanism involved in this lack of insulin secretion is unclear.The level of vascular endothelial growth factor B(VEGF-B) is significantly increased in T2 D patients.The inactivation of VEGF-B could restore insulin sensitivity in db/db mice by reducing fatty acid accumulation.It is speculated that VEGF-B is related to pancreatic β-cell dysfunction and is an important factor affecting β-cell secretion of insulin.As an in vitro model of normal pancreatic β-cells,the MIN6 cell line can be used to analyze the mechanism of insulin secretion and related biological effects.AIM To study the role of VEGF-B in the insulin secretion signaling pathway in MIN6 cells and explore the effect of VEGF-B on blood glucose regulation.METHODS The MIN6 mouse pancreatic islet β-cell line was used as the model system.By administering exogenous VEGF-B protein or knocking down VEGF-B expression in MIN6 cells,we examined the effects of VEGF-B on insulin secretion,Ca2+ and cyclic adenosine monophosphate(cAMP) levels,and the insulin secretion signaling pathway.RESULTS Exogenous VEGF-B inhibited the secretion of insulin and simultaneously reduced the levels of Ca2+ and cAMP in MIN6 cells.Exogenous VEGF-B also reduced the expression of phospholipase C gamma 1(PLCγ1),phosphatidylinositol 3-kinase(PI3 K),serine/threonine kinase(AKT),and other proteins in the insulin secretion pathway.Upon knockdown of VEGF-B,MIN6 cells exhibited increased insulin secretion and Ca2+ and cAMP levels and upregulated expression of PLCγ1,PI3 K,AKT,and other proteins.CONCLUSION VEGF-B can regulate insulin secretion by modulating the levels of Ca2+ and cAMP.VEGF-B involvement in insulin secretion is related to the expression of PLCγ1,PI3 K,AKT,and other signaling proteins.These results provide theoretical support and an experimental basis for the study of VEGF-B in the pathogenesis of T2 D.
