1. Type 1 diabetes (due to b-cell destruction, usually leading to absolute insulin deficiency) 2. Type 2 diabetes (due to a progressive insulin secretory defect on the background of insulin resistance) 3. Gestational diabetes mellitus (GDM) (diabetes diagnosed in the second or third trimester of pregnancy that is not clearly overt diabetes) 4. Specific types of diabetes due to other causes, e.g., monogenic diabetes syndromes (such as neonatal diabetes and maturity-onset diabetes of the young [MODY]), diseases of the exocrine pancreas (such as cystic fibrosis), and drugor chemical-induced diabetes (such as in the treatment of HIV/AIDS or after organ transplantation)

Classification and diagnosis of diabetes

Type 1 diabetes mellitus (T1DM) is an autoimmune disorder that affects an estimated 30 million people worldwide. It is characterized by the destruction of pancreatic β cells by the immune system, which leads to lifelong dependency on exogenous insulin and imposes an enormous burden on patients and health-care resources. T1DM is also associated with an increased risk of comorbidities, such as cardiovascular disease, retinopathy, and diabetic kidney disease (DKD), further contributing to the burden of this disease. Although T cells are largely considered to be responsible for β-cell destruction in T1DM, increasing evidence points towards a role for B cells in disease pathogenesis. B cell-depletion, for example, delays disease progression in patients with newly diagnosed T1DM. Loss of tolerance of islet antigen-reactive B cells occurs early in disease and numbers of pancreatic CD20+ B cells correlate with β-cell loss. Although the importance of B cells in T1DM is increasingly apparent, exactly how these cells contribute to disease and its comorbidities, such as DKD, is not well understood. Here we discuss the role of B cells in the pathogenesis of T1DM and how these cells are activated during disease development. Finally, we speculate on how B cells might contribute to the development of DKD.

/pdf/b-cells-in-type-1-diabetes-mellitus-and-diabetic-kidney-54bs8ridj9.pdf

B cells in type 1 diabetes mellitus and diabetic kidney disease

The involvement of angiogenesis in disease and its potential as a therapeutic target have been firmly established over recent decades. Endothelial cells (ECs) are central elements in vessel homeostasis and regulate the passage of material and cells into and out of the bloodstream. EC proliferation and migration are modified by alterations to mitochondrial biogenesis and dynamics resulting from several signals and environmental cues, such as oxygen, hemodynamics, and nutrients. As intermediary signals, mitochondrial ROS are released as important downstream modulators of the expression of angiogenesis-related genes. In this review, we discuss the physiological actions of these signals and aberrant responses during vascular disorders.

Mitochondria in endothelial cells: Sensors and integrators of environmental cues.

Up-regulated lnc-SNHG1 contributes to osteosarcoma progression through sequestration of miR-577 and activation of WNT2B/Wnt/β-catenin pathway.

Fibroblast growth factor 21 (FGF21) is important in glucose, lipid homeostasis and insulin sensitivity. However, it remains unknown whether FGF21 is involved in insulin expression and secretion that are dysregulated in type 2 diabetes mellitus (T2DM). In this study, we found that FGF21 was down-regulated in pancreatic islets of db/db mice, a mouse model of T2DM, along with decreased insulin expression, suggesting the possible involvement of FGF21 in maintaining insulin homeostasis and islet β-cell function. Importantly, FGF21 knockout exacerbated palmitate-induced islet β-cell failure and suppression of glucose-stimulated insulin secretion (GSIS). Pancreatic FGF21 overexpression significantly increased insulin expression, enhanced GSIS, improved islet morphology and reduced β-cell apoptosis in db/db mice. Mechanistically, FGF21 promoted expression of insulin gene transcription factors and soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE) proteins, the major regulators of insulin secretion, as well as activating phosphatidylinositol 3-kinase (PI3K)/Akt signaling in islets of db/db mice. In addition, pharmaceutical inhibition of PI3K/Akt signaling effectively suppressed FGF21-induced expression of insulin gene transcription factors and SNARE proteins, suggesting an essential role of PI3K/Akt signaling in FGF21-induced insulin expression and secretion. Taken together, our results demonstrate a protective role of pancreatic FGF21 in T2DM mice through inducing PI3K/Akt signaling-dependent insulin expression and secretion.

https://www.onlinelibrary.wiley.com/doi/pdf/10.1111/jcmm.14007

Pancreatic fibroblast growth factor 21 protects against type 2 diabetes in mice by promoting insulin expression and secretion in a PI3K/Akt signaling‐dependent manner

Pancreatic β-cell dysfunction is a central component of the pathogenesis of pediatric diabetes. MicroRNA (miRNA) have become one of the most encouraging and fruitful fields in biological research, and have been implicated as new players in the pathogenesis of diabetes and diabetes-associated complications. The role of miRNA in diabetes begins with the development of pancreatic islets. Fibroblast growth factor (FGF)-21 enhances glucose uptake in adipocytes, protecting transgenic animals from diet-induced obesity when overexpressed, and lowers blood glucose and triglyceride levels in diabetic animals (when administered); therefore, it is a good way to treat diabetes. However, the mechanism of miRNA in regulation of FGF21 is not known. In this study, FGF-21 was predicted to be the target of miR-577. Therefore, we investigated the effects of miR-577 on β-cell function and survival by targeting FGF-21. We demonstrated that, although FGF-21 does not acutely stimulate insulin secretion in isolated islets from normal rats, it increases insulin secretion and insulin content in diabetic islets and protects β-cells from apoptosis via the activation of extracellular signal-regulated kinase 1/2 and Akt signaling pathways.

/pdf/mir-577-inhibits-pancreatic-b-cell-function-and-survival-by-3yr00awqlx.pdf

MiR-577 inhibits pancreatic β-cell function and survival by targeting fibroblast growth factor 21 (FGF-21) in pediatric diabetes.

Endothelial cells (ECs) apoptosis induced by hyperglycemia is intimately involved in the pathophysiology of diabetes and its complication Although PGC-1α is known for its role in glucose metabolism, its role in ECs injury caused by high glucose milieu is still unclear Therefore, this study aims to investigate whether PGC-1α participates in ECs apoptosis under high glucose condition Human umbilical vein endothelial cells (HUVECs) were down-regulated PGC-1α expression by adenovirus-mediated PGC-1α specific siRNA (Ad-shPGC-1α) and exposed to high glucose Cell viability, apoptosis, mitochondrial membrane permeability, apoptotic marker, reactive oxygen species (ROS), and expression of PGC-1α and VDAC isoforms were studied Our results showed that high glucose-induced cell apoptosis was associated with an obvious decrease in PGC-1α expression Lack of PGC-1α exacerbated high glucose-induced cell apoptosis, inner mitochondrial membrane permeabilization, mitochondrial cytochrome c release into cytoplasm and caspases activation; while further decreased cell viability and mitochondrial membrane potential Analysis of apoptotic markers (Bcl-2, Bax), intracellular ROS and endoplasmic reticulum stress revealed that these mechanisms were not accounted for the effects of Ad-shPGC-1α on apoptosis However, we found silencing PGC-1α further increased high glucose-induced VDAC1 expression The pharmacological inhibition of VDAC1 with 4,4’-diisothiocyanostilbene-2,2’-disulfonic acid (DIDS) inhibited the increased apoptosis in high glucose-treated PGC-1α knockdown cells These findings strongly suggest that PGC-1α defect is one of the major mechanisms for ECs apoptosis under high glucose condition, and provide a novel strategy to prevent endothelial dysfunction in diabetes

Lack of PGC-1α exacerbates high glucose-induced apoptosis in human umbilical vein endothelial cells through activation of VADC1.

The interleukin-1α (IL-1α) gene appears to play a role in the pathogenesis of type 1 diabetes (T1D). Therefore, the aim of this study was to investigate the contribution of the IL-1 rs1800587 gene polymorphism to susceptibility to T1D in Chinese children. This case-control study included 332 Chinese children with T1D and 332 healthy controls. Identification of genetic variants of rs1800587 in the IL-1α gene was performed by polymerase chain reaction amplification. The IL-1α rs1800587 polymorphism demonstrated a significant association with T1D risk. The allelic frequency significantly differed between the T1D and control groups [odds ratio (OR) = 0.7; 95% confidence interval (CI) = 0.52-0.86; P = 0.002]. Furthermore, significant differences were observed in the dominant model (CC/CT + TT; OR = 0.6; 95%CI = 0.46-0.85; P = 0.003). In T1D patients, the prevalence of hypertension in T allele carriers was 4.2-fold higher than that in C allele carriers, (95%CI = 2.67-6.58; P < 0.001). In conclusion, the present study found evidence of a significant association between the rs1800587 polymorphism in the IL-1α gene and T1D.

/pdf/association-of-il-1a-gene-polymorphism-with-susceptibility-rq3ga2dddt.pdf

Association of IL-1α gene polymorphism with susceptibility to type 1 diabetes in Chinese children.

Background
Several studies have reported the association of PTPN2 gene with type 1 diabetes mellitus (T1DM) in many populations but not in the Chinese Han population. Therefore, the goal of our study was to replicate the reported association between 2 single-nucleotide polymorphisms (SNPs; rs478582 and rs2542151) in the PTPN2 gene and T1DM in Chinese Han children.

/pdf/genetic-variants-of-ptpn2-gene-in-chinese-children-with-type-41xyxe606b.pdf

Genetic Variants of PTPN2 Gene in Chinese Children with Type 1 Diabetes Mellitus

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MiR-577 inhibits pancreatic β-cell function and survival by targeting fibroblast growth factor 21 (FGF-21) in pediatric diabetes.

Lack of PGC-1α exacerbates high glucose-induced apoptosis in human umbilical vein endothelial cells through activation of VADC1.

Association of IL-1α gene polymorphism with susceptibility to type 1 diabetes in Chinese children.

Genetic Variants of PTPN2 Gene in Chinese Children with Type 1 Diabetes Mellitus