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Neuroendocrine Factors
Published in Michael H. Stone, Timothy J. Suchomel, W. Guy Hornsby, John P. Wagle, Aaron J. Cunanan, Strength and Conditioning in Sports, 2023
Michael H. Stone, Timothy J. Suchomel, W. Guy Hornsby, John P. Wagle, Aaron J. Cunanan
Glucagon is a peptide hormone secreted from the alpha cells in the islets of Langerhans of the pancreas. Glucagon functions in energy substrate control, particularly for glucose. The primary regulation of glucagon appears to occur through stimulation or inhibition by nutrients (108). A rise in serum glucose results in a reduction in serum glucagon, and vice versa (107, 126). In animals, fatty acids and ketones inhibit glucagon secretion and glucose metabolism (126). Gastric inhibitory peptide (GIP) and secretin are released as a result of gastrointestinal and hormonal signals; GIP may stimulate glucagon secretion, while secretin may decrease glucagon secretion (126, 210). Glucagon is also stimulated by the sympathetic nervous system and sympathomimetic amines (126). Glucagon has several primary effects including (109, 126, 202, 210): Antagonism of the actions of insulin.Serving to mobilize energy substrates (i.e., glucose and fatty acids).Having thermogenic and anorectic effects.Being mediated by cAMP, and its metabolic effects in the liver and adipose tissue are essentially similar to those of EPI.
Diabetes Mellitus Type 1 (DM1)/Juvenile Diabetes/Insulin Dependent Diabetes Mellitus (IDDM)
Published in Charles Theisler, Adjuvant Medical Care, 2023
In type 1 diabetes, the pancreas produces little or no insulin. Juvenile-onset diabetes is usually caused by an autoimmune process wherein the immune system begins destroying healthy insulin-producing pancreatic beta cells within the islets of Langerhans. This destructive process can go on for months or years before symptoms appear, often relatively suddenly. Eventually, without adequate amounts of insulin, glucose cannot enter into the body’s cells. Thereafter, blood sugar levels build up and remain high, causing symptoms such as increased thirst, fatigue, unintended weight loss, mood changes, excessive urination, and increased hunger.
Disorders of the digestive tract
Published in Judy Bothamley, Maureen Boyle, Medical Conditions Affecting Pregnancy and Childbirth, 2020
The pancreas is a small gland well-known for its endocrine function. Specialist cells distributed in the pancreas, known as the Islets of Langerhans, produce insulin and glucagon that have an essential role in the control of blood sugar (see Chapter 1). The pancreas also has an exocrine function. It produces pancreatic juice, which contains enzymes that digest carbohydrates, proteins and fats. The common bile duct, coming from the liver, joins the pancreatic duct just before it enters the duodenum.
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
Impacts of the COVID-19 pandemic on a human research islet program
Published in Islets, 2022
Tina J. Dafoe, Theodore Dos Santos, Aliya F. Spigelman, James Lyon, Nancy Smith, Austin Bautista, Patrick E. MacDonald, Jocelyn E. Manning Fox
Human pancreatic tissue and isolated islets of Langerhans are vital to research, where they are used to study islet morphology, β-cell proliferation, genomics, insulin and glucagon secretion, fuel-induced toxicity, transcription factor regulation, transplantation, and many other aspects of endocrine physiology and diabetes. Characterization of human islet function is central to understanding diabetes, given the key role that islets play in disease pathophysiology1 and genetic susceptibility,2–4 and to regenerative strategies including the production of mature human β-cells from stem cells.5–7 Increased interest in – and need for – these areas of research, along with awareness of the limitations of non-human models, has elevated the demand for human research islets. Concerns have been raised regarding future access8,9 with data from the European Consortium for Islet Transplantation (ECIT) suggesting a growing gap between human research islet supply and demand,10 a trend first reported by the Islet Cell Resource Consortium (the predecessor to the Integrated Islet Distribution Program, or IIDP).11
HSC70 is a novel binding partner involved in the capture of immunoglobulins on B cells in the NOD mouse
Published in Autoimmunity, 2022
Emma Renman, Rifat Ekici, Mia Sundström, Kristina Lejon
Although clearly important in the host defense against foreign pathogens, B cells are also involved in the development of several autoimmune diseases, including Type 1 diabetes [6]. This disease has been readily investigated in the non-obese diabetic (NOD) mouse strain, which spontaneously develops diabetes as a result of an auto-destruction of pancreatic β cells in the islets of Langerhans [7]. B cells infiltrate the pancreatic islets of NOD mice early in the disease development [8], and autoantibodies against islet antigens indicate an increased risk of disease [9]. Depletion of B cells in NOD have a protective role in the development of Type 1 diabetes [10–12] and B cells of NOD play a critical role as disease-promoting antigen-presenting cells in their interaction with T cells, which primes pro-inflammatory T cell responses to β cell antigens [13–15]. Moreover, NOD mice display enhanced and prolonged immune responses [16,17] as well as an aberrant VH gene utilisation pattern [18]. We have previously described an enhanced capture of IgG and IgM antibodies by B cells of NOD compared to those of C57BL/6 mice, a trait contributing to increased IC trapping by NOD B cells [19]. We excluded that the binding was due to the poly-reactive immunoglobulin repertoire in NOD as well as potential receptors such as the FcR and complement receptors CR1/2 [19]. The phenomenon was concluded to be restricted to the extracellular part of the B cell plasma membrane as an act of an unknown binding partner. In this study, we sought to identify the binding partner responsible for the increased IgG and IgM capturing on NOD B cells.