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Topic Review
Type I Diabetes Pathoetiology and Pathophysiology
Type 1 diabetes mellitus (T1DM) arises from the failure of pancreatic β-cells to produce adequate insulin, usually as a consequence of extensive pancreatic β-cell destruction. T1DM is classed as an immune-mediated condition. However, the processes that drive pancreatic β-cell apoptosis remain to be determined, resulting in a failure to prevent ongoing cellular destruction. Alteration in mitochondrial function is clearly the major pathophysiological process underpinning pancreatic β-cell loss in T1DM. This entry highlights the role of intercellular interactions among different cell types in pancreatic islets. It is proposed that the pathoetiology of T1DM arises from mitochondrial interactions among different pancreatic cells, leaving pancreatic B-cells with suppressed capacity to induce the mitochondrial melatonergic pathway, with the associated decrease in pancreatic B-cell melatonin leading to suboptimal mitochondrial function and increased oxidative stress that suppresses PINK1/parkin/mitophagy, leading increased major histocompatibility complex (MHC)-1. This results in the chemoattraction of CD8+ T cells and immune-mediated cell destruction. Variations in different gut bacteria and fungi contribute to pancreatic B-cell loss via their impacts on mitochondrial function within the interacting cells of the pancreatic islets. T1DM may therefore be more of a ‘mitochondria/metabolic’ disorder than an ‘autoimmune’ or ‘immune-mediated’ disorder.
  • 293
  • 15 Feb 2023
Topic Review
Type I Diabetes Mellitus
A considerable endeavor had taken place in order to understand the associated challenges for children and adolescents with Specific Learning Disorder (SLD) and Type 1 Diabetes Mellitus (T1DM) but also in order to describe the necessary skills and approaches that the care givers have to develop to assist both children and parents.
  • 763
  • 14 Feb 2021
Topic Review
Type 2 Diabetes with Metabolic Syndrome in Youth
In the frame of metabolic syndrome, type 2 diabetes emerges along a continuum of the risk from the clustering of all its components, namely visceral obesity, high blood pressure and lipids, and impaired glucose homeostasis. Insulin resistance is the hallmark common to all the components and, in theory, is a reversible condition. Nevertheless, the load that this condition can exert on the β-cell function at the pubertal transition is such as to determine its rapid and irreversible deterioration leading to plain diabetes.
  • 273
  • 06 May 2023
Topic Review
Type 2 Diabetes Pathogenesis
Since the discovery of insulin a century ago, insulin injection has been a primary treatment for both type 1 (T1D) and type 2 diabetes (T2D). T2D is a complicated disease that is triggered by the dysfunction of insulin-producing β cells and insulin resistance in peripheral tissues. Insulin injection partially compensates for the role of endogenous insulin which promotes glucose uptake, lipid synthesis and organ growth.
  • 289
  • 20 Mar 2023
Topic Review
Type 2 Diabetes and Postprandial Dysmetabolism
The postprandial state is known as the metabolic assessment period during and after a meal (6–12 h), which involves the digestion and absorption of nutrients, mainly fatty acids and carbohydrates from food. This state spans most of the day, more than 16 h, and is characterized by an increase in glycemia and lipidemia associated with systemic low-grade inflammation. Inflammation is an essential component of innate (nonspecific) immunity and host defense, but a chronic systemic low-grade inflammatory state is also the basis of the metabolic syndrome.
  • 180
  • 19 Dec 2023
Topic Review
Type 2 Diabetes and P450
 The most frequent form of diabetes is type 2 diabetes mellitus (T2DM) which is often part of a metabolic syndrome (hyperglycaemia, hypertension, hypercholesterolemia, abdominal obesity) that usually requires the use of several medications from different drug classes to bring each of these conditions under control. T2DM is associated with an increase in inflammatory markers such as interleukin-6 (IL-6) and the tumor necrosis factor alpha (TNF-α). Higher levels of IL-6 and TNF-α are associated with a downregulation of several drug metabolizing enzymes, especially the cytochrome P450 (P450) isoforms CYP3As and CYP2C19. A decrease in these P450 isoenzymes may lead to unexpected rise in plasma levels of substrates of these enzymes. It could also give rise to a mismatch between the genotypes determined for these enzymes, the predicted phenotypes based on these genotypes and the phenotypes observed clinically. This phenomenon is described as phenoconversion. Phenoconversion typically results from either a disease (such as T2DM) or concomitant administration of medications inducing or inhibiting (including competitive or non-competitive inhibition) a P450 isoenzyme used by other substrates for their elimination. Phenoconversion could have a significant impact on drug effects and genotypic-focused clinical outcomes.
  • 655
  • 11 Oct 2021
Topic Review
Type 2 Cystatins in Human Immune and Cancer
Type 2 cystatins are a group of small secreted protease inhibitors that regulate cysteine protease cathepsins and legumain. These enzymes regulate important cellular processes that are linked to the immune response and tumor progression, playing important roles in both autoimmune diseases and various types of cancers. Cysteine cathepsins are associated with the development of autoimmune diseases, tumor progression, and metastasis. Cystatins are categorized into three subfamilies: type 1, type 2, and type 3. The type 2 cystatin subfamily is the largest, containing 10 members, and consists entirely of small secreted proteins. Although type 2 cystatins have many shared biological roles, each member differs in structure, post-translational modifications (e.g., glycosylation), and expression in different cell types. These distinctions allow the type 2 cystatins to have unique biological functions and properties.
  • 156
  • 01 Dec 2023
Topic Review
Type 1 Diabetes Mellitus
Patients with type 1 diabetes mellitus (T1DM) present elevated levels of cytokines including interleukin-1a (IL), IL-1β, IL-2, IL-6 and tumor necrosis factor alpha (TNF-α), suggesting the pre-existence of chronic inflammation, which, in turn, has been considered the major risk factor of adverse COVID-19 outcomes in many cohorts. Even more importantly, oxidative stress is a key player in COVID-19 pathogenesis and determines disease severity. It is well-known that extreme glucose excursions, the prominent feature of T1DM, are a potent mediator of oxidative stress through several pathways including the activation of protein kinase C (PKC) and the increased production of advanced glycation end products (AGEs). Additionally, chronic endothelial dysfunction and the hypercoagulant state observed in T1DM, in combination with the direct damage of endothelial cells by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), may result in endothelial and microcirculation impairment, which contribute to the pathogenesis of acute respiratory syndrome and multi-organ failure. The binding of SARS-CoV-2 to angiotensin converting enzyme 2 (ACE2) receptors in pancreatic b-cells permits the direct destruction of b-cells, which contributes to the development of new-onset diabetes and the induction of diabetic ketoacidosis (DKA) in patients with T1DM. Large clinical studies are required to clarify the exact pathways through which T1DM results in worse COVID-19 outcomes. 
  • 486
  • 19 May 2021
Topic Review
Tyk2 Targeting in Immune-Mediated Inflammatory Diseases
Genetic linkage has related dysfunction of Tyrosine kinase 2 (Tyk2)—the first member of the Jak family that was described—to protection from psoriasis. Furthermore, Tyk2 dysfunction has been related to IMID prevention, without increasing the risk of serious infections; thus, Tyk2 inhibition has been established as a promising therapeutic target, with multiple Tyk2 inhibitors under development.
  • 739
  • 20 Feb 2023
Topic Review
TYK2 in Cancer Metastases
Genomic, transcriptomic and proteomic assays have led to identification of tyrosine kinase 2 (TYK2) mutations, fusion proteins and expression changes in a variety of hematological cancers, carcinomas and soft-tissue sarcomas. TYK2 is an approximately 134 kDa protein identified in 1990 as the first member of the Janus kinase (JAK) family, which includes non-receptor tyrosine kinases that mediate cytokine signaling. In humans, the TYK2 gene is found on chromosome 19, and is ubiquitously expressed at varying levels throughout the body.
  • 444
  • 30 Aug 2021
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