China 
Africa 
Explore chapters and articles related to this topic
Diabetes Mellitus, Obesity, Lipoprotein Disorders and other Metabolic Diseases
Published in John S. Axford, Chris A. O'Callaghan, Medicine for Finals and Beyond, 2023
Up to 1 in 10 patients with type 1 diabetes experience a ‘honeymoon’ phase after starting on insulin therapy – blood glucose levels fall into the normal range and insulin doses either substantially reduce or even stop. This is thought to be due to elimination of any ‘glucose toxicity’ to the pancreas due to hyperglycaemia. In 90% of cases the honeymoon phase lasts <1 year. Transplantation of purified human pancreatic islet cells has been used to ameliorate type 1 diabetes, but the effect wanes, often over a few years. Pancreatic transplantation can reverse type 1 diabetes but, due to the surgical risks and need for immunosuppression, this is usually reserved for patients requiring a kidney transplant for diabetic kidney disease.
Nanotechnology in Stem Cell Regenerative Therapy and Its Applications
Published in Harishkumar Madhyastha, Durgesh Nandini Chauhan, Nanopharmaceuticals in Regenerative Medicine, 2022
Multipotent pancreatic stem cells (PSCs) are isolated from the human foetal pancreas, derived from the foregut endoderm and reformed into progenitor lineages, essential for the growing pancreas (Jiang and Morahan 2014). Islet cell transplantation can reverse the damage of pancreatic islets cells in Type 1 diabetes (Ma et al. 2008).
Beta Cells and Diabetes
Published in Raj K. Keservani, Anil K. Sharma, Rajesh K. Kesharwani, Nutraceuticals and Dietary Supplements, 2020
Shivani Srivastava, Durgavati Yadav, Kumar Sandeep, Harsh Pandey, Surya Kumar Singh, Yamini Bhusan Tripathi
GLUT-2 is essential for GSIS. GLUT-2-dependent glucose-sensing controls pancreatic islet cell mass and function through the nervous system. GSIS and glucose uptake get suppressed by genetic inactivation of GLUT in beta cells of rodents (Thorens, 2015).
A primer on modelling pancreatic islets: from models of coupled β-cells to multicellular islet models
Published in Islets, 2023
Gerardo J. Félix-Martínez, J. Rafael Godínez-Fernández
Pancreatic islets, also known as islets of Langerhans, are mainly composed of ɑ, β and δ-cells, endocrine cells that secrete glucagon, insulin and somatostatin, respectively, critical hormones for the regulation of blood glucose. Insulin, the only hormone capable of reducing glucose levels directly, is secreted when blood glucose rises, producing its hypoglycemic effect by promoting the uptake of glucose by hepatic, muscular and adipose tissues. On the contrary, glucagon is secreted when blood glucose decreases, promoting the release of the stored glucose (i.e., glycogen) mainly from the liver to restore the normal glucose levels. Finally, somatostatin, secreted by δ-cells, is not involved in the regulation of blood glucose directly, although it has a relevant indirect role by inhibiting the secretion of both glucagon and insulin from ɑ and β-cells, respectively.1
Species-dependent impact of immunosuppressive squalene-gusperimus nanoparticles and adipose-derived stem cells on isolated human and rat pancreatic islets
Published in Islets, 2022
Carlos E. Navarro Chica, Tian Qin, Erika Pinheiro-Machado, Bart J. de Haan, M.M. Faas, Alexandra M. Smink, Ligia Sierra, Betty L. López, Paul de Vos
Transplantation of pancreatic islets is a promising alternative for exogenous insulin in patients with type 1 diabetes mellitus (T1DM). The advantage of islet transplantation over other therapies is that it regulates glucose on a minute-to-minute level.1 This approach has reached a certain degree of success, but its broad application is hampered by the high variation in the survival rate of the islets after the grafting procedure. The high variation has been attributed to factors such as differences in islet quality but also sensitivity to hypoxia and low nutrient conditions after implantation as well as to the cellular and humoral response triggered after transplantation.1,2 To overcome this, many strategies have been proposed to increase islet survival. Among these strategies is the use of new, safe immunosuppressive agents that are released in a controlled fashion to provide an anti-inflammatory microenvironment around islets in the transplantation site as well as the use of mesenchymal stromal cells that have shown to increase islets survival rate.3–9
Reconstructing human pancreatic islet architectures using computational optimization
Published in Islets, 2020
Gerardo J. Félix-Martínez, Aurelio N. Mata, J. Rafael Godínez-Fernández
Pancreatic islets constitute the endocrine part of the pancreas and are essential for glucose homeostasis. It has been estimated that a healthy human pancreas has ∼3 million islets dispersed throughout the pancreas with a mean diameter of 108.9 ± 6.2 μm.1 Pancreatic islets are mainly composed of insulin-producing β-cells (∼65%), glucagon- producing α-cells (∼30%) and somatostatin-producing δ-cells (∼5%),2,3 with other cells such as the ghreling-producing ε-cells4 and the pancreatic polypeptide-producing (PP-) cells5 also present but in a much lower proportion than the α, β and δ-cells.6 Insulin is the only hormone capable of lowering glucose levels directly and glucagon is the main hyperglycemic hormone.7 Somatostatin, on the other hand, inhibits both insulin and glucagon secretion, thus participating indirectly in the regulation of glucose levels.8–10