In the last decade, the incidence of diabetes in Canada has nearly doubled and is now estimated to affect one in three individuals. Type 2 diabetes (T2D) is a serious public health problem: governments and health care professional are working to control its propagation, offer better treatment alternatives and reduce its impact on patient quality of life. Insulin resistance is an early event in the development of T2D. Due to its mass and important role in the maintenance of glucose homeostasis, skeletal muscle is believed to play a central role in the development of insulin resistance. The development of this metabolic disorder is multifaceted with obesity, physical activity and diet receiving the most research interest. It is recognized that mitochondrial dysfunction, increased oxidative stress and inflammation are implicated in the development of insulin resistance in muscle. Recently, the environmental hypothesis has been advanced to explain the increased number of patients with T2D. Various persistent organic pollutants (POPs), such as polychlorinated biphenyls (PCBs), bisphenol A (BPA) and p, p-dichlorodiphenylchloroethane (DDT) are being investigated in their relation to T2D. However, despite the importance of skeletal muscle in the development of insulin resistance and T2D, very few studies have focused on the effect of POPs on skeletal muscle energy metabolism. This review will highlight the implication of POPs in the development of diabetes and present work being done to asses POPs’ involvement in observed metabolic disarrangements, specifically at the level of skeletal muscle.

https://ccsenet.org/journal/index.php/enrr/article/download/64352/34621

Role of Environmental Pollutants in Skeletal Muscle Insulin Resistance and Mitochondrial Dysfunction

A diverse combination of etiologies such as vascular and inflammatory factors and social and physical inactivity may take place in the etiology of cognitive dysfunction (CD) Diabetes mellitus (DM) may contribute to CD over insulin resistance, inflammation, and vascular risk factors However, mechanisms included in the process are not very clear We aimed to investigate serum levels of selected biomarkers as a proliferation-inducing ligand (APRIL), FGF-21, P-selectin, soluble vascular cell, and intercellular adhesion molecules-1 (sVCAM-1 and sICAM-1) in elderly patients with DM in relation to cognitive function A group of 80 elderly type 2 diabetic patients from the outpatient clinic, consisting of 40 patients with CD (mini-mental state examination (MMSE) score < 24) and 40 individuals without CD were enrolled in the study Anthropometric, sociodemographic, and functional-glycemic evaluations were determined Biomarker levels were determined by enzyme-linked immunosorbent assay Median sICAM-1 and FGF-21 levels were higher, and P-selectin level, activities of daily living (ADL), instrumental ADL, MNA, and MMSE scores were lower in the CD group (p = 0002, p = 0010, p = 0001, p = 0001, p < 0001, p = 0005, p < 0001, respectively) There was no significant difference between the groups regarding age, gender, living status, education, cigarette and alcohol consumption, antidiabetic therapy as well as comorbidities such as hypertension and other diseases, depression, body composition, sVCAM-1, APRIL levels, and related biochemical values Median sICAM-1 and FGF-21 levels were higher and P-selectin level was lower in older diabetic patients with CD than in patients with normal cognitive status Understanding the mechanisms may lead to the prevention or delay of CD in those patients

Human APRIL and FGF-21 and adhesion molecules in relation to cognitive function in elderly diabetic patients

APRIL (A Proliferation-Inducing Ligand), a member of the TNF superfamily, was initially described for its ability to promote proliferation of tumor cells in vitro. Moreover, this cytokine has been related to the pathogenesis of different chronic inflammatory diseases, such as rheumatoid arthritis. This study aimed to evaluate the ability of APRIL in regulating B cell-mediated immune response in the antigen-induced arthritis (AIA) model in mice. AIA was induced in previously immunized APRIL-transgenic (Tg) mice and their littermates by administration of antigen (mBSA) into the knee joints. Different inflammatory cell populations in spleen and draining lymph nodes were analyzed using flow cytometry and the assay was performed in the acute and chronic phases of the disease, while cytokine levels were assessed by ELISA. In the acute AIA, APRIL-Tg mice developed a less severe condition and a smaller inflammatory infiltrate in articular tissues when compared with their littermates. We also observed that the total cellularity of draining lymph nodes was decreased in APRIL-Tg mice. Flow cytometry analysis revealed an increase of CD19+IgM+CD5+ cell population in draining lymph nodes and an increase of CD19+CD21hiCD23hi (B regulatory) cells in APRIL-Tg mice with arthritis as well as an increase of IL-10 and CXCL13 production in vitro. 

Anti-inflammatory role of APRIL by modulating regulatory B cells in antigen-induced arthritis

Hashimoto’s thyroiditis (HT) is an autoimmune and inflammatory disease in which antibodies are directed against the thyroid gland leading to chronic inflammation and hypothyroidism. The autoimmunity against thyroid antigens can be associated to genetic background and environmental factors. Thyroid peroxidase (TPO) and thyroglobulin (TG) are the major autoantigens for characterizing the disease. And the pathogenic mechanism is related to the activation of autoreactive CD4+ T cells, CD8+ cytotoxic T cells and antithyroid antibody producing-B cells. The treatment for hypothyroidism is based on thyroid hormone replacement, the levothyroxine. This review briefly discusses the clinical and pathogenic profile of HT and the importance of a correct diagnostics.

/pdf/current-concepts-in-endocrinology-for-clinicians-and-medical-4e3c1v73em.pdf

Current Concepts in Endocrinology for Clinicians and Medical Students. Hashimoto’s Thyroiditis: clinical and subclinical thyroid dysfunction

/pdf/role-of-adipose-to-muscle-communication-in-pcb126-induced-588kv3eo11.pdf

Role of Adipose-to-Muscle Communication in PCB126-induced Metabolic Defects

Diabetes mellitus is a chronic disease that affects over 382 million people worldwide. Type-1 Diabetes (T1D) is classified as an autoimmune disease that results from pancreatic β-cell destruction and insulin deficiency. Type-2 Diabetes (T2D) is characterized principally by insulin resistance in target tissues followed by decreased insulin production due to β-cell failure. It is challenging to identify immunological markers such as inflammatory molecules that are triggered in response to changes during the pathogenesis of diabetes. APRIL is an important member of the TNF family and has been linked to chronic inflammatory processes of various diseases since its discovery in 1998. Therefore, this study aimed to evaluate APRIL serum levels in T1D and T2D. For this, we used the ELISA assay to measure serum APRIL levels of 33 T1D and 30 T2D patients, and non-diabetic subjects as control group. Our data showed a decrease in serum APRIL levels in T1D patients when compared with healthy individuals. The same pattern was observed in the group of T2D patients when compared with the control. The decrease of serum APRIL levels in diabetic patients suggests that this cytokine has a role in T1D and T2D. Diabetes is already considered as an inflammatory condition with different cytokines being implicated in its physiopathology. Our data suggest that APRIL can be considered as a potential modulating cytokine in the inflammatory process of diabetes.

/pdf/decreased-circulating-levels-of-april-questioning-its-role-1g2elzjzfc.pdf

Decreased Circulating Levels of APRIL: Questioning Its Role in Diabetes

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Decreased Circulating Levels of APRIL: Questioning Its Role in Diabetes