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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.
Beta Cells and Diabetes
Published in Raj K. Keservani, Anil K. Sharma, Rajesh K. Kesharwani, Nutraceuticals and Dietary Supplements, 2020
Shivani Srivastava, Durgavati Yadav, Kumar Sandeep, Harsh Pandey, Surya Kumar Singh, Yamini Bhusan Tripathi
The location of 42-amino acid hormone GIP on the human chromosome is 17q21.3-q22 with six exons. This hormone is secreted from K cells of the upper small intestine (duodenum and jejunum) through proteolytic processing of pre-pro GIP. After secretion active GIP directly acts on the pancreatic islet to secrete insulin from β cells (Seino et al., 2010).
Biocatalyzed Synthesis of Antidiabetic Drugs
Published in Peter Grunwald, Pharmaceutical Biocatalysis, 2019
Incretins are gut hormones that potentiate insulin secretion after meal ingestion in a glucose-dependent manner (Campbell and Drucker, 2013). The incretin effect, a term that refers to the observation that orally administered glucose results in a larger increase in plasma insulin levels and insulin-dependent decrease in blood glucose concentration when compared to the same amount of glucose given intravenously (Rondas et al., 2013), is responsible for 50%-70% insulin production. The two best studied incretins are glucose-dependent insulinotropic polypeptide (also named gastric inhibitory polypeptide, GIP), a 42 amino acid peptide synthesized in and secreted from enteroendocrine K cells located primarily in the duodenum and proximal jejunum, although CNS production of GIP has also been described);glucagon-like peptide-1 (GLP-1) a 30 amino acid residue peptide, originated from preproglucagon, synthesized in the l-cells in the distal ileum, in the pancreas and in the brain.
Design of novel therapeutics targeting the glucose-dependent insulinotropic polypeptide receptor (GIPR) to aid weight loss
Published in Expert Opinion on Drug Discovery, 2023
The remainder of the review will focus on how GLP-1R-based therapies are being improved by the addition of drugs targeting GIPR. GIP is a 42 amino acid peptide derived from the pre-pro-GIP gene, found in the enteroendocrine K cells present in the duodenum and the upper jejunum. It was discovered prior to GLP-1 in the early 1970s by Brown and Pederson working at the University of British Columbia [16]. GIP was initially believed to be an enterogastrone, an acid inhibitory factor that is released from the small intestinal mucosa by fat. Thus, it was given the name gastric inhibitory polypeptide. However, shortly after its initial discovery, Dupre, in collaboration with Brown, showed that an intravenous infusion of GIP in humans during a glucose tolerance test potentiated insulin secretion [17]. This finding was mirrored ex vivo, as Pederson showed that GIP could increase insulin secretion in a perfused rat pancreas in a glucose-dependent manner [18]. It quickly became apparent that its incretin action was a more important function of the peptide, and thus GIP became known as glucose-dependent insulinotropic polypeptide. In fact, in normal physiology, GIP is overall a more important contributor to the incretin effect than GLP-1, although in type 2 diabetes, GIP becomes less effective due to GIP resistance, whereas GLP-1 retains its incretin activity.
Circulating glucagon-like peptide-1 level in patients with liver cirrhosis
Published in Archives of Physiology and Biochemistry, 2023
Masoud Nouri-Vaskeh, Neda Khalili, Amirreza Khalaji, Pouya Behnam, Leila Alizadeh, Sara Ebrahimi, Neda Gilani, Mehdi Mohammadi, Seyed Alisalar Madinehzadeh, Mohammad Zarei
Glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are gut-derived incretin hormones that stimulate insulin secretion from pancreatic β-cells after meal ingestion. Oral glucose intake causes a much greater increase in insulin secretion as opposed to intravenous glucose administration. This is due to the presence of the incretin hormones and/or glucose-responsive nerves in the gastrointestinal tract. The incretin effect is responsible for as high as 70% of the total insulin secretion after food intake in healthy individuals (Nauck et al.1986, Kuhre et al.2015). GLP-1 is mainly released from L-cells that are located all across the small intestine; however, these cells tend to increase in number when approaching the distal ileum (Holst, 2007). The circulating levels of GLP-1 and GIP increase rapidly from 5–10 pmol/L to 15–50 pmol/L after nutrient ingestion within half an hour. Besides its glucose-dependent insulinotropic effect, GLP-1 has several regulatory roles; it is involved in reducing gastrointestinal motility, decreasing appetite, suppressing glucagon release from the pancreatic α-cells, and regulating postprandial nutrient distribution (Junker et al.2015, Muskiet et al.2017).
Considerations when prescribing pharmacotherapy for metabolic associated fatty liver disease
Published in Expert Opinion on Pharmacotherapy, 2022
Lucia Brodosi, Francesca Marchignoli, Giulio Marchesini, Maria Letizia Petroni
DPP-4Is (mainly sitagliptin) are considered neutral for liver disease. As for GLP-1RAs, in a small phase 2 study (LEAN study), liraglutide treatment improved NASH histology after 48 weeks [13], but activity resolution was not associated with fibrosis regression. Semaglutide, a longer-acting, weekly dosing GLP-1 analog, has recently been tested in a placebo-controlled 72-week trial in 320 patients with NASH; it confirmed a significant effect on liver disease activity, but failed to reach the confirmatory endpoint of fibrosis improvement [14], despite a remarkable weight loss. A few positive effects were also reported with dulaglutide, another weekly dosing GLP-1RA, but very few histologic data are available. Synergistic effects may be achieved by combining GLP-1RAs with lifestyle intervention [15] or with receptor agonists of gastric inhibitory polypeptide (GIP). Treatment with a GIP/GLP-1 combined agonist, tirzepatide, has been reported to exert a robust effect on metabolic control [16], as well as to improve several hepatic biomarkers.