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Macronutrients
Published in Chuong Pham-Huy, Bruno Pham Huy, Food and Lifestyle in Health and Disease, 2022
Chuong Pham-Huy, Bruno Pham Huy
Amylin, a 37-amino-acid-peptide, is a pancreatic β-cell hormone that produces effects in several different organ systems (45). Amylin’s major role is as a glucoregulatory hormone, and it is an important regulator of energy metabolism in health and disease. Other amylin actions have also been reported, such as on the cardiovascular system or on bone. Amylin acts principally in the circumventricular organs of the central nervous system and functionally interacts with other metabolically active hormones such as cholecystokinin, leptin, and estradiol. The amylin-based peptide, pramlintide, is used clinically to treat Type 1 and Type 2 diabetes. Clinical studies in obesity have shown that amylin agonists could also be useful for weight loss, especially in combination with other agents (45).
Endocrine Functions of Brain Dopamine
Published in Nira Ben-Jonathan, Dopamine, 2020
Amylin is a 37-amino-acid peptide belonging to the calcitonin gene-related peptide (CGRP) family. It is co-secreted with insulin from pancreatic beta cells in response to prandial stimuli and in direct proportion to the meal size. Circulating amylin can cross the BBB, but amylin-immunoreactive neurons have also been detected in the hypothalamus [52]. With respect to the feeding behavior, amylin inhibits food intake following both systemic or ICV administration at low doses. Interactions between amylin and DA are supported by the demonstration that amylin inhibited the release of DA, but not NE or serotonin, from hypothalamic synaptosomes. The authors concluded that the anorectic effects of amylin involve inhibition of the release of DA in the hypothalamus. Another study reported that amylin acts in the VTA to reduce palatable food intake [53]. Although a direct interaction of amylin with DA was not tested in this study, based on the well-established role of DA in reward-related processes, the authors proposed that the effects of amylin are mediated by the blunting of DA.
The physiology of glucose metabolism
Published in Janet Titchener, Diabetes Management, 2020
Amylin This is another pancreatic hormone. It is co-secreted with insulin from the pancreatic β-cells following the ingestion of food. Amylin suppresses postprandial glucagon secretion, thereby decreasing glucagon-stimulated hepatic glucose output (as described above). Amylin also slows the rate of gastric emptying. This reduces the rate at which glucose is delivered to the small intestine for absorption, thereby playing an important role in the control of postprandial blood sugars. By slowing gastric emptying, it is also possible that amylin reduces food intake and body weight – i.e. amylin has similar actions to the incretin hormones (see below).
Physico-chemical stability of co-formulation of PEGylated human amylin with insulin
Published in Pharmaceutical Development and Technology, 2019
Celimar Sinésia, Caio Victor M. F. do Nascimento, Paulo G. S. Lacativa, Luís Maurício T. R. Lima
Amylin, also known as islet amyloid polypeptide (IAPP) – is a 37 amino acid peptide produced by the pancreatic islet β cells (Clodi et al. 1998; Bennett et al. 2000; Knowles et al. 2002) and co-secreted with insulin (Kahn et al. 1990; Stridsberg et al. 1993). In addition to the complementary biological functions, amylin also interacts molecularly with insulin, both soluble and crystalline forms, in vitro and in vivo (Jaikaran et al. 2004; Larson and Miranker 2004; Gilead et al. 2006; Knight et al. 2008; Sellin et al. 2010). Such interaction is likely to be mediated by the domains comprising amino acids 7 to 19 of amylin and amino acids 9 to 20 of insulin’s B chain (Gilead et al. 2006; Younk et al. 2011). Under physiologic conditions, the variation of amylin concentration in plasma mirrors insulin fluctuation, both during postprandial and basal levels between meals (Kruger et al. 1999). Synergistically with insulin, amylin contributes for the maintenance of glucose homeostasis by reducing the post-meal gastric emptying rate, promoting satiety and inhibiting the secretion of glucagon.
Closed-loop insulin delivery: current status of diabetes technologies and future prospects
Published in Expert Review of Medical Devices, 2018
Strategies to address the immediate postprandial period by delaying carbohydrate appearance are currently being studied. Amylin is a hormone co-secreted with insulin by the pancreatic beta-cell and is deficient in people with T1D [84]. It delays gastric emptying, inhibits glucagon secretion, and plays a role in achieving satiety, thereby facilitating a reduction in postprandial glycaemic burden [85]. The effects of pramlintide, a synthetic analog of amylin, on postprandial glycaemia have recently been evaluated in small clinical research facility studies [86]. Co-administration with insulin in a CLS has shown a reduction of postprandial glycaemic excursions compared to single-hormone CLS alone [87]. Reported side effects of amylin include nausea and vomiting [88]. Larger studies are still needed to establish efficacy and tolerance in CLS.
What is on the horizon for type 2 diabetes pharmacotherapy? – An overview of the antidiabetic drug development pipeline
Published in Expert Opinion on Drug Discovery, 2020
Karl Sebastian Johansson, David Peick Sonne, Filip Krag Knop, Mikkel Bring Christensen
Amylin is co-secreted with insulin in response to food intake and reduces glucagon secretion and food intake as well as delays gastric emptying, thereby leading to improved glycemic control and reduced bodyweight [13–15]. The amylin receptor has the same core structure as the calcitonin receptor and dual amylin-calcitonin receptor agonists bind to both receptors. This leads to a more potent activation of the amylin receptor and, thus, more effective reductions in glucagon secretion and bodyweight [16]. Pramlintide, a pure amylin agonist approved as an adjunct to mealtime insulin therapy in both type 1 diabetes (T1D) and T2D in the US, lowers HbA1 c by 0.3% and bodyweight by 2.2 kg when added to already established insulin therapy [17].