Effects of vitamin D supplementation on glucose and lipid metabolism in patients with type 2 diabetes mellitus and risk factors for insulin resistance.

BACKGROUND: Type 2 diabetes mellitus (T2DM) is a chronic metabolic disease featured by insulin resistance (IR) and decreased insulin secretion. Currently, vitamin D deficiency is found in most patients with T2DM, but the relationship between vitamin D and IR in T2DM patients requires further investigation. AIM: To explore the risk factors of IR and the effects of vitamin D supplementation on glucose and lipid metabolism in patients with T2DM. METHODS: Clinical data of 162 T2DM patients treated in First Affiliated Hospital of Harbin Medical University between January 2019 and February 2022 were retrospectively analyzed. Based on the diagnostic criteria of IR, the patients were divided into a resistance group (n = 100) and a non-resistance group (n = 62). Subsequently, patients in the resistance group were subdivided to a conventional group (n = 44) or a joint group (n = 56) according to the treatment regimens. Logistic regression was carried out to analyze the risk factors of IR in T2DM patients. The changes in glucose and lipid metabolism indexes in T2DM patients with vitamin D deficiency were evaluated after the treatment. RESULTS: Notable differences were observed in age and body mass index (BMI) between the resistance group and the non-resistance group (both P < 0.05). The resistance group exhibited a lower 25-hydroxyvitamin D3 (25(OH)D3) level, as well as notably higher levels of 2-h postprandial blood glucose (2hPG), fasting blood glucose (FBG), and glycosylated hemoglobin (HbA1c) than the non-resistance group (all P < 0.0001). Additionally, the resistance group demonstrated a higher triglyceride (TG) level but a lower high-density lipoprotein-cholesterol (HDL-C) level than the non-resistance group (all P < 0.0001). The BMI, TG, HDL-C, 25(OH)D3, 2hPG, and HbA1c were found to be risk factors of IR. Moreover, the post-treatment changes in levels of 25(OH)D3, 2hPG, FBG and HbA1c, as well as TG, total cholesterol, and HDL-C in the joint group were more significant than those in the conventional group (all P < 0.05). CONCLUSION: Patients with IR exhibit significant abnormalities in glucose and lipid metabolism parameters compared to the non-insulin resistant group. Logistic regression analysis revealed that 25(OH)D3 is an independent risk factor influencing IR. Supplementation of vitamin D has been shown to improve glucose and lipid metabolism in patients with IR and T2DM.

Effect of DHCR7 for the co-occurrence of hypercholesterolemia and vitamin D deficiency in type 2 diabetes: Perspective of health prevention.

Type 2 diabetes mellitus (T2DM) is a complex disease caused by multiple factors, which are often accompanied by the disorder of glucose and lipid metabolism and the lack of vitamin D.Over the years, researchers have conducted numerous studies into the pathogenesis and prevention strategies of diabetes. In this study, diabetic SD rats were randomly divided into type 2 diabetes group, vitamin D intervention group, 7-dehydrocholesterole reductase (DHCR7) inhibitor intervention group, simvastatin intervention group, and naive control group. Before and 12 weeks after intervention, liver tissue was extracted to isolate hepatocytes. Compared with naive control group, in the type 2 diabetic group without interference, the expression of DHCR7 increased, the level of 25(OH)D3 decreased, the level of cholesterol increased. In the primary cultured naive and type 2 diabetic hepatocytes, the expression of genes related to lipid metabolism and vitamin D metabolism were differently regulated in each of the 5 treatment groups. Overall, DHCR7 is an indicator for type 2 diabetic glycolipid metabolism disorder and vitamin D deficiency. Targeting DHCR7 will help with T2DM therapy.The management model of comprehensive health intervention can timely discover the disease problems of diabetes patients and high-risk groups and reduce the incidence of diabetes.

Impact of metabolic syndrome on sex hormones and reproductive function: a meta-analysis of 2923 cases and 14062 controls.

Current evidence is inconsistent regarding the impact of metabolic syndrome (MetS) on sex hormones and reproductive function, and this meta-analysis aimed to illuminate the association. A literature search was conducted in public databases to identify all relevant studies, and study-specific standardized mean differences (SMD) and 95% confidence intervals (CI) were pooled using a random-effects model. Finally, 21 studies were identified with a total of 2923 MetS cases and 14062 controls. In males, MetS cases had a lower level of testosterone, inhibin B, total sperm count, sperm concentration, sperm normal morphology, sperm total motility, sperm progressive motility and sperm vitality, and a higher level of DNA fragmentation and mitochondrial membrane potential. In females, MetS cases had a higher level of testosterone. No significant difference was detected for follicle-stimulating hormone, luteinizing hormone, oestradiol, prolactin, anti-Müllerian hormone and semen volume in males, and for oestradiol, follicle-stimulating hormone, luteinizing hormone and progesterone in females. In conclusion, this meta-analysis indicated the impact of MetS on sex hormones and reproductive function, and MetS cases had a potential risk of infertility.

CircHIPK3 Promotes Thyroid Cancer Tumorigenesis and Invasion through the Mirna-338-3p/RAB23 Axis.

Objective：Thyroid cancer is a common type of endocrine malignancy, and its incidence has been steadily increasing in many regions of the world. Numerous studies have found that the circRNAs in various cancer types are aberrantly expressed, which could be potential biological diagnostic markers and therapeutic targets. The purpose of this study was to investigate the role of circHIPK3 in the development and progression of thyroid cancer and its mechanism. Subject and Methods：qRT-PCR was used to detect the relative expression levels of circHIPK3 in thyroid cancer cell lines (K1, CAL-62, TPC1), human thyroid normal cells (Nthy-ori 3-1), 10 pairs of thyroid cancer tissues and corresponding adjacent normal tissues. CCK-8 and Transwell assays were used to detect the proliferation and metastasis ability of cells. The targeted relationships between circHIPK3-miR-338-3p and miR-338-3p-RAB23 were predicted by bioinformatics analysis and verified by dual-luciferase reporter assays. Results and Conclusion: The downregulation of circHIPK3 significantly reduced the migration, invasion and proliferation of thyroid carcinoma. Then, we demonstrated that circHIPK3 up-regulated the expression of its target gene RAB23 by sponging miR-338-3p to promote the tumorigenesis and invasiveness of thyroid cancer. This study is the first to find that circHIPK3 plays the role of oncogenetic circRNA in thyroid cancer, which may provide new insights into how circRNA affects the progression of thyroid cancer. Our study also showed that circHIPK3 could be a novel biomarker for thyroid cancer.

The function of SNHG7/miR-449a/ACSL1 axis in thyroid cancer.

Thyroid cancer (TC) has been characterized as the most common malignant malady of the endocrine system. Small nucleolar RNA host gene 7 (SNHG7) has been reported to serve as a key regulator in a large number of human cancer types, but its role in TC and the underlying regulatory mechanism have never been evaluated yet. The present study indicated that the expression of SNHG7 was markedly higher in TC cell lines. Knockdown of SNHG7 led to a suppression of TC cell progression and migration. Acyl-CoA synthetase long-chain family member 1 (ACSL1) has also been demonstrated as an oncogene in many cancers. Herein an inhibition of ACSL1 after SNHG7 knockdown was captured. Further, the suppressing effects of SNHG7 knockdown on TC cell processes were counteracted by ACSL1 overexpression. Data from online bioinformatics analysis, RNA immunoprecipitation, and luciferase reporter assays validated the interaction between microRNA-449a (miR-449a) and SNHG7 or ACSL1. It was also verified that SNHG7 sequestered miR-449a and therefore elevated ACSL1 expression levels. To conclude, the current study indicated that SNHG7 promoted proliferation and migration of TC cells by sponging miR-449a and therefore upregulating ACSL1. The present study may provide more explorations about the molecular regulation mechanism of long noncoding RNAs in TC progression.