Pancreas insulin production

Diabetes mellitus is a complicated, chronic disorder characterized by either insufficient insulin production by the beta cells of die pancreas or by cellular resistance to insulin. Insulin insufficiency results in elevated blood glucose levels, or hyperglycemia As a result of the disease, individuals with diabetes are at greater risk for a number of disorders, including myocardial infarction, cerebrovascular accident (stroke), blindness, kidney disease, and lower limb amputations. 

Those with type 1 diabetes mellitus produce insulin in insufficient amounts and tiierefore must have insulin supplementation to survive Type 1 diabetes usually has a rapid onset, occurs before die age of 20 years, produces more severe symptoms tiian type 2 diabetes, and is more difficult to control. Major symptoms of type 1 diabetes include hyperglycemia, polydipsia (increased thirst), polyphagia (increased appetite), polyuria (increased urination), and weight loss. Treatment of type 1 diabetes is particularly difficult to control because of the lack of insulin production by die pancreas. Treatment requires a strict regimen tiiat typically includes a carefully calculated diet, planned physical activity, home glucose testing several times a day, and multiple daily insulin injections. 

A pancreas with normal (3-cell function is able to adjust insulin production to maintain normal blood glucose levels. 

Insulin production takes place in the islet tissue of the pancreas, and the individual variation in the amount of this tissue is large. It is estimated that a substantial percentage of the pancreases in a population (78 per cent in one study) 13 have from 0.9 to 3.5 per cent of islet tissue. Those individuals having less than 0.9 per cent are likely to be diabetics, and those having more than 3.5 per cent are likely to be actual or potential sufferers from hyperinsulinism. 14... 

Generai This human insulin product differs from animal-source insulins because it is structurally identical to the insulin produced by the body s pancreas and because of its unique manufacturing process. 

In their report the researchers describe a culturing technique that can turn mouse embryonic stem cells into cell clusters that resemble pancreatic islets. The clusters inner cells produced insulin, while outer cells produced glucagon and somatostatin, two other proteins typically synthesized by pancreatic cells. Most important, the embryonic stem cell-derived pancreas cells produce insulin in response to glucose, the fundamental role of beta cells that regulate insulin secretion. The major shortcoming of the system at this time is the low levels of insulin production. Refinements in culture technique or drug manipulation may be needed to achieve therapeutic levels. 

The receptor for l,25(OH)2D exists in a wide variety of tissues—not just bone, gut, and kidney. In these "nonclassic" tissues, l,25(OH)2D exerts a number of actions including regulation of parathyroid hormone secretion from the parathyroid gland, insulin secretion from the pancreas, cytokine production by macrophages and T cells, and proliferation and differentiation of a large number of cells, including cancer cells. Thus, the clinical utility of l,25(OH)2D and its... 

The human intestine has evolved as a highly efficient organ to digest (i.e. hydrolyse) practically all the macromolecules in the human diet (albeit with the help of a few trillion bacteria ) with the exception of some plant fibres. To do this it possesses a formidable array of enzymes. This is particularly true for the digestion of proteins and peptides where peptidases are found in the stomach, are secreted by the pancreas in considerable quantities and are found on the surface of and inside intestinal epithelial cells. These enzymes work in a co-ordinated fashion to rapidly hydrolyse proteins. They present the major difficulty for designing oral delivery systems for therapeutic peptides, which may explain why 86 years after the first attempt to orally administer insulin (Bliss 1982), there is still not an oral insulin product available for diabetics. 

Treatment of insulin-dependent diabetes involves the administration of insulin. In less severe cases of this diabetic form or in patients with adult-onset diabetes who have retained some /3 cell function, it is possible to "squeeze" the pancreas with such drugs as tolbutamide (orinase), tolazamide, or chlorpropamide, which act directly on the pancreas to increase insulin production. In most non-insulin-dependent diabetes situations, the dietary restriction of carbohydrate and fat is sufficient to control the disease. 

Some of the effects of GH may be a consequence of its stimulation of synthesis and secretion of insulin by the pancreas. Such effects have been demonstrated in various systems [93], as have actions on cell growth in islets of Langerhans. The pancreas is a site of production of somatomedin C, and the possibility that this factor may mediate the actions of GH on insulin production has not been excluded. 

A key component of DKA is that there is no or very little circulating insulin so it occurs mainly (but not exclusively) in type 1 diabetes (because type 1 diabetes is characterised by a lack of insulin production in the pancreas). It is much less common in type 2 diabetes which is closely related to cell insensitivity to insulin, rather than shortage or absence of insulin. 

Diabetes mellitus (DM) is an increasingly common disease of sugar metabolism. Juvenile-onset diabetes, also known as Type I or insulin-dependent diabetes (IDDM), is an autoimmune disease that results in decreased release of insulin by the pancreas. Late-onset diabetes, also known as Type II or non-insulin-dependent diabetes (NIDDM), results from reduced sensitivity of cells to the insulin signal. A convenient animal model for studying diabetes and testing alternative therapies is the streptozotocin-freated diabetic rat. Streptozotocin (STZ) attacks the pancreas and decreases insulin production and release, thus, mimicking many aspects of the human disease. Since insulin is not orally absorbed, the oral administration of vanadium compounds that are insuhn-mimetic or insulin-enhancing would be a very attractive therapy ... 

The mechanism of this child s diabetes was as follows. Impaired insulin production resulted from destruction, by antibodies, of many of the i-cells of the pancreas. Antibodies are proteins synthesized by cells of the immune system that recognize and tightly bind to macromolecules to form antibody-target complexes. These complexes are then destroyed by w hite blood cells. A normally acting immune system produces only antibodies that recognize foreign structures however, this child produced antibodies that recognized components of the child s own p-cells,... 

Diabetes mellitus is a chronic disease characterized by inherited or acquired dehciency in insulin production by the pancreas or by resistance of tissues to insulin. Traditionally, the disorder has been divided into type 1 (insulin-dependent) and type 2 (noninsulin dependent) forms, although this distinction is not always clear [44-46]. 

Type II diabetes mellitus Type II diabetes mellitus (age-onset diabetes) is when the pancreas ability to produced insulin is either diminished (age) or is insufficient to metabolize the excess serum glucose (overweight, lack of exercise). Insulin is produced but is not effective. The patient controls Type II diabetes mellitus by diet, exercise, and oral diabetes medication that stimulate insulin production in the pancreas and other organs. This is referred to as non-insulin-dependent diabetes (NIDDM). 

Insuhn is a protein hormone produced by the (5-ceUs of the islets of Langerhans in the pancreas. Insulin was the first protein hormone to be sequenced, the first substance to be measured by radioimmunoassay (RIA), and the first compound produced by recombinant DNA technology for practical use. It is an anaboUc hormone that stimulates the uptake of glucose into fat and muscle, promotes the conversion of glucose to glycogen or fat for storage, inhibits glucose production by the liver, stimulates protein synthesis, and inhibits protein brealcdown. 

Diabetes mellitus type 1 (T1D). Autoimmune form of diabetes mellitus caused by immune-mediated destruction of insulin-producing beta cells in the pancreas with irreversible loss of insulin production. Islet cell autoantibodies and autoantibodies directed against glutamic acid decarboxylase, insulin, and the IA2-antigen are diagnostic markers for T1D as well as risk markers for the development of this disease. 

Di Abietes has insulin-dependent diabetes mellitus (type 1), a disease associated with a severe deficiency or absence of insulin production by the p cells of the pancreas. One of the effects of insulin is to stimulate production of LPL. Because of low insulin levels, Di Abietes tends to have low levels of this enzyme. Flydrolysis of the triacylglycerols in chylomicrons and in VLDL is decreased, and hypertriglyceridemia results. 

Dbsty2 2149844 PDGF-a receptor 486984 Interacts with hedgehog, involved in insulin production in pancreas [97]... 

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