血浆肾素-血管紧张素-醛固酮系统活性和 2 型糖尿病患者微量白蛋白尿的相关性研究简

目的：探讨血浆肾素-血管紧张素-醛固酮系统（RAAS）活性和2型糖尿病患者微量白蛋白尿之间的关系。方法用放射免疫法检测116例2型糖尿病患者的 RAAS活性,计算血浆醛固酮/肾素活性比值、尿微量白蛋白/肌酐比值和其他生化指标,采用多因素回归分析观察这些指标和微量白蛋白尿之间的关系。结果经过性别、年龄、BMI、病程校正后,单因素分析结果：糖尿病视网膜病变（DR）、血浆醛固酮、血管紧张素Ⅰ、醛固酮肾素活性比值、空腹血糖与糖尿病微量白蛋白尿显著相关（P＜0．05）;多因素分析结果：空腹血糖、血浆醛固酮、DR与糖尿病微量白蛋白尿显著相关（P＜0．05）。结论空腹血糖、血浆醛固酮、DR是微量白蛋白尿的独立相关因子。     

红光联合护理干预及药物治疗糖尿病合并带状疱疹神经痛的疗效观察

目的:探讨红光照射联合护理干预及药物治疗糖尿病合并带状疱疹神经痛的疗效。方法:选取此类患者56例,随机分为观察组和对照组,各28例。对照组用更昔洛韦加泼尼松、甲钴胺片、维生素B1片进行治疗,观察组在对照组治疗的基础上加用红光照射,两组护理干预方法保持一致,2周后评价疗效。结果:对照组治愈率为32.1%,总愈显率为60.7%,观察组上述数据分别为64.3%、89.3%,观察组疗效显著优于对照组。结论:红光照射联合护理干预及药物治疗糖尿病合并带状疱疹神经痛疗效显著,值得临床推广。     

红光照射联合伐昔洛韦护理治疗糖尿病合并带状疱疹的疗效观察

目的:探讨红光照射联合伐昔洛韦护理治疗糖尿病合并带状疱疹的疗效。方法:将96例糖尿病合并带状疱疹患者随机分为观察组和对照组,各48例。两组均采取相同的护理干预,对照组给予口服伐昔洛韦,观察组在对照组治疗的基础上采用红光治疗仪病灶部位照射。结果:观察组在水疱结痂、疼痛缓解和疼痛基本消失时间与对照组相比明显缩短。结论:红光照射联合伐昔洛韦及护理治疗糖尿病合并带状疱疹起效快,疗效显著。     

医院-社区-患者模式对糖调节受损患者转归的影响

目的探讨医院-社区-患者模式对糖调节受损（IGR）患者转归的影响。方法在江西省南昌市不同社区内分别建立医院-患者和医院-社区-患者保健体系干预模式,对IGR人群进行生活干预,定期行糖耐量试验,了解糖尿病发展及转归的情况。结果医院-社区-患者模式组干预2年后糖尿病发生率低于医院-患者模式组,差异有统计学意义（P〈0.01）,而糖耐量转归为正常者高于医院-患者模式组,差异有统计学意义（P〈0.05）。结论医院-社区-患者一级预防模式是有效的糖尿病预防保健体系。     

鼠曲草总黄酮对糖尿病小鼠血脂代谢紊乱改善作用的研究

鼠曲草总黄酮对糖尿病小鼠糖脂代谢紊乱的改善作用。首先采用腹腔注射链脲佐菌素构建小鼠糖尿病模型,通过检测连续21d灌胃不同剂量的鼠曲草黄酮对糖尿病小鼠体质量、糖耐量、糖化血清蛋白含量、肝糖原含量和血脂代谢的影响,研究鼠曲草总黄酮调节糖尿病小鼠糖脂代谢紊乱的作用。实验结果显示,连续21d灌胃鼠曲草黄酮(50mg/kg·d)可显著改善糖尿病小鼠糖耐量、降低体内的糖化血清蛋白、总胆固醇、甘油三酯、低密度脂蛋白含量,升高糖尿病小鼠的肝糖原和高密度脂蛋白水平的作用。鼠曲草总黄酮具有有效调节糖尿病小鼠糖脂代谢紊乱的作用。      

Pleiotropic Effects of APOB Variants on Lipid Profiles,Metabolic Syndrome,and the Risk of Diabetes Mellitus

Apolipoprotein B (ApoB) plays a crucial role in lipid and lipoprotein metabolism. The effects of APOB locus variants on lipid profiles, metabolic syndrome, and the risk of diabetes mellitus (DM) in Asian populations are unclear. We included 1478 Taiwan Biobank participants with whole-genome sequence (WGS) data and 115,088 TWB participants with Axiom genome-wide CHB array data and subjected them to genotype–phenotype analyses using APOB locus variants. Five APOB nonsynonymous mutations, including Asian-specific rs144467873 and rs13306194 variants, were selected from participants with the WGS data. Using a combination of regional association studies, a linkage disequilibrium map, and multivariate analysis, we revealed that the APOB locus variants rs144467873, rs13306194, and rs1367117 were independently associated with total, low-density lipoprotein (LDL), and non-high-density lipoprotein (non-HDL) cholesterol levels; rs1318006 was associated with HDL cholesterol levels; rs13306194 and rs35131127 were associated with serum triglyceride levels; rs144467873, rs13306194, rs56213756, and rs679899 were associated with remnant cholesterol levels; and rs144467873 and rs4665709 were associated with metabolic syndrome. Mendelian randomization (MR) analyses conducted using weighted genetic risk scores from three or two LDL-cholesterol-level-associated APOB variants revealed significant association with prevalent DM (p = 0.0029 and 8.2 × 10⁻⁵, respectively), which became insignificant after adjustment for LDL-C levels. In conclusion, these results indicate that common and rare APOB variants are independently associated with various lipid levels and metabolic syndrome in Taiwanese individuals. MR analyses supported APOB variants associated with the risk of DM through their associations with LDL cholesterol levels.     

Insights into the Genetics and Signaling Pathways in Maturity-Onset Diabetes of the Young

Diabetes Mellitus (DM) is a complex disease with a significant impact in today’s world. Studies have emphasized the crucial role of genetics in DM, unraveling the distinction of monogenic diabetes from the most common types that have been recognized over the years, such as type 1 diabetes (T1DM) and type 2 diabetes (T2DM). A literature search was carried out to scrutinize the subtypes of maturity-onset diabetes of the young (MODY), as well as the connection between the recognized genetic and molecular mechanisms responsible for such phenotypes. Thus far, 14 subtypes of MODY have been identified. Here, the authors review the pathophysiological and molecular pathways in which monogenic diabetes genes are involved. Despite being estimated to affect approximately 2% of all T2DM patients in Europe, the exact prevalence of MODY is still unknown, enhancing the need for research focused on biomarkers. Due to its impact in personalized medicine, a follow-up of associated complications, and genetic implications for siblings and offspring of affected individuals, it is imperative to diagnose the monogenic forms of DM accurately. Currently, advances in the genetics field has allowed for the recognition of new DM subtypes, which until now were considered to be slight variations of the typical forms. New molecular insights can define therapeutic strategies, aiming for the prevention, correction, or at least delay of β-cell dysfunction. Thus, it is imperative to act in the close interaction between genetics and clinical manifestations to improve diagnosis and individualize treatment.     

Organokines,Sarcopenia, and Metabolic Repercussions: The Vicious Cycle and the Interplay with Exercise

Sarcopenia is a disease that becomes more prevalent as the population ages, since it is directly linked to the process of senility, which courses with muscle atrophy and loss of muscle strength. Over time, sarcopenia is linked to obesity, being known as sarcopenic obesity, and leads to other metabolic changes. At the molecular level, organokines act on different tissues and can improve or harm sarcopenia. It all depends on their production process, which is associated with factors such as physical exercise, the aging process, and metabolic diseases. Because of the seriousness of these repercussions, the aim of this literature review is to conduct a review on the relationship between organokines, sarcopenia, diabetes, and other metabolic repercussions, as well the role of physical exercise. To build this review, PubMed-Medline, Embase, and COCHRANE databases were searched, and only studies written in English were included. It was observed that myokines, adipokines, hepatokines, and osteokines had direct impacts on the pathophysiology of sarcopenia and its metabolic repercussions. Therefore, knowing how organokines act is very important to know their impacts on age, disease prevention, and how they can be related to the prevention of muscle loss.     

Impact of Sulfated Hyaluronan on Bone Metabolism in Diabetic Charcot Neuroarthropathy and Degenerative Arthritis

Bone in diabetes mellitus is characterized by an altered microarchitecture caused by abnormal metabolism of bone cells. Together with diabetic neuropathy, this is associated with serious complications including impaired bone healing culminating in complicated fractures and dislocations, especially in the lower extremities, so-called Charcot neuroarthropathy (CN). The underlying mechanisms are not yet fully understood, and treatment of CN is challenging. Several in vitro and in vivo investigations have suggested positive effects on bone regeneration by modifying biomaterials with sulfated glycosaminoglycans (sGAG). Recent findings described a beneficial effect of sGAG for bone healing in diabetic animal models compared to healthy animals. We therefore aimed at studying the effects of low- and high-sulfated hyaluronan derivatives on osteoclast markers as well as gene expression patterns of osteoclasts and osteoblasts from patients with diabetic CN compared to non-diabetic patients with arthritis at the foot and ankle. Exposure to sulfated hyaluronan (sHA) derivatives reduced the exaggerated calcium phosphate resorption as well as the expression of genes associated with bone resorption in both groups, but more pronounced in patients with CN. Moreover, sHA derivatives reduced the release of pro-inflammatory cytokines in osteoclasts of patients with CN. The effects of sHA on osteoblasts differed only marginally between patients with CN and non-diabetic patients with arthritis. These results suggest balancing effects of sHA on osteoclastic bone resorption parameters in diabetes.