Interaction of sleep quality and sleep duration on glycemic control in patients with type 2 diabetes mellitus

Background Copious evidence from epidemiological and laboratory studies has revealed that sleep status is associated with glucose intolerance, insulin resistance, thus increasing the risk of developing type 2 diabetes. The aim of this study was to reveal the interaction of sleep quality and sleep quantity on glycemic control in patients with type 2 diabetes mellitus. Methods From May 2013 to May 2014, a total of 551 type 2 diabetes patients in Tianjin Metabolic Diseases Hospital were enrolled. Blood samples were taken to measure glycosylated hemoglobin （HbAlc）, and all the patients completed the Chinese version of the Pittsburgh Sleep Quality Index （PSQI） questionnaire to evaluate their sleep status. ＂Good sleep quality＂ was defined as PQSI 〈5, ＂average sleep quality＂ was defined as PQSI 6-8, and ＂poor sleep quality＂ was defined as PQSI 〉8. Poor glycemic control was defined as HbAlc 〉7%. Sleep quantity was categorized as 〈6, 6-8, and 〉8 hours/ night. Short sleep time was defined as sleep duration 〈6 hours/night. Results In the poor glycemic control group, the rate of patients who had insufficient sleep was much higher than that in the other group （X2=11.16, P=0.037）. The rate of poor sleep quality in poor glycemic control group was much greater than that in the average control group （X2=9.79, P=-0.007）. After adjusted by gender, age, body mass index, and disease duration, the adjusted PSQI score＇s OR was 1.048 （95% CI 1.007-1.092, P=0.023） for HbAlc level. The sleep duration＇s OR was 0.464 （95% CI 0.236-0.912, P=0.026） for HbAlc level. One-way analysis of variance showed that the poor sleep quality group had the highest homeostasis model assessment-insulin resistance （P 〈0.01）. Conclusions Inadequate sleep, in both quality and quantity, should be regarded as a plausible risk factor for glycemic control in type 2 diabetes. Poor sleep might bring much more serious insulin resistance and could be the reason for bad glycemic control. A good night＇s sleep should be seen as a critical health component tool in the prevention and treatment of type 2 diabetes. It is important for clinicians to target the root causes of short sleep duration and/or poor sleep quality.

Iodine deficiency up-regulates monocarboxylate transporter 8 expression of mouse thyroid gland

Background Iodine deficiency is a major factor affecting thyroid auto-regulation,the quantity of iodine may greatly influence the synthesis of thyroid hormones （THs）.It has long been believed that TH enters the cell through passive diffusion.Recent studies have suggested that several transporters could facilitate transportation of TH.The monocarboxylate transporter 8 （MCT8） was identified as a very active and specific TH transporter.The purpose of this study was to investigate whether iodine insufficient affected the expression of MCT8 in the thyroid gland.Methods Sixty BALB/c mice were randomly divided into two groups：control group was fed with standard feed （iodine concentration of 300 μg/kg）; while low-iodine （LI） group received iodine-insufficient feed （iodine concentration of 20-40 μg/kg）.After 3 months,10 mice of each group were sacrificed.The remaining 20 mice of each group were kept till 6 months.From the LI group,we randomly selected 15 mice and injected triiodothyronine （T3,100 μg/kg body weight per day） intraperitoneally for 24,48 or 72 hours （5 mice for each time-point）.Then,all the mice were sacrificed.Mouse serum thyroxine （T4）,T3,and thyroid-stimulating hormone （TSH） levels were determined by chemiluminescence immunoassay （CIA）.The protein content or messenger RNA （mRNA） level of thyroid MCT8 was measured by Western blotting analysis or real time RT-PCR respectively.MCT8 subcellular location in thyroid tissues was probed with immunohistochemistry （IHC） assay.Results We found that mouse serum T3 and T4 levels decreased and TSH level increased by the end of the third month.Consistent with these findings,there was significant goiter and hypothyroidism in the LI group.Meanwhile,the MCT8 mRNA increased to 1.36-fold of the level in the control group at the 3rd month.At 6th month,the serum T4 level in LI mice remained at a lower level,and MCT8 mRNA expression continued rising to nearly 1.60-fold compared with the control group.The protein content was also about 3 times higher than that in the control group.IHC results also revealed MCT8 was of higher expression and localized in the cytoplasm of thyroid follicular cells.After providing exogenous T3 to iodine deficient mice,the serum T3 and T4 gradually increased,whereas MCT8 mRNA and protein both started to decrease and returned to the same level as the control group.Conclusion There is a compensatory increase in thyroid MCT8 expression to enhance its capability to transport TH from thyroid to the blood circulation in iodine deficient mice.

Biphasic insulin aspart 30 improved glycemic control in Chinese patients with type 2 diabetes poorly controlled on oral glucose-lowering drugs： a subgroup analysis of the A1chieve study

Background The effectiveness and safety of initiating biphasic insulin aspart 30 in patients who were poorly controlled on oral glucose-lowering drugs were studied in randomized controlled trials,while results from clinical practice remain limited.This subgroup analysis was to provide such findings from a large-scale non-interventional study.Methods A1chieve was a multinational,prospective,open-label,non-interventional,24-week study in patients with type 2 diabetes initiating insulin analogues in 28 countries across Asia,Africa,Europe,and Latin America.After physician had taken the decision to use this insulin,any patient with type 2 diabetes who was not treated with or who had started the study insulin within 4 weeks before inclusion was eligible.Patients were treated with study insulin alone or in combination with oral glucose-lowering drugs.Data on adverse drug reactions,hypoglycemia and glycemic control were collected at baseline,week 12 and 24.This is a report of a Chinese subgroup analysis from the A1chieve study.Results Totally,4 100 patients constituted this subgroup.No serious adverse drug reactions were reported.Rates of total,major,nocturnal hypoglycemic events （events/patient per year） were 1.47,0.10,0.31 at baseline and 1.35,0.00,0.22 at week 24,respectively.Glycemic control was improved as measured by hemoglobin A1c （mean 9.3％ to 7.0％,reduction -2.3％）,fasting plasma glucose （mean 10.2 to 6.8 mmol/L,reduction-3.5 mmol/L） and postprandial plasma glucose （mean 14.4 to 8.8 mmol/L,reduction-5.6 mmol/L）,all P ＜0.001.Change in mean body weight was ＋0.3 kg （P ＜0.001）.Conclusion In this subgroup analysis of the A1chieve study,biphasic insulin aspart 30 improved glycemic control with low risk of hypoglycemia.

Early intervention with Di-Dang Decoction prevents macrovascular fibrosis in diabetic rats by regulating the TGF-β1/Smad signalling pathway

Macroangiopathy is a complication of Type II Diabetes Mellitus(T2 DM),which is mainly caused by fibrosis of blood vessels.Using T2 DM rat models,we investigated whether the traditional Chinese medicine,Di-Dang Decoction(DDD),exhibited antifibrotic actions on great vessels.T2 DM rats were randomly divided into non-intervention group,early-,middle-,late-stage DDD intervention groups and control groups,including pioglitazone group and aminoguanidine group.After administration of DDD to T2 DM rats at different times,we detected the amount of extracellular matrix(ECM)deposition in the thoracic aorta.The results showed that early-stage intervention with DDD could effectively protect great vessels from ECM deposition.Considering that TGF-β1 is the master regulator of fibrosis,we further validated at the molecular level that,compared to middle-and late-stage intervention with DDD,early-stage intervention with DDD could significantly decrease the expression levels of factors related to the activated TGF-β1/Smad signalling pathway,as well as the expression levels of downstream effectors including CTGF,MMP and TIMP family proteins,which were directly involved in ECM remodelling.Therefore,early-stage intervention with DDD can reduce macrovascular fibrosis and prevent diabetic macroangiopathy.

实现基于缺陷能级稀土双掺氧化锌上转换发光（英文）

上转换白光由红色、绿色和蓝色组成,而上转换白光通常是通过复杂的三掺杂稀土离子如Yb^(3+)、Er^(3+)和Tm^(3+)实现的.本文报道了一个新型村料,通过Yb^(3+)、Tm^(3+)双掺ZnO实现上转换白光输出.体系获得475 nm(~1G_4→~3H_6)上转换蓝光和652 nm(~1G_4→~3F_4)上转换红光,上转换绿光发射源于ZnO基质村料缺陷(氧空位)发光.此外,通过调节OH-的浓度可以调控纳米村料形貌.尤其是铅笔状结构纳米棒由于表面具有高浓度的氧空位,实现了上转换绿光辐射.同时氧空位缺陷作为能量传递过程的中间态能级,提高了上转换蓝光以及上转换红光的发光强度.我们的研究首次将缺陷发光机理和上转换发光机理相结合,为实现上转换白光输出开辟了新道路.