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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
Glucagon is a peptide hormone produced by alpha cells of the pancreas and works to raise the level of glucose and fatty acids in blood. Its effect is opposite to that of insulin. Together with insulin, it is a regulator of glucose in blood. Moreover, it hydrolyzes triglycerides into fatty acids and glycerol (38, 42).
Diabetes
Published in Michael Horvat, Ronald V. Croce, Caterina Pesce, Ashley Fallaize, Developmental and Adapted Physical Education, 2019
Michael Horvat, Ronald V. Croce, Caterina Pesce, Ashley Fallaize
The alpha cells produce and secrete a hormone called glucagon, which raises the blood sugar level by changing the stored glycogen in the liver to glucose, which is transported to the cells by insulin (Figure 17.2). Glucagon is a hormone secreted when the blood glucose concentration is low, primarily to convert liver glycogen into glucose to elevate blood glucose (Horton, 1989). In reality, glucagon actually helps increase the uptake of amino acids and stimulates gluconeogenesis. It also has glycogenolytic properties in the liver and, with epinephrine, is a major glucose counter-regulatory hormone during exercise (Horton, 1989). A balance is maintained, with the glucagon keeping the blood glucose from becoming too low while the insulin keeps it from becoming too high. If this does not occur and the balance is distorted, the body cannot use the available sugar to supply its own energy requirement and relies on the energy in fat stored in the body. This occurs in normal metabolism.
The Role of Gut Microbiota in the Pathogenesis and Treatment of Diabetes
Published in Emmanuel C. Opara, Sam Dagogo-Jack, Nutrition and Diabetes, 2019
Stephen J. Walker, Shaun P. Deveshwar
Individuals with DM-1 have malfunctioning pancreatic beta islet cells, which are unable to secrete insulin into the bloodstream to facilitate storage of excess sugar as glycogen [4,5]. However, pancreatic alpha cells are still able to secrete the antagonist hormone to insulin, glucagon, into the bloodstream and therefore deplete the body of its stored glycogen through glycogenolysis. Individuals with untreated DM-1 will experience severe weight loss and ketoacidosis. Moreover, the body feels the need to urinate more frequently, resulting in the excretion of important nutrients due to the increased glucose concentration in the bloodstream.
Design of novel therapeutics targeting the glucose-dependent insulinotropic polypeptide receptor (GIPR) to aid weight loss
Published in Expert Opinion on Drug Discovery, 2023
GLP-1 is a hormone released from enteroendocrine L cells in response to a nutrient stimulus such as carbohydrates, amino acids, and fatty acids. It is derived from the alternative processing of the proglucagon gene in L cells and also neurones, in distinction to alpha cell processing which leads to glucagon secretion. GLP-1’s insulinotropic function was first investigated in vitro by the Holst group [5] and in vivo by Kreymann and Bloom [6]. GLP-1, alongside GIP (see section 3) were found to be incretins, i.e. they are gut hormones that are responsible for the enhanced secretion of insulin when glucose is given enterically compared to when an isoglycemic load is given intravenously. As a result, GLP-1 is effective at improving glycemia in diabetics. In addition to this, GLP-1 also has an appetite suppressive effect in animals [7] and in man [8], possibly mediated by GLP-1 receptor expressing neurones in the hypothalamus, known to be important for appetite regulation [9].
Evidence for the existence and potential roles of intra-islet glucagon-like peptide-1
Published in Islets, 2021
Scott A. Campbell, Janyne Johnson, Peter E. Light
Although induction of the GCG gene is critical for proglucagon production, the subsequent processing of proglucagon into glucagon or glucagon-related peptides (such as GLP-1 and GLP-2) is critically dependent on the relative expression levels of PC2 and PC1/3 (Figure 1). Greater PC1/3 expression favors GLP-1 production, whereas greater PC2 expression favors glucagon production (Figure 1). In this regard, PC1/3 is highly expressed in juvenile human islets, although its expression is decreased in adult alpha cells. Instead, mature islets preferentially express the nonfunctional “long-noncoding” PC1/3 gene lncPCSK1.46 Despite its decreased expression in aging, alpha cell PC1/3 expression is still well-documented in adult alpha cells where it correlates positively with BMI.47 Indeed, PC1/3 expression is detectable in FACS-sorted alpha cells from the adult, non-diabetic human pancreas and alpha cell PC1/3 expression is elevated in T2D alpha cells.44,48 This is supported by our own recent research that demonstrates that islets from T2D donors contain a higher proportion of GLP-1 positive alpha cells than islets from non-diabetic donors.44 While there is substantial evidence that the adult human endocrine pancreas can express intra-islet GLP-1, the precise signaling pathways regulating alpha cell PC1/3 expression is an active research area and several potential pathways that regulate alpha cell PC1/3 expression have been identified and are described below.
Closed-loop control in insulin pumps for type-1 diabetes mellitus: safety and efficacy
Published in Expert Review of Medical Devices, 2020
In type 1 diabetes, insulin-producing pancreatic beta cells are destroyed by an immune-mediated process. Beta and alpha cells produce insulin, amylin, and glucagon, all of which are hormones required to maintain the body’s glucose homeostasis. Prior to insulin therapy, type 1 diabetes was universally fatal. Nowadays, insulin is either replaced with multiple daily injections (MDI) using both short- and long-acting insulins, or by continuous infusion of rapid-acting insulin via an insulin pump. Even with insulin replacement therapy and frequent self-monitoring of blood glucose levels, people with diabetes are at risk of multiple long-term complications if glucose control is suboptimal [1], as well as the immediate risks posed by dangerously low (hypoglycemia) or high (hyperglycemia) glucose levels if insulin is acutely over- or under-dosed.