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Microencapsulation Of Living Cells and Tissues
Published in Max Donbrow, Microcapsules and Nanoparticles in Medicine and Pharmacy, 2020
Anthony M. Sun, Ivan Vacek, Isaballa Tai
Although insulin therapy prolongs the lives of diabetic patients, it has failed to prevent the chronic complications of diabetes, such as retinopathy, neuropathy, nephropathy, and vascular disease, which, in turn cause premature death. The basic problem of immunological rejection has prevented whole-organ transplantation from being a practical alternative treatment for diabetes. Given these problems, the transplantation of pancreatic islets constitutes a promising approach to a cure. However, although islet transplantation offers many advantages over whole-organ transplantation, the problem of immunogenic rejection remains. One approach to overcoming this problem is the introduction of a semipermeable physical barrier between the transplanted islets and the host immune system. The potential clinical benefit of this approach is that diabetic patients would be provided with normal pancreatic islets which not only would be protected from immunorejection but would secrete, in addition to insulin, other hormones such as glucagon, somatostatin, pancreatic polypeptides and possibly other islet proteins — in response to physiological demand. Perhaps this therapy could ultimately prevent the development of diabetes-related complications and lead to a cure for the disease.
New Developments in Oral Insulin Delivery
Published in Emmanuel Opara, Controlled Drug Delivery Systems, 2020
Alec Jost, Mmesoma Anike, Emmanuel Opara
Insulin is a double-chain polypeptide synthesized by beta cells in the pancreatic islets that serve primarily to regulate the storage and processing of surplus serum glucose. It is released from storage vesicles within the Golgi along with cleavage product C-peptide under stimulation by elevated serum glucose as well as a variety of other signaling compounds including glucagon-like peptide 1 and acetylcholine (Wilcox 2005). The level of insulin release in response to an intravenous glucose bolus typically occurs in two phases – an initial burst release followed by prolonged basal secretion. Insulin release following oral glucose stimulation is markedly less predictable, in part due to the influence of other signaling molecules which are implicated in gastrointestinal activity (Donner 2000).
Biocatalyzed Synthesis of Antidiabetic Drugs
Published in Peter Grunwald, Pharmaceutical Biocatalysis, 2019
Diabetes mellitus (DM) is a disorder of metabolic homeostasis, showing hyperglycemia and altered lipid metabolism caused by dysfunction of pancreatic islets, which do not produce enough insulin (a hormone that regulates blood sugar, or glucose), or rather caused when the body cannot effectively use the insulin it produces (WHO, 2016). According to this, there are three main types of DM (Ramachandran et al., 2017): Type 1 DM (DM1) results from the inherent pancreas’s failure to produce enough insulin, being this type formerly known as “insulin-dependent diabetes mellitus” (IDDM) or “juvenile diabetes.”Type 2 DM (DM2) is caused by insulin resistance, and it was previously referred to as “non insulin-dependent diabetes mellitus” (NIDDM) or “adult-onset diabetes.”Finally, gestational diabetes is the third main form and occurs when pregnant women without a previous history of diabetes develop high blood-sugar levels.
Bio-medical potential of chalcone derivatives and their metal complexes as antidiabetic agents: a review
Published in Journal of Coordination Chemistry, 2021
The α-glucosidase converts dietary starch and complex carbohydrates (oligosaccharides and polysaccharides) into simple sugars viz. glucose by breaching the glycosidic bonds present in them and also delays carbohydrate digestion/absorption [45]. Alpha cells of the small intestine, especially α-glucosidase which is present predominantly in the proximal half [46], produces glucagon which upon gluconeogenesis produces glucose followed by its release to the bloodstream [47]. This increase of excess glucose in the bloodstream causes hyperglycemia and this leads to development of T2DM because of lack of response of adipose tissues to insulin. In detailed mechanism, excessive glutamate consumption with food disturbs the glutamate homeostatis and elevated glutamate concentrations activate the α-cells via AMPA/kinate receptors and stimulates glucagon secretion [48, 49]. Glucagon secreted by the pancreatic alpha cells of the pancreatic islets is the body’s principal hyperglycemic hormone. Glucagon secretion is also under paracrine control by insulin and follows the ‘switch-off’ hypothesis, which means hyper secretion of glucagon when insulin secretion is low [50]. This whole mechanism is shown in Figure 3 in the form of a cycle.
Fucoidan-based hydrogels particles as versatile carriers for diabetes treatment strategies
Published in Journal of Biomaterials Science, Polymer Edition, 2022
Lara L. Reys, Simone S. Silva, Diana Soares da Costa, Rui L. Reis, Tiago H. Silva
Diabetes mellitus is a life-threating disease that affects 450 million of people in the world, being the seventh most common cause of death. Diabetes is a metabolic disease characterized by abnormally high levels of glucose in the blood caused by insufficient production of insulin, or resistance to this hormone, which is secreted by β cells within the pancreatic islets [1, 2]. Etiologically, diabetes can be subdivided into different types, namely type I, type II, and gestational diabetes [3, 4], although recently some researchers suggested a more complex organization related with disease outcomes and associated complications [5]. Type I diabetes (T1D) is characterized by an absolute deficiency in the production of insulin by the pancreas, as a result of autoimmune destruction of the insulin-producing β cells. As insulin is the hormone promoting the uptake of glucose by cells, this sugar is not metabolized for the production of energy and hyperglycemia occurs, resulting in severe complications [6]. Without insulin treatment, T1D patients are exposed to the risk of death from acute ketoacidosis [7]. By its turn, type II diabetes (T2D) is characterized by the development of resistance to insulin by cells and, over time, insulin production by β-cells becomes insufficient to sustain a proper glucose metabolism [3, 8]. The pathogenesis of T2D is mainly associated with increasing age, unhealthy diets, obesity, and a sedentary lifestyle, which explains why the mainstay of both treatment and prevention of T2D is dieting and physical activity, although some anti-diabetic drugs can be also prescribed, as insulin sensitizers (as thiazolidinediones) or secretagogues (as sulphonyreas) [1, 9].