"as digestive chymotrypsinogen enzymes and pancreatic lipase PNLIP, or expressed in the various cells of the endocrine pancreatic islets and have functions related to secreted hormones such as insulin, glucagon, somatostatin and pancreatic polypeptide. A perforation of the pancreas, which may lead to the secretion of digestive enzymes such as lipase and amylase into the abdominal cavity as well as subsequent pancreatic self-digestion and digestion and damage to organs within the abdomen, generally requires prompt and experienced medical intervention. It is possible for one to live without a pancreas, provided that the person takes insulin for proper regulation of blood"
"the pancreas islets appear to be the major if not only site where ALOX12 is expressed in these patients. The studies propose that in the islets of Langerhans ALOX12 and its 12(""S"")-HETE product cause excessive production of reactive oxygen species and inflammation which lead to losses in insulin-secreting beta cells and thereby types 1 and 2 diabetes and that in adipose tissue the excess in AlOX12, 12(""S"")-HETE, reactive oxygen species, and inflammation lead to fat cell dysfunction (also see 12-HETE#Inflammation and inflammatory diseases and 12-HETE#Diabetes). Indeed, in one study a Single-nucleotide polymorphism, rs2073438, located in an intron region of the"
"in promoting leukocytic infiltration into the pancreas prior to pancreatic beta-cell destruction. Insulitis Insulitis is an inflammation of the islets of Langerhans, a collection of endocrine tissue located in the pancreas. The islets containing the pancreatic β-cells, and in some cases, the exocrine tissues, become infiltrated by T and B lymphocytes, macrophages and dendritic cells. This innate immune cell and lymphocyte infiltration can result in destruction of the insulin producing beta cells of the islets, and clinical diabetes. Insulitis is often studied in the multiple low dose streptozotocin (MLDS) mouse model or the non-obese diabetic (NOD) mouse model of type"
"it is reduced to fragments, whereupon all activity is lost. There has been some research into ways to protect insulin from the digestive tract, so that it can be administered orally or sublingually. In 1869, while studying the structure of the pancreas under a microscope, Paul Langerhans, a medical student in Berlin, identified some previously unnoticed tissue clumps scattered throughout the bulk of the pancreas. The function of the ""little heaps of cells"", later known as the ""islets of Langerhans"", initially remained unknown, but Édouard Laguesse later suggested they might produce secretions that play a regulatory role in digestion. Paul"
"region called Islets of Langerhans. In the islets of Langerhans, there are beta-cells, which are responsible for production and storage of insulin. Insulin is secreted as a response mechanism for counteracting the increasing excess amounts of glucose in the blood. Glucose in the body increases after food consumption. This is primarily due to carbohydrate intake, but to a much lesser degree protein intake ()(). Depending on the tissue type, the glucose enters the cell through facilitated or passive diffusion. In muscle and adipose tissue, glucose enters through GLUT 4 receptors via facilitated diffusion (). In brain, kidney and retina, glucose"
"Insulitis Insulitis is an inflammation of the islets of Langerhans, a collection of endocrine tissue located in the pancreas. The islets containing the pancreatic β-cells, and in some cases, the exocrine tissues, become infiltrated by T and B lymphocytes, macrophages and dendritic cells. This innate immune cell and lymphocyte infiltration can result in destruction of the insulin producing beta cells of the islets, and clinical diabetes. Insulitis is often studied in the multiple low dose streptozotocin (MLDS) mouse model or the non-obese diabetic (NOD) mouse model of type 1 diabetes. The chemokine family of proteins may play a key role"
"in the blood which was then excreted in urine. Attempts to extract insulin from ground-up pancreas cells were unsuccessful, likely because of the destruction of the insulin by the proteolysis enzyme of the pancreas. The challenge was to find a way to extract insulin from the pancreas prior to its being destroyed. Moses Barron published an article in 1920 which described experimental closure of the pancreatic duct by ligature; this further influenced Banting's thinking. The procedure caused deterioration of the cells of the pancreas that secrete trypsin which breaks down insulin, but it left the islets of Langerhans intact. Banting"
"islet of Langerhans and in rat β TC3 cells. Research has shown that in the pancreases of Type II diabetic mouse models, there is a deficiency of C16:0. Additional research has shown that C16:0 plays an important role in assisting to improve insulin crystal preservation, and as the β cells in the pancreas secrete insulin, sulfatide aids in the monomerization of insulin, which is the breakdown of insulin into its basics components or monomers. Consequently, sulfatide is needed in order to maintain normal insulin secretion, which sulfatide is capable of mediating through stimulation of calcium dependent exocytosis and adenosine triphosphate"
"effect of increasing glucose uptake and storage. Finally, insulin is degraded, terminating the response. In mammals, insulin is synthesized in the pancreas within the beta cells. One million to three million pancreatic islets form the endocrine part of the pancreas, which is primarily an exocrine gland. The endocrine portion accounts for only 2% of the total mass of the pancreas. Within the pancreatic islets, beta cells constitute 65–80% of all the cells. Insulin consists of two polypeptide chains, the A- and B- chains, linked together by disulfide bonds. It is however first synthesized as a single polypeptide called preproinsulin in"
"Paul Langerhans Paul Langerhans (25 July 1847 – 20 July 1888) was a German pathologist, physiologist and biologist, credited with the discovery of the cells that secrete insulin, named after him as the islets of Langerhans. Langerhans was born in Berlin on 25 July 1847, the son of a physician. He later entered the renowned Graues Kloster in the same city. Due to his outstanding performance he was exempted from the final oral examinations. He began his medical studies at the University of Jena and completed them in Berlin. In February 1869, he presented a thesis entitled “Contributions to the"
"alpha cells. The insulin concentration within the fetal pancreas is 3.6 pmol/g at seven to ten weeks, which rises to 30 pmol/g at 16–25 weeks of gestation. Near term, the insulin concentration increases to 93 pmol/g. The endocrine cells have dispersed throughout the body within 10 weeks. At 31 weeks of development, the islets of Langerhans have differentiated. While the fetal pancreas has functional beta cells by 14 to 24 weeks of gestation, the amount of insulin that is released into the bloodstream is relatively low. In a study of pregnant women carrying fetuses in the mid-gestation and near term"
"moves through the digestive system). The pancreatic islets make up the endocrine part of the pancreas, and synthesize and secrete hormones including insulin into the bloodstream. There is evidence that the beta cells in the islets that synthesize insulin contain dopamine receptors, and that dopamine acts to reduce the amount of insulin they release. The source of their dopamine input is not clearly established—it may come from dopamine that circulates in the bloodstream and derives from the sympathetic nervous system, or it may be synthesized locally by other types of pancreatic cells. Dopamine as a manufactured medication is sold under"
"These supply the head of the pancreas. The body and neck of the pancreas drain into the splenic vein; the head drains into the superior mesenteric and portal veins. The pancreas contains tissue with an endocrine and exocrine role, and this division is also visible when the pancreas is viewed under a microscope. The tissues with an endocrine role can be seen under staining as lightly-stained clusters of cells, called pancreatic islets (also called islets of Langerhans). Darker-staining cells form clusters called acini, which are arranged in lobes separated by a thin fibrous barrier. The secretory cells of each acinus"
"only amino acid change mutations found in the B domain lead to the disease. Proinsulin Proinsulin is the prohormone precursor to insulin made in the beta cells of the islets of Langerhans, specialized regions of the pancreas. In humans, proinsulin is encoded by the ""INS"" gene. The islets of Langerhans only secrete between 1% and 3% of proinsulin intact. However, because proinsulin has a longer half life than insulin, it can account for anywhere from 5–30% of the insulin-like structures circulating in the blood. There are higher concentrations of proinsulin after meals and lower levels when a person is fasting."
"example, rat pancreatic cells are microencapsulated, they receive nutrients and release insulin through nanopores being totally isolated from their neighboring environment i.e. foreign cells. This knowledge can help to replace nonfunctional islets of Langerhans cells in the pancreas (responsible for producing insulin), by harvested piglet cells. They can be implanted underneath the human skin without the need of immunosuppressants which put diabetic patients at a risk of infection. Nanopore A nanopore is a pore of nanometer size. It may, for example, be created by a pore-forming protein or as a hole in synthetic materials such as silicon or graphene. When"
"Langerhans' son, Archibald, also helped to understand this regulatory role. The term ""insulin"" originates from ""insula"", the Latin word for islet/island. In 1889, the physician Oskar Minkowski, in collaboration with Joseph von Mering, removed the pancreas from a healthy dog to test its assumed role in digestion. On testing the urine, they found sugar, establishing for the first time a relationship between the pancreas and diabetes. In 1901, another major step was taken by the American physician and scientist Eugene Lindsay Opie, when he isolated the role of the pancreas to the islets of Langerhans: ""Diabetes mellitus when the result"
"of a lesion of the pancreas is caused by destruction of the islands of Langerhans and occurs only when these bodies are in part or wholly destroyed"". Over the next two decades researchers made several attempts to isolate the islets' secretions. In 1906 George Ludwig Zuelzer achieved partial success in treating dogs with pancreatic extract, but he was unable to continue his work. Between 1911 and 1912, E.L. Scott at the University of Chicago tried aqueous pancreatic extracts and noted ""a slight diminution of glycosuria"", but was unable to convince his director of his work's value; it was shut down."
"Pancreatic islet macrophage Islet resident macrophages are the predominant myeloid cell of the pancreatic islets of langerhans. Islet resident macrophages are uniquely found within the endocrine tissue (islet), while nearby in the nearby acinar tissue, macrophages express a different repertoire of CD (cluster of differentiation) markers and come from a different developmental origin. In terms of expression markers, islet macrophages are positive for; F4/80, CD11b, CD11c, MHC-II, CD64, CD68, LyzM (lysozyme), Cx3cr1 and are negative for; CD206 (mannose receptor), CD301, CD103. The mesoderm gives rise to myeloid progenitor cells, which further differentiate into macrophage populations. As opposed to macrophages in"
"enters passively. In the beta-cells of the pancreas, glucose enters through the GLUT 2 receptors (process described below). Insulin biosynthesis is regulated by transcriptional and translational levels. The β-cells promote their protein transcription in response to nutrients. The exposure of rat Langerhans islets to glucose for 1 hour is able to remarkably induce the intracellular proinsulin levels. It was noted that the proinsulin mRNA remained stable. This suggests that the acute response to glucose of the insulin synthesis is independent of mRNA synthesis in the first 45 minutes, because the blockage of the transcription decelerated the insulin accumulation during that"
"Édouard Laguesse Gustave-Édouard Laguesse (23 April 1861 – 6 November 1927) was a French pathologist and histologist born in Dijon. In 1885 he received his medical doctorate in Paris and from 1891 performed scientific research in Lille. In 1896 he became a professor of histology. Laguesse is remembered for his histopathological work involving the pancreas. In 1893 he named the small cellular clusters of the pancreas the ""Islets of Langerhans"", in honor of their discoverer Paul Langerhans (1847-1888). At the time of its discovery, Langerhans provided an excellent description of the structures, but offered no further conclusions as to their"
"Incretin Incretins are a group of metabolic hormones that stimulate a decrease in blood glucose levels. Incretins are released after eating and augment the secretion of insulin released from pancreatic beta cells of the islets of Langerhans by a blood glucose-dependent mechanism. Incretins also inhibit glucagon release from the alpha cells of the islets of Langerhans. In addition, they slow the rate of absorption of nutrients into the blood stream by reducing gastric emptying and may directly reduce food intake. The two main candidate molecules that fulfill criteria for an incretin are the intestinal peptides glucagon-like peptide-1 (GLP-1) and gastric"
"induction and inhibited by insulin. Conversely, intestinal proglucagon gene expression is reduced during fasting and stimulated upon food consumption. In mammals, the transcription gives rise to identical mRNA in all three cell types, which is further translated to the 180 amino acid precursor called proglucagon. However, as a result of tissue-specific posttranslational processing mechanisms, different peptides are produced in the different cells. In the pancreas (α-cells of the islets of Langerhans), proglucagon is cleaved by prohormone convertase (PC) 2 producing glicentin-related pancreatic peptide (GRPP), glucagon, intervening peptide-1 (IP-1) and major proglucagon fragment (MPGF). In the gut and brain, proglucagon is"
"cells in the pancreatic islets are among the most well understood and important. If the blood glucose level falls to dangerous levels (as during very heavy exercise or lack of food for extended periods), the alpha cells of the pancreas release glucagon, a hormone whose effects on liver cells act to increase blood glucose levels. They convert glycogen into glucose (this process is called glycogenolysis). The glucose is released into the bloodstream, increasing blood sugar. Hypoglycemia, the state of having low blood sugar, is treated by restoring the blood glucose level to normal by the ingestion or administration of dextrose"
"shown improvements towards the treatment of type 1 diabetics who are prone to hypoglycemic unawareness. However, the two major hurdles faced in this technique are the limited availability of donor organs and with the need for immunosuppresents to prevent an immune response in the patient's body. Several studies have been dedicated towards the development of bioartificial pancreas involving the immobilization of islets of Langerhans inside polymeric capsules. The first attempt towards this aim was demonstrated in 1980 by Lim et al. where xenograft islet cells were encapsulated inside alginate polylysine microcapsules and showed significant in vivo results for several weeks."
"glucagon to increase the levels of glucose, and insulin to decrease it. The islets are crisscrossed by a dense network of capillaries. The capillaries of the islets are lined by layers of islet cells, and most endocrine cells are in direct contact with blood vessels, either by cytoplasmic processes or by direct apposition. The islets function independently from the digestive role played by the majority of pancreatic cells. Activity of the cells in the islets is affected by the autonomic nervous system: The pancreas plays a vital role in the digestive system. It secretes a fluid that contains enzymes into"
"life-threatening state in type 1 diabetes, rather than focus on removing the need for insulin injections entirely . Researchers use a mixture of highly purified enzymes (Collagenase) to isolate islets from the pancreas of a deceased donor. Collagenase solution is injected into the pancreatic duct which runs through the head, body and tail of the pancreas. Delivered this way, the enzyme solution causes distension of the pancreas, which is subsequently cut into small chunks and transferred into so-called Ricordi's chamber, where digestion takes place until the islets are liberated and removed from the solution. Isolated islets are then separated from"
"pancreas. Production, which is otherwise freerunning, is suppressed/regulated by insulin from the adjacent beta cells. (Actually, GABA is the interlock signal chemical that prevents simultaneous insulin and glucagon production in the pancreas. It is produced by the pancreatic ß cells at the same time insulin is being produced. It prevents the α cells from being switched on.) When blood sugar drops, insulin production drops and more glucagon is produced In rodents, the alpha cells are located in the outer rim of the islet. Human islet structure is much less segregated, and alpha cells are distributed throughout the islet in close"
"as well, by contributing to islet inflammation. The origin and turnover in the normal state was characterized by Emil Unanue in 2015. Pancreatic islet macrophage Islet resident macrophages are the predominant myeloid cell of the pancreatic islets of langerhans. Islet resident macrophages are uniquely found within the endocrine tissue (islet), while nearby in the nearby acinar tissue, macrophages express a different repertoire of CD (cluster of differentiation) markers and come from a different developmental origin. In terms of expression markers, islet macrophages are positive for; F4/80, CD11b, CD11c, MHC-II, CD64, CD68, LyzM (lysozyme), Cx3cr1 and are negative for; CD206 (mannose"
"syndrome. Experimental evidence shows that there is substantial increase of ceramide levels upon adding palmitate. Ceramide accumulation activates PP2A and the subsequent dephosphorylation and inactivation of AKT, a crucial mediator in metabolic control and insulin signaling. This results in a substantial decrease in insulin responsiveness (i.e. to glucose) and in the death of insulin-producing cells in the pancreas called islets of Langerhans. Inhibition of ceramide synthesis in mice via drug treatments or gene-knockout techniques prevented insulin resistance induced by fatty acids, glucocorticoids or obesity. An increase in ""in vitro"" activity of acid SMase has been observed after applying multiple stress"
"10 milligrams. Glipizide sensitizes the beta cells of pancreatic islets of Langerhans insulin response, meaning that more insulin is released in response to glucose than would be without glipizide ingestion. Glipizide acts by partially blocking potassium channels among beta cells of pancreatic islets of Langerhans. By blocking potassium channels, the cell depolarizes, which results in the opening of voltage-gated calcium channels. The resulting calcium influx encourages insulin release from beta cells. Glipizide Glipizide is an oral rapid- and short-acting anti-diabetic medication from the sulfonylurea class. It is classified as a second-generation sulfonylurea, which means that it undergoes enterohepatic circulation. Second-generation"
"a role for the pancreas in diabetes is generally ascribed to Joseph von Mering and Oskar Minkowski, who in 1889 found that dogs whose pancreas was removed developed all the signs and symptoms of diabetes and died shortly afterwards. In 1910, Sir Edward Albert Sharpey-Schafer suggested that people with diabetes were deficient in a single chemical that was normally produced by the pancreas—he proposed calling this substance insulin, from the Latin ""insula"", meaning island, in reference to the insulin-producing islets of Langerhans in the pancreas. The endocrine role of the pancreas in metabolism, and indeed the existence of insulin, was"
"endocrine cell types that will form the islets of Langerhans. The absence of ""Hes1"" in the developing intestine of mice promotes the increase of Math1 (a protein required for the production of intestinal secretory cell types), which leads to an increase of goblet, enteroendocrine, and Paneth cells. When ""Hes1"" is deleted in mouse and zebrafish, surplus goblet cells and enteroendocrine cells are made while few enterocytes are made. Liver progenitor cells differentiate into two different cell types: hepatocytes and biliary epithelial cells. When ""Hes1"" expression is low, hepatocytes form normally, but bile ducts are completely absent. This phenotype resembles Alagille"
"produced by the human pancreas. They help the person digest fats, starches, and proteins. Pancreatic enzymes have been used as medications since at least the 1800s. They are on the World Health Organization's List of Essential Medicines, the most effective and safe medicines needed in a health system. In the United Kingdom a typical month's supply costs the NHS about £11.64. In the United States a month of treatment typically costs $50 to $100. Pancrelipases are generally a first line approach in treatment of exocrine pancreatic insufficiency and other digestive disorders, accompanying cystic fibrosis, complicating surgical pancreatectomy, or resulting from"