Vitamin D plays an important role in insulin secretion. As the enzyme that initiates degradation of the active metabolite of vitamin D (1,25-(OH)2 vitamin D), 24-hydroxylase encoded by CYP24A1 may be associated with insulin secretion. In this study, we aimed at investigating the association between copy number of CYP24A1 and the concentration of insulin. Included in the study were 1528 rural people from Henan Province of China. The copy number of CYP24A1 and the concentrations of serum 25(OH) vitamin D3 and insulin were determined. Association between copy number of CYP24A1 and vitamin D deficiency was investigated with logistic regression model. Correlation between copy number of CYP24A1 and serum insulin was observed by Spearman correlation. The results suggested that copy number variation of CYP24A1 was associated with vitamin D deficiency. Higher copy number of CYP24A1 was a risk factor for vitamin D deficiency (adjusted odds ratio: 1.199; 95% confidence interval: 1.028-1.397; P = 0.021). Furthermore, copy number of CYP24A1 was positive correlated with the concentration of serum insulin (r = 0.115; P < 0.001), regardless of vitamin D status, age, and body mass index (BMI). Increased copy number of CYP24A1 is associated with not only vitamin D deficiency but also increased serum insulin. Vitamin D supplement may be beneficial to individuals with high copy number of CYP24A1. Novelty Increased copy number of CYP24A1 was a risk factor of vitamin D deficiency. Increased copy number of CYP24A1 was associated with increased serum concentration of insulin independent of age, BMI, and vitamin D status.

To evaluate price, availability and affordability of insulin products in Shaanxi Province, western China.
We used a simplified and adapted WHO/Health Action International method to obtain the availability and prices of insulin products and five oral anti-diabetic medicines as comparators in public general hospitals and private retail outlets. In addition, we investigated the price components of eight selected insulin products by tracing the supply chain.
All three kinds of insulin products, prandial, basal and premixed insulin, are 100% available in public hospitals, and have fairly high availability in the private sector (62.5-68.8%). The prices of most insulin products were higher than international reference prices in both sectors (ranging from 0.95 times to 2.33 times). All insulin products were unaffordable as they would cost 3.5-17.1 days\' wage of the lowest-paid government workers in Shaanxi. The manufacturer\'s markup (selling price), which comprised more than 60% of the final price of all insulin products surveyed, was the largest price component.
Although availability of insulin products was high in public general hospitals and private retail pharmacies, their high price made them unaffordable to diabetes patients, especially low-income patients. The government should increase insurance compensation for those who need these life-saving medicines or decrease the cost of insulin products through negotiation with suppliers.

MicroRNAs (miRNAs) are a class of noncoding single-stranded RNA molecules encoded by endogenous genes of about 22 nucleotides, which are involved in post-transcriptional gene expression regulation in animals and plants. Type 1 diabetes (T1D) is an autoimmune disease that is clinically silent until the majority of β cells are destroyed, and a large number of studies have shown that miRNAs are involved in the pathological mechanism of T1D. In this review, we searched the related research in recent years and summarized the important roles of miRNAs in T1D diagnosis and treatment. Furthermore, we summarized the current understanding of miRNA-mediated regulation mechanisms of gene expression in the T1D pathogenesis as well as related signaling pathways with a focus on the important roles of miRNAs and their antagonists in T1D pathogenesis, and brought insight into the potential therapeutic value of miRNAs for T1D patients. In view of the important roles of miRNAs in T1D pathology, disordered miRNAs may be important diagnostic markers and therapeutic targets for patients with T1D.

OBJECTIVE: Although extensive data have shown that galanin can regulate the food intake and glucose metabolism of animals, little is known regarding the galanin concentration in patients with impaired glucose tolerance (IGT). Therefore, the aims of this study were to investigate whether serum galanin levels and other metabolic parameters are changed in patients with IGT compared with controls with normal glucose tolerance (NGT).
METHODS: Data regarding serum galanin levels and relative metabolic parameters were collected in 12 patients with IGT and 12 healthy patients with NGT.
RESULTS: At 1 hour and 2 hours after dinner, serum galanin, insulin and glucose levels were significantly higher in patients with IGT than in controls with NGT. Additionally, the body weights of patients with IGT was higher than those of the controls. Furthermore, a negative correlation was found between galanin levels and 1-hour glucose concentrations (r=-0.580; p=0.048) in patients with IGT.
CONCLUSIONS: The higher serum galanin levels as well as the negative correlation between galanin levels and 1-hour glucose content in patients with IGT may result from the interaction between insulin and galanin in differing conditions, suggesting that the galanin level may be used as a potential biomarker for the prediction of IGT in clinical settings.

Obstructive sleep apnea (OSA) is a breathing disorder during sleep, with a most prominent character of chronic intermittent hypoxia (CIH), which induces the generation of reactive oxygen species (ROS) that damages multiple tissues and causes metabolic disorders. In this study, we established a rat model of varying OSA with different grades of CIH (12.5% O2, 10% O2, 7.5% O2, and 5% O2) for 12 weeks, and found that CIH stimulated insulin secretion, reduced the insulin:proinsulin ratio in pancreatic tissue, and caused pancreatic tissue lesions and cell apoptosis in a dose-dependent manner. Moreover, CIH promoted the production of tumor necrosis factor (TNF)-α, interleukin (IL)-1β and IL-6, and activated mitogen-activated protein kinase (MAPK) family members, extracellular regulated protein kinase (ERK), c-Jun N-terminal kinase (JNK), and P38, depending on the O2 concentration. In summary, CIH disturbed insulin secretion, and caused inflammation, lesions, and cell apoptosis in pancreatic tissue via the MAPK signaling pathway, which may be of great significance for clinical treatment of OSA and type 2 diabetes mellitus (T2DM).