Background: Diabetes and diabetes-related complications are major causes of morbidity and mortality in the United States. Depressive symptoms and perceived stress have been identified as possible risk factors for beta...Background: Diabetes and diabetes-related complications are major causes of morbidity and mortality in the United States. Depressive symptoms and perceived stress have been identified as possible risk factors for beta cell dysfunction and diabetes. The purpose of this study was to assess associations between depression symptoms and perceived stress with beta cell function between African and Haitian Americans with and without type 2 diabetes. Participants and Methods: Informed consent and data were available for 462 participants (231 African Americans and 231 Haitian Americans) for this cross-sectional study. A demographic questionnaire developed by the Primary Investigator was used to collect information regarding age, gender, smoking, and ethnicity. Diabetes status was determined by self-report and confirmed by fasting blood glucose. Anthropometrics (weight, and height and waist circumference) and vital signs (blood pressure) were taken. Blood samples were drawn after 8 10 hours over-night fasting to measure lipid panel, fasting plasma glucose and serum insulin concentrations. The homeostatic model assessment, version 2 (HOMA2) computer model was used to calculate beta cell function. Depression was assessed using the Beck Depression Inventory-II (BDI-II) and stress levels were assessed using the Perceived Stress Scale (PSS). Results: Moderate to severe depressive symptoms were more likely for persons with diabetes (p = 0.030). There were no differences in perceived stress between ethnicity and diabetes status (p = 0.283). General linear models for participants with and without type 2 diabetes using beta cell function as the dependent variable showed no association with depressive symptoms and perceived stress;however, Haitian Americans had significantly lower beta cell function than African Americans both with and without diabetes and adjusting for age, gender, waist circumference and smoking. Further research is needed to compare these risk factors in other race/ethnic groups.展开更多
AIM: To analyze the associations of pancreatic fat with other fat depots and β-cell function in pediatric nonalcoholic fatty liver disease(NAFLD).METHODS: We examined 158 overweight/obese children and adolescents, 80...AIM: To analyze the associations of pancreatic fat with other fat depots and β-cell function in pediatric nonalcoholic fatty liver disease(NAFLD).METHODS: We examined 158 overweight/obese children and adolescents, 80 with NAFLD [hepatic fat fraction(HFF) ≥ 5%] and 78 without fatty liver. Visceral adipose tissue(VAT), pancreatic fat fraction(PFF) and HFF were determined by magnetic resonance imaging. Estimates of insulin sensitivity were calculated using the homeostasis model assessment of insulin resistance(HOMA-IR), defined by fasting insulin and fasting glucose and whole-body insulin sensitivity index(WBISI), based on mean values of insulin and glucose obtained from oral glucose tolerance test and the corresponding fasting values. Patients were considered to have prediabetes if they had either:(1) impaired fasting glucose, defined as a fasting glucose level ≥ 100 mg/d L to < 126 mg/d L;(2) impaired glucose tolerance, defined as a 2 h glucose concentration between ≥ 140 mg/d L and < 200 mg/d L; or(3) hemoglobin A1 c value of ≥ 5.7% to < 6.5%.RESULTS: PFF was significantly higher in NAFLD patients compared with subjects without liver involvement. PFF was significantly associated with HFF and VAT, as well as fasting insulin, C peptide, HOMA-IR, and WBISI. The association between PFF and HFF was no longer significant after adjusting for age, gender, Tanner stage, body mass index(BMI)-SD score, and VAT. In multiple regression analysis withWBISI or HOMA-IR as the dependent variables, against the covariates age, gender, Tanner stage, BMI-SD score, VAT, PFF, and HFF, the only variable significantly associated with WBISI(standardized coefficient B,-0.398; P = 0.001) as well as HOMA-IR(0.353; P = 0.003) was HFF. Children with prediabetes had higher PFF and HFF than those without. PFF and HFF were significantly associated with prediabetes after adjustment for clinical variables. When all fat depots where included in the same model, only HFF remained significantly associated with prediabetes(OR = 3.38; 95%CI: 1.10-10.4; P = 0.034).CONCLUSION: In overweight/obese children with NAFLD, pancreatic fat is increased compared with those without liver involvement. However, only liver fat is independently related to prediabetes.展开更多
目的探讨初诊肥胖2型糖尿病患者血清Betatrophin水平与胰岛β细胞功能的关系。方法方便选择2014年1月—2015年1月初诊肥胖2型糖尿病患者100例为研究对象(观察组),另选择同期该院体检健康者(NGT)者100名为对照观察(对照组)。测量人体指标...目的探讨初诊肥胖2型糖尿病患者血清Betatrophin水平与胰岛β细胞功能的关系。方法方便选择2014年1月—2015年1月初诊肥胖2型糖尿病患者100例为研究对象(观察组),另选择同期该院体检健康者(NGT)者100名为对照观察(对照组)。测量人体指标,检测相关代谢血生化指标,采用酶联免疫吸附实验(ELISA)法测定空腹血清Betatrophin水平,采用直线相关分析研究betatrophin与胰岛β细胞功能、体测及代谢指标的相关关系。结果观察组血清Betatrophin水平(422.5±247.60)pg/m L明显高于对照组(316.3±293.30)pg/m L,差异有统计学意义(P<0.05);相关性分析提示Betatrophin与腰臀比、HOMA-IR、FPG、2 h PG、HbA1c、FINS、TG呈正相关(r=0.215、0.216、0.249、0.447、0.338、0.452、0.470,P<0.01),与HDL-C、HOMA-β成负相关(r=-0.256、-0.363,P<0.05),差异有统计学意义(P<0.05)。结论初诊肥胖2型糖尿病患者的血清betatrophin水平较NGT组明显升高,并且与胰岛β细胞功能密切相关,推测其参与了糖尿病的发生。展开更多
目的通过比较聚乙二醇洛塞那肽与利拉鲁肽治疗肥胖2型糖尿病的疗效,为临床治疗该类疾病选择更高效的用药方案。方法选取东南大学医学院附属南京同仁医院2022年1月至2023年10月予以相应治疗的肥胖2型糖尿病患者共136例作为此次试验对象,...目的通过比较聚乙二醇洛塞那肽与利拉鲁肽治疗肥胖2型糖尿病的疗效,为临床治疗该类疾病选择更高效的用药方案。方法选取东南大学医学院附属南京同仁医院2022年1月至2023年10月予以相应治疗的肥胖2型糖尿病患者共136例作为此次试验对象,按照随机数字表法分成68例A组(聚乙二醇洛塞那肽治疗)与68例B组(利拉鲁肽治疗)。比较治疗前后两组肥胖相关指标、治疗前后两组血脂相关指标、治疗前后两组血糖指标以及治疗后不良反应发生率。结果治疗后两组体质量、腰臀比、体质量指数(BMI)和腰围均下降,B组体质量和BMI[分别为(80.31±7.62)kg和(24.13±1.82)kg·m^(-2)]低于A组体质量[分别为(83.65±7.93)kg和BMI(25.34±1.84)kg·m^(-2)](体质量:t=2.504,P=0.014;BMI:t=3.855,P<0.05);治疗后两组甘油三酯(TG)、血清总胆固醇(TC)和低密度脂蛋白(LDL)均下降,高密度脂蛋白胆固醇(HDL-C)上升(均P<0.05);治疗后两组餐后2 h血糖(2 h FBG)、空腹血糖(FBG)、糖化血红蛋白(HbAlc)、胰岛素抵抗指数(HOMA-IR)水平均下降,空腹血糖胰岛素(FINS)、β细胞功能指数(HOMA-β)水平均上升,A组2 h FBG、FBG[分别为(7.86±1.12)mmol·L^(-1)、(6.18±0.71)mmol·L^(-1)]低于B组[分别为2 h FBG(8.72±1.34)mmol·L^(-1)和FBG(7.02±0.62)mmol·L^(-1)](2 h FBG:t=4.061,P<0.05;FBG:t=7.349,P<0.05),A组HOMA-β[(74.62±3.78)%]高于B组[(62.79±3.56)%](t=18.937,P<0.05);两组不良反应发生率比较差异无统计学意义(20.59%vs 25.00%,χ^(2)=0.376,P=0.540)。结论对于肥胖2型糖尿病患者,聚乙二醇洛塞那肽与利拉鲁肽均能有效减轻体质量、调节血脂、降低血糖水平以及增强胰岛β细胞的功能,且安全性相似。然而,在降低体质量方面,利拉鲁肽的效果更为显著,而聚乙二醇洛塞那肽在改善胰岛β细胞功能和降低血糖方面则表现更为出色。展开更多
Type 2 diabetes(T2D)is a multifactorial metabolic disorder affecting more than 450 million people across the globe.With the increasing prevalence of T2D and obesity,the role of fat accumulation at sites other than sub...Type 2 diabetes(T2D)is a multifactorial metabolic disorder affecting more than 450 million people across the globe.With the increasing prevalence of T2D and obesity,the role of fat accumulation at sites other than subcutaneous adipose tissue has received significant attention in the pathophysiology of T2D.Over the past decade and a half,a pressing concern has emerged on investigating the association of pancreatic fat accumulation or pancreatic steatosis with the development of disease.While a few reports have suggested a possible association between pancreatic fat and T2D and/or impaired glucose metabolism,a few reports suggest a lack of such association.Pancreatic fat has also been linked with genetic risk of developing T2D,prediabetes,reduced insulin secretion,and beta cell dysfunction albeit some confounding factors such as age and ethnicity may affect the outcome.With the technological advancements in clinical imaging and progress in assessment of pancreatic beta cell function,our understanding of the role of pancreatic fat in causing insulin resistance and development of various etiologies of T2D has significantly improved.This review summarizes various findings on the possible association of pancreatic fat accumulation with the pathophysiology of T2D.展开更多
目的 探究甘精胰岛素联合利拉鲁肽对2型糖尿病患者胰岛β细胞功能及脂代谢的影响。方法 选取2021年6月—2022年12月于北京市西城区展览路医院就医的80例2型糖尿病患者为研究对象,根据随机数表法分为对照组和观察组,各40例。对照组采用...目的 探究甘精胰岛素联合利拉鲁肽对2型糖尿病患者胰岛β细胞功能及脂代谢的影响。方法 选取2021年6月—2022年12月于北京市西城区展览路医院就医的80例2型糖尿病患者为研究对象,根据随机数表法分为对照组和观察组,各40例。对照组采用甘精胰岛素进行治疗,观察组则采用甘精胰岛素联合利拉鲁肽进行治疗。比较两组治疗前后的血糖检测指标、胰岛功能指标[胰岛素抵抗指数(homeostatic model assessment of insulin resistance index,HOMA-IR)及胰岛β细胞功能指数(homeostatic model assessment of β-cell function,HOMA-β)]及脂代谢相关指标。结果 治疗前,两组的血糖检测指标、胰岛β细胞功能指标及脂代谢相关指标比较,差异无统计学意义(P>0.05)。治疗3个月后,观察组的血糖检测指标、HOMA-IR、瘦素及血脂指标显著低于对照组,血清脂联素及HOMA-β显著高于对照组,且两组的检测结果显著优于治疗前,差异有统计学意义(P<0.05)。结论 甘精胰岛素联合利拉鲁肽对2型糖尿病患者中的应用效果较好,且可显著改善胰岛β细胞功能及脂代谢状态,因此在2型糖尿病患者中的应用价值较高。展开更多
Background Women with a history of gestational diabetes mellitus （GDM） are at higher risk of future development of diabetes. This study investigated the risk factors associated with early postpartum abnormal glucose...Background Women with a history of gestational diabetes mellitus （GDM） are at higher risk of future development of diabetes. This study investigated the risk factors associated with early postpartum abnormal glucose regulation （AGR） among Chinese women with a history of GDM. Methods A total of 186 women with a history of GDM were screened for early postpartum AGR at 6-8 weeks after delivery. Those with AGR were given lifestyle intervention therapy and reevaluated in 6-12 months. The demographic, anthropometric, prenatal and delivery data were recorded. The plasma high-sensitivity C-reactive protein （HsCRP） and lipid concentration were measured, and insulin secretion were analyzed. Insulinogenic index △ins30＇/△BG30＇, the homeostasis model assessment index （HOMA）-B, and HOMA-IR were calculated. Multiple regression analysis was performed to identify the risk factors. Results Of the GDM women 28.0% （52/186） had AGR at 6-8 weeks after delivery; 45.2% （17/40） of these AGR women reminded abnormal after 6-12 month lifestyle intervention. Compared to the women who reverted to normal, women with consistent AGR showed significantly lower fasting insulin concentration, lower △ins30＇/△BG30＇ as well as lower HOMA-B. No significant differences in age, body mass index （BMI）, waist circumference, blood pressure, lipid level HsCRP and HOMA-IR were observed between the two groups. Pre-pregnancy BMI ≥25 kg/m^2, fasting glucose level ≥5.6 mmol/L and/or 75 g oral glucose tolerance test （OGTT） 2 hours glucose level ≥11.1 mmol/L during pregnancy were predictors for the AGR at 6-8 weeks after delivery. △ins30＇/△BG30≤1.05 was a significant risk contributor to the consistent early postpartum AGR. Conclusion There is a high incidence of early postpartum AGR among Chinese woman with prior GDM. Beta-cell dysfunction, rather than insulin resistance or inflammation, is the predominant contributor to the early onset and consistent AGR after delivery.展开更多
Background Abnormal insulin secretion of pancreatic beta cells is now regarded as the more primary defect than the insulin function in the etiology of type 2 diabetes.Previous studies found impaired mitochondrial func...Background Abnormal insulin secretion of pancreatic beta cells is now regarded as the more primary defect than the insulin function in the etiology of type 2 diabetes.Previous studies found impaired mitochondrial function and impaired Ca2＋ influx in beta cells in diabetic patients and animal models,suggesting a role for these processes in proper insulin secretion.The aim of this study was to investigate the detailed relationship of mitochondrial function,Ca2＋ influx,and defective insulin secretion.Methods We investigated mitochondrial function and morphology in pancreatic beta cell of diabetic KK-Ay mice and C57BL/6J mice.Two types of Ca2＋ channel activities,L-type and store-operated Ca2＋ （SOC）,were evaluated using whole-cell patch-clamp recording.The glucose induced Ca2＋ influx was measured by a non-invasive micro-test technique （NMT）.Results Mitochondria in KK-Ay mice pancreatic beta cells were swollen with disordered cristae,and mitochondrial function decreased compared with C57BL/6J mice.Ca2＋ channel activity was increased and glucose induced Ca2＋ influx was impaired,but could be recovered by genipin.Conclusion Defective mitochondrial function in diabetic mice pancreatic beta cells is a key cause of abnormal insulin secretion by altering Ca2＋ influx,but not via Ca2＋ channel activity.展开更多
文摘Background: Diabetes and diabetes-related complications are major causes of morbidity and mortality in the United States. Depressive symptoms and perceived stress have been identified as possible risk factors for beta cell dysfunction and diabetes. The purpose of this study was to assess associations between depression symptoms and perceived stress with beta cell function between African and Haitian Americans with and without type 2 diabetes. Participants and Methods: Informed consent and data were available for 462 participants (231 African Americans and 231 Haitian Americans) for this cross-sectional study. A demographic questionnaire developed by the Primary Investigator was used to collect information regarding age, gender, smoking, and ethnicity. Diabetes status was determined by self-report and confirmed by fasting blood glucose. Anthropometrics (weight, and height and waist circumference) and vital signs (blood pressure) were taken. Blood samples were drawn after 8 10 hours over-night fasting to measure lipid panel, fasting plasma glucose and serum insulin concentrations. The homeostatic model assessment, version 2 (HOMA2) computer model was used to calculate beta cell function. Depression was assessed using the Beck Depression Inventory-II (BDI-II) and stress levels were assessed using the Perceived Stress Scale (PSS). Results: Moderate to severe depressive symptoms were more likely for persons with diabetes (p = 0.030). There were no differences in perceived stress between ethnicity and diabetes status (p = 0.283). General linear models for participants with and without type 2 diabetes using beta cell function as the dependent variable showed no association with depressive symptoms and perceived stress;however, Haitian Americans had significantly lower beta cell function than African Americans both with and without diabetes and adjusting for age, gender, waist circumference and smoking. Further research is needed to compare these risk factors in other race/ethnic groups.
基金Supported by Sapienza University of Rome(Progetti di Ricerca Universitaria 2011-2012)
文摘AIM: To analyze the associations of pancreatic fat with other fat depots and β-cell function in pediatric nonalcoholic fatty liver disease(NAFLD).METHODS: We examined 158 overweight/obese children and adolescents, 80 with NAFLD [hepatic fat fraction(HFF) ≥ 5%] and 78 without fatty liver. Visceral adipose tissue(VAT), pancreatic fat fraction(PFF) and HFF were determined by magnetic resonance imaging. Estimates of insulin sensitivity were calculated using the homeostasis model assessment of insulin resistance(HOMA-IR), defined by fasting insulin and fasting glucose and whole-body insulin sensitivity index(WBISI), based on mean values of insulin and glucose obtained from oral glucose tolerance test and the corresponding fasting values. Patients were considered to have prediabetes if they had either:(1) impaired fasting glucose, defined as a fasting glucose level ≥ 100 mg/d L to < 126 mg/d L;(2) impaired glucose tolerance, defined as a 2 h glucose concentration between ≥ 140 mg/d L and < 200 mg/d L; or(3) hemoglobin A1 c value of ≥ 5.7% to < 6.5%.RESULTS: PFF was significantly higher in NAFLD patients compared with subjects without liver involvement. PFF was significantly associated with HFF and VAT, as well as fasting insulin, C peptide, HOMA-IR, and WBISI. The association between PFF and HFF was no longer significant after adjusting for age, gender, Tanner stage, body mass index(BMI)-SD score, and VAT. In multiple regression analysis withWBISI or HOMA-IR as the dependent variables, against the covariates age, gender, Tanner stage, BMI-SD score, VAT, PFF, and HFF, the only variable significantly associated with WBISI(standardized coefficient B,-0.398; P = 0.001) as well as HOMA-IR(0.353; P = 0.003) was HFF. Children with prediabetes had higher PFF and HFF than those without. PFF and HFF were significantly associated with prediabetes after adjustment for clinical variables. When all fat depots where included in the same model, only HFF remained significantly associated with prediabetes(OR = 3.38; 95%CI: 1.10-10.4; P = 0.034).CONCLUSION: In overweight/obese children with NAFLD, pancreatic fat is increased compared with those without liver involvement. However, only liver fat is independently related to prediabetes.
文摘目的探讨初诊肥胖2型糖尿病患者血清Betatrophin水平与胰岛β细胞功能的关系。方法方便选择2014年1月—2015年1月初诊肥胖2型糖尿病患者100例为研究对象(观察组),另选择同期该院体检健康者(NGT)者100名为对照观察(对照组)。测量人体指标,检测相关代谢血生化指标,采用酶联免疫吸附实验(ELISA)法测定空腹血清Betatrophin水平,采用直线相关分析研究betatrophin与胰岛β细胞功能、体测及代谢指标的相关关系。结果观察组血清Betatrophin水平(422.5±247.60)pg/m L明显高于对照组(316.3±293.30)pg/m L,差异有统计学意义(P<0.05);相关性分析提示Betatrophin与腰臀比、HOMA-IR、FPG、2 h PG、HbA1c、FINS、TG呈正相关(r=0.215、0.216、0.249、0.447、0.338、0.452、0.470,P<0.01),与HDL-C、HOMA-β成负相关(r=-0.256、-0.363,P<0.05),差异有统计学意义(P<0.05)。结论初诊肥胖2型糖尿病患者的血清betatrophin水平较NGT组明显升高,并且与胰岛β细胞功能密切相关,推测其参与了糖尿病的发生。
文摘目的通过比较聚乙二醇洛塞那肽与利拉鲁肽治疗肥胖2型糖尿病的疗效,为临床治疗该类疾病选择更高效的用药方案。方法选取东南大学医学院附属南京同仁医院2022年1月至2023年10月予以相应治疗的肥胖2型糖尿病患者共136例作为此次试验对象,按照随机数字表法分成68例A组(聚乙二醇洛塞那肽治疗)与68例B组(利拉鲁肽治疗)。比较治疗前后两组肥胖相关指标、治疗前后两组血脂相关指标、治疗前后两组血糖指标以及治疗后不良反应发生率。结果治疗后两组体质量、腰臀比、体质量指数(BMI)和腰围均下降,B组体质量和BMI[分别为(80.31±7.62)kg和(24.13±1.82)kg·m^(-2)]低于A组体质量[分别为(83.65±7.93)kg和BMI(25.34±1.84)kg·m^(-2)](体质量:t=2.504,P=0.014;BMI:t=3.855,P<0.05);治疗后两组甘油三酯(TG)、血清总胆固醇(TC)和低密度脂蛋白(LDL)均下降,高密度脂蛋白胆固醇(HDL-C)上升(均P<0.05);治疗后两组餐后2 h血糖(2 h FBG)、空腹血糖(FBG)、糖化血红蛋白(HbAlc)、胰岛素抵抗指数(HOMA-IR)水平均下降,空腹血糖胰岛素(FINS)、β细胞功能指数(HOMA-β)水平均上升,A组2 h FBG、FBG[分别为(7.86±1.12)mmol·L^(-1)、(6.18±0.71)mmol·L^(-1)]低于B组[分别为2 h FBG(8.72±1.34)mmol·L^(-1)和FBG(7.02±0.62)mmol·L^(-1)](2 h FBG:t=4.061,P<0.05;FBG:t=7.349,P<0.05),A组HOMA-β[(74.62±3.78)%]高于B组[(62.79±3.56)%](t=18.937,P<0.05);两组不良反应发生率比较差异无统计学意义(20.59%vs 25.00%,χ^(2)=0.376,P=0.540)。结论对于肥胖2型糖尿病患者,聚乙二醇洛塞那肽与利拉鲁肽均能有效减轻体质量、调节血脂、降低血糖水平以及增强胰岛β细胞的功能,且安全性相似。然而,在降低体质量方面,利拉鲁肽的效果更为显著,而聚乙二醇洛塞那肽在改善胰岛β细胞功能和降低血糖方面则表现更为出色。
文摘Type 2 diabetes(T2D)is a multifactorial metabolic disorder affecting more than 450 million people across the globe.With the increasing prevalence of T2D and obesity,the role of fat accumulation at sites other than subcutaneous adipose tissue has received significant attention in the pathophysiology of T2D.Over the past decade and a half,a pressing concern has emerged on investigating the association of pancreatic fat accumulation or pancreatic steatosis with the development of disease.While a few reports have suggested a possible association between pancreatic fat and T2D and/or impaired glucose metabolism,a few reports suggest a lack of such association.Pancreatic fat has also been linked with genetic risk of developing T2D,prediabetes,reduced insulin secretion,and beta cell dysfunction albeit some confounding factors such as age and ethnicity may affect the outcome.With the technological advancements in clinical imaging and progress in assessment of pancreatic beta cell function,our understanding of the role of pancreatic fat in causing insulin resistance and development of various etiologies of T2D has significantly improved.This review summarizes various findings on the possible association of pancreatic fat accumulation with the pathophysiology of T2D.
文摘目的 探究甘精胰岛素联合利拉鲁肽对2型糖尿病患者胰岛β细胞功能及脂代谢的影响。方法 选取2021年6月—2022年12月于北京市西城区展览路医院就医的80例2型糖尿病患者为研究对象,根据随机数表法分为对照组和观察组,各40例。对照组采用甘精胰岛素进行治疗,观察组则采用甘精胰岛素联合利拉鲁肽进行治疗。比较两组治疗前后的血糖检测指标、胰岛功能指标[胰岛素抵抗指数(homeostatic model assessment of insulin resistance index,HOMA-IR)及胰岛β细胞功能指数(homeostatic model assessment of β-cell function,HOMA-β)]及脂代谢相关指标。结果 治疗前,两组的血糖检测指标、胰岛β细胞功能指标及脂代谢相关指标比较,差异无统计学意义(P>0.05)。治疗3个月后,观察组的血糖检测指标、HOMA-IR、瘦素及血脂指标显著低于对照组,血清脂联素及HOMA-β显著高于对照组,且两组的检测结果显著优于治疗前,差异有统计学意义(P<0.05)。结论 甘精胰岛素联合利拉鲁肽对2型糖尿病患者中的应用效果较好,且可显著改善胰岛β细胞功能及脂代谢状态,因此在2型糖尿病患者中的应用价值较高。
文摘Background Women with a history of gestational diabetes mellitus （GDM） are at higher risk of future development of diabetes. This study investigated the risk factors associated with early postpartum abnormal glucose regulation （AGR） among Chinese women with a history of GDM. Methods A total of 186 women with a history of GDM were screened for early postpartum AGR at 6-8 weeks after delivery. Those with AGR were given lifestyle intervention therapy and reevaluated in 6-12 months. The demographic, anthropometric, prenatal and delivery data were recorded. The plasma high-sensitivity C-reactive protein （HsCRP） and lipid concentration were measured, and insulin secretion were analyzed. Insulinogenic index △ins30＇/△BG30＇, the homeostasis model assessment index （HOMA）-B, and HOMA-IR were calculated. Multiple regression analysis was performed to identify the risk factors. Results Of the GDM women 28.0% （52/186） had AGR at 6-8 weeks after delivery; 45.2% （17/40） of these AGR women reminded abnormal after 6-12 month lifestyle intervention. Compared to the women who reverted to normal, women with consistent AGR showed significantly lower fasting insulin concentration, lower △ins30＇/△BG30＇ as well as lower HOMA-B. No significant differences in age, body mass index （BMI）, waist circumference, blood pressure, lipid level HsCRP and HOMA-IR were observed between the two groups. Pre-pregnancy BMI ≥25 kg/m^2, fasting glucose level ≥5.6 mmol/L and/or 75 g oral glucose tolerance test （OGTT） 2 hours glucose level ≥11.1 mmol/L during pregnancy were predictors for the AGR at 6-8 weeks after delivery. △ins30＇/△BG30≤1.05 was a significant risk contributor to the consistent early postpartum AGR. Conclusion There is a high incidence of early postpartum AGR among Chinese woman with prior GDM. Beta-cell dysfunction, rather than insulin resistance or inflammation, is the predominant contributor to the early onset and consistent AGR after delivery.
基金This study was supported by grants from Fund of Capital Medical Development and Research （No. 2009-1020） and Tsinghua-Yue-Yuen Medical Science Foundation （No.20240000531 and No.20240000568）
文摘Background Abnormal insulin secretion of pancreatic beta cells is now regarded as the more primary defect than the insulin function in the etiology of type 2 diabetes.Previous studies found impaired mitochondrial function and impaired Ca2＋ influx in beta cells in diabetic patients and animal models,suggesting a role for these processes in proper insulin secretion.The aim of this study was to investigate the detailed relationship of mitochondrial function,Ca2＋ influx,and defective insulin secretion.Methods We investigated mitochondrial function and morphology in pancreatic beta cell of diabetic KK-Ay mice and C57BL/6J mice.Two types of Ca2＋ channel activities,L-type and store-operated Ca2＋ （SOC）,were evaluated using whole-cell patch-clamp recording.The glucose induced Ca2＋ influx was measured by a non-invasive micro-test technique （NMT）.Results Mitochondria in KK-Ay mice pancreatic beta cells were swollen with disordered cristae,and mitochondrial function decreased compared with C57BL/6J mice.Ca2＋ channel activity was increased and glucose induced Ca2＋ influx was impaired,but could be recovered by genipin.Conclusion Defective mitochondrial function in diabetic mice pancreatic beta cells is a key cause of abnormal insulin secretion by altering Ca2＋ influx,but not via Ca2＋ channel activity.
