scholarly journals Drugs from the Sea: A Marine Sponge-Derived Compound Prevents Type 1 Diabetes

2001 ◽  
Vol 1 ◽  
pp. 630-632 ◽  
Author(s):  
Luc Van Kaer

More than one million Americans have Type 1 diabetes. This disease — also known as autoimmune or juvenile diabetes — strikes children suddenly, makes them dependent on insulin injections for life, and carries the constant threat of devastating complications. While it can and does strike adults, nearly half of all new cases are diagnosed in children. A child is diagnosed with Type 1 diabetes every hour. Type 1 diabetes is caused by the inability of a person’s pancreas to produce sufficient amounts of insulin to control their blood sugar levels and sustain life. While insulin injections allow affected individuals to control their blood sugar and stay alive, it is not a cure nor does it prevent the devastating complications of this disease, which include kidney failure, blindness, amputations, heart attack, and stroke. In Type 1 diabetes, the body’s own immune system goes awry, attacking and destroying insulin-producing cells in the pancreas.

Author(s):  
Suguru Watanabe ◽  
Jun Kido ◽  
Mika Ogata ◽  
Kimitoshi Nakamura ◽  
Tomoyuki Mizukami

Summary Hyperglycemic hyperosmolar state (HHS) and diabetic ketoacidosis (DKA) are the most severe acute complications of diabetes mellitus (DM). HHS is characterized by severe hyperglycemia and hyperosmolality without significant ketosis and acidosis. A 14-year-old Japanese boy presented at the emergency room with lethargy, polyuria and polydipsia. He belonged to a baseball club team and habitually drank sugar-rich beverages daily. Three weeks earlier, he suffered from lassitude and developed polyuria and polydipsia 1 week later. He had been drinking more sugar-rich isotonic sports drinks (approximately 1000–1500 mL/day) than usual (approximately 500 mL/day). He presented with HHS (hyperglycemia (1010 mg/dL, HbA1c 12.3%) and mild hyperosmolality (313 mOsm/kg)) without acidosis (pH 7.360), severe ketosis (589 μmol/L) and ketonuria. He presented HHS in type 1 diabetes mellitus (T1DM) with elevated glutamate decarboxylase antibody and islet antigen 2 antibody. Consuming beverages with high sugar concentrations caused hyperglycemia and further exacerbates thirst, resulting in further beverage consumption. Although he recovered from HHS following intensive transfusion and insulin treatment, he was significantly sensitive to insulin therapy. Even the appropriate amount of insulin may result in dramatically decreasing blood sugar levels in patients with T1DM. We should therefore suspect T1DM in patients with HHS but not those with obesity. Moreover, age, clinical history and body type are helpful for identifying T1DM and HHS. Specifically, drinking an excess of beverages rich in sugars represents a risk of HHS in juvenile/adolescent T1DM patients. Learning points: Hyperglycemic hyperosmolar state (HHS) is characterized by severe hyperglycemia and hyperosmolality without significant ketosis and acidosis. The discrimination between HHS of type 1 diabetes mellitus (T1DM) and type 2 diabetes mellitus (T2DM) in initial presentation is difficult. Pediatrician should suspect T1DM in patients with HHS but not obesity. Age, clinical history and body type are helpful for identifying T1DM and HHS. Children with T1DM are very sensitive to insulin treatment, and even appropriate amount of insulin may result in dramatically decreasing blood sugar levels.


2004 ◽  
Vol 7 (2) ◽  
pp. 14-19
Author(s):  
CAMILLO RICORDI

The discovery of insulin changed the course of history in the treatment of diabetes. However, despite tremendous progress in insulin formulations and treatment strategies, insulin treatment still cannot fully prevent chronic complications and intensive insulin treatment to improve metabolic control, has often paralleled an increased risk of severe hypoglycemia. A cure for Type 1 diabetes should include: ? Restoration of self tolerance, to prevent recurrence of autoimmunity ? Restoration of physiologic metabolism by replacement of the biologic function (insulin producing cells) that was partially of completely impaired as a result of the disease process. ? Prevention of destruction of the new insulin producing cells by the recipient immune system in the absence of any treatment that could introduce an additional risk to the patient, which could be comparable to, or higher than the risk imposed by disease progression under exogenous insulin treatment. Pancreatic islets could be considered an ideal and more physiologic alternative to insulin, as they can restore metabolic control after transplantation, preventing the development of chronic complications. In fact, islets are capable of perfectly timed insulin release and can keep glucose levels in the normal range, functioning for an entire lifetime, if they are not destroyed by the recipient's immune system. Significant progress has been recently reported in the translational research approach towards the development of a cure for Type 1 diabetes. There is now strong evidence for the technical feasibility of human islet isolation and purification procedures. Proof of function of isolated human islets has been clearly established both in animal models and in pilot clinical trials of human islet allotransplantation in patients with surgical and Type 1 diabetes. Additional research in now needed to improve the current clinical results in terms of long term prevention of rejection and recurrence of autoimmunity, the development of safe, non diabetogenic immunomodulation strategies and ultimately the achievement of donor specific immune tolerance. If success will be achieved in these areas, then we will face the critical challenge of identifying sufficient and suitable sources of insulin producing tissue to treat the increasing number of patients who could benefit from this form of therapy and which would not be limited to Type 1 diabetes. That is why the work on xenogeneic islets, embryonic and adult stem cells, islet regeneration and proliferation, as well as engineering of insulin producing cells must be continued, to identify the most ideal source of insulin producing tissue that could be utilized on a large scale once the impediments and limitations of immunosuppression will be resolved.


Type1 diabetes is a sickness occurs when your immune system fighting against infection, affects and erode the insulin generating beta cells of the pancreas. In general, when the blood sugar stage increases, the pancreas makes more insulin. Insulin helps to go sugar out of the blood so it can be used for liveliness. Type 1 diabetes occurs due to the immune system which affects cells in the pancreas that make insulin. The pancreas cannot make adequate insulin, so the blood sugar level continues to increase. According to the children history of type 1 diabetes may enhance risk of their life. Type 1 diabetes cannot be cured, but it can be controlled and managed. In this study we use Naive Bayes, linear regression and k-means algorithm for data analysis and prediction. It predicts the diabetes affected children with maximum level of accuracy 96% by using of data mining algorithms.


2016 ◽  
Vol 22 (2) ◽  
pp. 158-163 ◽  
Author(s):  
Leehu Zysberg ◽  
Tal Bar Yoseph ◽  
Mor Goldman

Type 1 diabetes is a lifelong physical and emotional challenge. The concept of emotional intelligence may offer better understanding of personal resources facilitating management of such challenges. We therefore hypothesized that emotional intelligence will negatively associate with two measures of diabetic management: HA1c and blood sugar levels. A total of 78 young adults with type 1 diabetes mellitus reported their last HA1c test result and their blood sugar level, as well as demographics and took the audio-visual test of emotional intelligence. The results showed a negative association between emotional intelligence and HA1c and marginal results in the same direction with blood sugar levels even when controlling for demographics.


Author(s):  
Matthew J. Simmonds ◽  
Stephen C. L. Gough

Dysfunction within the endocrine system can lead to a variety of diseases with autoimmune attack against individual components being some of the most common. Endocrine autoimmunity encompasses a spectrum of disorders including, e.g., common disorders such as type 1 diabetes, Graves’ disease, Hashimoto’s thyroiditis, and rarer disorders including Addison’s disease and the autoimmune polyendocrine syndromes type 1 (APS 1) and type 2 (APS 2) (see Table 1.6.1). Autoimmune attack within each of these diseases although aimed at different endocrine organs is caused by a breakdown in the immune system’s ability to distinguish between self and nonself antigens, leading to an immune response targeted at self tissues. Investigating the mechanisms behind this breakdown is vital to understand what has gone wrong and to determine the pathways against which therapeutics can be targeted. Before discussing how self-tolerance fails, we first have to understand how the immune system achieves self-tolerance.


2019 ◽  
Vol 7 (3) ◽  
pp. 67 ◽  
Author(s):  
Sidharth Mishra ◽  
Shaohua Wang ◽  
Ravinder Nagpal ◽  
Brandi Miller ◽  
Ria Singh ◽  
...  

Type 1-diabetes (T1D) is an autoimmune disease characterized by immune-mediated destruction of pancreatic beta (β)-cells. Genetic and environmental interactions play an important role in immune system malfunction by priming an aggressive adaptive immune response against β-cells. The microbes inhabiting the human intestine closely interact with the enteric mucosal immune system. Gut microbiota colonization and immune system maturation occur in parallel during early years of life; hence, perturbations in the gut microbiota can impair the functions of immune cells and vice-versa. Abnormal gut microbiota perturbations (dysbiosis) are often detected in T1D subjects, particularly those diagnosed as multiple-autoantibody-positive as a result of an aggressive and adverse immunoresponse. The pathogenesis of T1D involves activation of self-reactive T-cells, resulting in the destruction of β-cells by CD8+ T-lymphocytes. It is also becoming clear that gut microbes interact closely with T-cells. The amelioration of gut dysbiosis using specific probiotics and prebiotics has been found to be associated with decline in the autoimmune response (with diminished inflammation) and gut integrity (through increased expression of tight-junction proteins in the intestinal epithelium). This review discusses the potential interactions between gut microbiota and immune mechanisms that are involved in the progression of T1D and contemplates the potential effects and prospects of gut microbiota modulators, including probiotic and prebiotic interventions, in the amelioration of T1D pathology, in both human and animal models.


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