AIM： To investigate the possible involvement of 25-hydroxyvitamin D3-1cx-hydroxylase [1α-25（OH）2D3] in butyrate-induced differentiation in human intestinal cell line Caco-2 cells. METHODS： Caco-2 cells were incub...AIM： To investigate the possible involvement of 25-hydroxyvitamin D3-1cx-hydroxylase [1α-25（OH）2D3] in butyrate-induced differentiation in human intestinal cell line Caco-2 cells. METHODS： Caco-2 cells were incubated either with 3 mmol/L butyrate and 1 umol/L 25（OH）2D3 or with 1 umol/L 1α-25（OH）2D3 for various time intervals ranging from 0 to 72 h. Additionally, cells were co-incubated with butyrate and either 25（OH）2D3 or 1α-25（OH）2D3. 1α-25（OH）2D3 mRNA was determined semi-quantitatively using the fluorescent dye PicoGreen. Immunoblotting was used for the detection of 1α-25（OH）2D3 protein. Finally, enzymatic activity was measured by ELISA. RESULTS： Both butyrate and 1α-25（OH）2D3 stimulated differentiation of Caco-2 cells after a 48 h incubation period, while 25（OH）2D3 had no impact on cell differentiation. Synergistic effects on differentiation were observed when cells were co-incubated with butyrate and vitamin D metabolite. Butyrate transiently upregulated 1α-25（OH）2D3 mRNA followed by a timely delayed protein upregulation. Coincidently, enzymatic activity was enhanced significantly. The induction of the enzyme allowed for comparable differentiating effects of both vitamin D metabolites. CONCLUSION： Our experimental data provide a further mechanism for the involvement of the vitamin D signaling pathway in colonic epithelial cell differentiation by butyrate. The enhancement of 1α-25（OH）2D3 followed by antiproliferative effects of the vitamin D prohormone in the Caco-2 cell line suggest that 25（OH）2D3 in combination with butyrate may offer a new therapeutic approach forthe treatment of colon cancer.展开更多
Background: Diabetes mellitus is a worldwide epidemic. In 2002 there were 173 million diabetic adults worldwide, and these numbers are expected to reach up to 300 million people by 2030. Meanwhile, vitamin D deficienc...Background: Diabetes mellitus is a worldwide epidemic. In 2002 there were 173 million diabetic adults worldwide, and these numbers are expected to reach up to 300 million people by 2030. Meanwhile, vitamin D deficiency has its worldwide prevalence directly influenced by factors as solar radiation, skin color, latitude and seasons, cultural habits of populations such as clothing and food, and these factors are important to explain the different prevalences of vitamin D deficiency in the world. Methods: A prospective cross-sectional cohort study was conducted with patients in the outpatient clinic of the Health Unit of the city of Mangueirinha, Paraná, Southern Brazil. Fifty-four type 2 diabetic patients were evaluated (38 women and 16 men), aged 55.8 ± 12.6 years. The following variables were evaluated: age, ethnicity, presence of type 2 diabetes (DM2), hypertension, dyslipidemia, weight, BMI, WC, blood pressure, blood glucose, glycated hemoglobin, ionized calcium, PTH, 25-OH Vit, total cholesterol, HDL, LDL, urea, creatinine, uric acid and red cell/hematocrit. Results: mean BMI was 30.2 ± 4.4 kg/m<sup>2</sup>, indicating class 1 obesity in this population. Fasting glucose levels were approximately 169.8 ± 74.5 mg/dL. The 25-OH vitamin D values for this population were 23.4 ± 8.3 ng/mL, and 13% of them showed 25-OH vitamin D levels above 30 mg/dL. Fifty percent of those patients had vitamin D levels lower than 30 mg/dL, and 37% had less than 20 mg/dL. Conclusions: this study suggests that vitamin D is associated with low levels of vitamin D in type 2 diabetic patients. Supplementation of vitamin D should be considered in diabetic patients, when levels under 30 mg/mL are found.展开更多
目的了解2型糖尿病患者血清25-羟维生素D(25-hydroxylvitamin D,25OHD)营养状况及其与骨密度(bone mineral density,BMD)的关系。方法选择2015年2月-2017年3月在北京同仁医院住院的2型糖尿病患者716例(男性410例,女性306例),年龄32~93岁...目的了解2型糖尿病患者血清25-羟维生素D(25-hydroxylvitamin D,25OHD)营养状况及其与骨密度(bone mineral density,BMD)的关系。方法选择2015年2月-2017年3月在北京同仁医院住院的2型糖尿病患者716例(男性410例,女性306例),年龄32~93岁,平均年龄(58.78±11.31)岁,检测血清25OHD水平,应用双能X线吸收检测法测定腰1-4、全髋及股骨颈的BMD。结果在716例2型糖尿病患者中,维生素D严重缺乏者为230例(32.1%),缺乏357例(49.9%),不足97例(13.5%),充足仅32例(4.5%)。不同年龄组别中,血清25OHD水平以及缺乏程度差异均无统计学意义(P>0.05)。Logistic回归分析显示年龄增长、女性及维生素D缺乏为2型糖尿病患者发生骨质疏松的危险因素。结论 2型糖尿病患者维生素D缺乏严重,女性更为明显。血清25OHD缺乏程度越重,骨质疏松的发生风险越高。展开更多
基金Supported by the Else Kroner-Fresenius Foundation, Bad Homburg, Germany
文摘AIM： To investigate the possible involvement of 25-hydroxyvitamin D3-1cx-hydroxylase [1α-25（OH）2D3] in butyrate-induced differentiation in human intestinal cell line Caco-2 cells. METHODS： Caco-2 cells were incubated either with 3 mmol/L butyrate and 1 umol/L 25（OH）2D3 or with 1 umol/L 1α-25（OH）2D3 for various time intervals ranging from 0 to 72 h. Additionally, cells were co-incubated with butyrate and either 25（OH）2D3 or 1α-25（OH）2D3. 1α-25（OH）2D3 mRNA was determined semi-quantitatively using the fluorescent dye PicoGreen. Immunoblotting was used for the detection of 1α-25（OH）2D3 protein. Finally, enzymatic activity was measured by ELISA. RESULTS： Both butyrate and 1α-25（OH）2D3 stimulated differentiation of Caco-2 cells after a 48 h incubation period, while 25（OH）2D3 had no impact on cell differentiation. Synergistic effects on differentiation were observed when cells were co-incubated with butyrate and vitamin D metabolite. Butyrate transiently upregulated 1α-25（OH）2D3 mRNA followed by a timely delayed protein upregulation. Coincidently, enzymatic activity was enhanced significantly. The induction of the enzyme allowed for comparable differentiating effects of both vitamin D metabolites. CONCLUSION： Our experimental data provide a further mechanism for the involvement of the vitamin D signaling pathway in colonic epithelial cell differentiation by butyrate. The enhancement of 1α-25（OH）2D3 followed by antiproliferative effects of the vitamin D prohormone in the Caco-2 cell line suggest that 25（OH）2D3 in combination with butyrate may offer a new therapeutic approach forthe treatment of colon cancer.
文摘Background: Diabetes mellitus is a worldwide epidemic. In 2002 there were 173 million diabetic adults worldwide, and these numbers are expected to reach up to 300 million people by 2030. Meanwhile, vitamin D deficiency has its worldwide prevalence directly influenced by factors as solar radiation, skin color, latitude and seasons, cultural habits of populations such as clothing and food, and these factors are important to explain the different prevalences of vitamin D deficiency in the world. Methods: A prospective cross-sectional cohort study was conducted with patients in the outpatient clinic of the Health Unit of the city of Mangueirinha, Paraná, Southern Brazil. Fifty-four type 2 diabetic patients were evaluated (38 women and 16 men), aged 55.8 ± 12.6 years. The following variables were evaluated: age, ethnicity, presence of type 2 diabetes (DM2), hypertension, dyslipidemia, weight, BMI, WC, blood pressure, blood glucose, glycated hemoglobin, ionized calcium, PTH, 25-OH Vit, total cholesterol, HDL, LDL, urea, creatinine, uric acid and red cell/hematocrit. Results: mean BMI was 30.2 ± 4.4 kg/m<sup>2</sup>, indicating class 1 obesity in this population. Fasting glucose levels were approximately 169.8 ± 74.5 mg/dL. The 25-OH vitamin D values for this population were 23.4 ± 8.3 ng/mL, and 13% of them showed 25-OH vitamin D levels above 30 mg/dL. Fifty percent of those patients had vitamin D levels lower than 30 mg/dL, and 37% had less than 20 mg/dL. Conclusions: this study suggests that vitamin D is associated with low levels of vitamin D in type 2 diabetic patients. Supplementation of vitamin D should be considered in diabetic patients, when levels under 30 mg/mL are found.
文摘目的了解2型糖尿病患者血清25-羟维生素D(25-hydroxylvitamin D,25OHD)营养状况及其与骨密度(bone mineral density,BMD)的关系。方法选择2015年2月-2017年3月在北京同仁医院住院的2型糖尿病患者716例(男性410例,女性306例),年龄32~93岁,平均年龄(58.78±11.31)岁,检测血清25OHD水平,应用双能X线吸收检测法测定腰1-4、全髋及股骨颈的BMD。结果在716例2型糖尿病患者中,维生素D严重缺乏者为230例(32.1%),缺乏357例(49.9%),不足97例(13.5%),充足仅32例(4.5%)。不同年龄组别中,血清25OHD水平以及缺乏程度差异均无统计学意义(P>0.05)。Logistic回归分析显示年龄增长、女性及维生素D缺乏为2型糖尿病患者发生骨质疏松的危险因素。结论 2型糖尿病患者维生素D缺乏严重,女性更为明显。血清25OHD缺乏程度越重,骨质疏松的发生风险越高。
