Glucagon-like peptide 1 (GLP-1) is a 30-amino acid peptide hormone produced in the intestinal epithelial endocrine L-cells by differential processing of proglucagon, the gene which is expressed in ...

The Physiology of Glucagon-like Peptide 1

The Pharmacological Basis of Therapeutics A Textbook of Pharmacology, Toxicology and Therapeutics for Physicians and Medical Students. By Prof. Louis Goodman and Prof. Alfred Gilman. Pp. xiii + 1383. (New York: The Macmillan Company, 1941.) 50s. net.

The Pharmacological Basis of Therapeutics

I. Introduction II. History of the Incretin Concept: Discovery of Gastric Inhibitory Polypeptide III. Discovery of GLP-1 IV. Structures of GLPs and Family of Glucagon-Related Peptides V. Tissue Distribution of the Expression of GLPs A. Pancreatic α-cells B. Intestinal L cells C. Central nervous system VI. Proglucagon Biosynthesis A. Organization/structure of the proglucagon gene B. Regulation of glucagon gene expression C. Posttranslational processing of proglucagon VII. Regulation of GLP Secretion A. Overview B. Intracellular signals C. Carbohydrates D. Fats E. Proteins F. Endocrine G. Neural H. GLP-2 VIII. Metabolism of GLPs A. GLP-1 B. GLP-2 IX. Physiological Actions of GLPs A. Overview B. Pancreatic islets C. Counterregulatory actions of GLP-1 and leptin on β-cells D. Stomach E. Lung F. Brain G. Liver, skeletal muscle, and fat H. Pituitary, hypothalamus, and thyroid I. Cardiovascular system J. GLP-2 X. GLP Receptors A. Structure B. Signaling C. Distribution D. Regulation E. GLP-2 XI. Pathophysiology o...

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The glucagon-like peptides.

Background The glucagon-like peptide-1 (GLP-1) is a multifaceted hormone with broad pharmacological potential. Among the numerous metabolic effects of GLP-1 are the glucose-dependent stimulation of insulin secretion, decrease of gastric emptying, inhibition of food intake, increase of natriuresis and diuresis, and modulation of rodent β-cell proliferation. GLP-1 also has cardio- and neuroprotective effects, decreases inflammation and apoptosis, and has implications for learning and memory, reward behavior, and palatability. Biochemically modified for enhanced potency and sustained action, GLP-1 receptor agonists are successfully in clinical use for the treatment of type-2 diabetes, and several GLP-1-based pharmacotherapies are in clinical evaluation for the treatment of obesity. Scope of review In this review, we provide a detailed overview on the multifaceted nature of GLP-1 and its pharmacology and discuss its therapeutic implications on various diseases. Major conclusions Since its discovery, GLP-1 has emerged as a pleiotropic hormone with a myriad of metabolic functions that go well beyond its classical identification as an incretin hormone. The numerous beneficial effects of GLP-1 render this hormone an interesting candidate for the development of pharmacotherapies to treat obesity, diabetes, and neurodegenerative disorders

https://spiral.imperial.ac.uk/bitstream/10044/1/74273/2/Glucagon-like%20peptide%201%20%28GLP-1%29%20Molecular%20Metabolism.pdf

Glucagon-like peptide 1 (GLP-1)

Glucagon-like peptide 1 (GLP1) is postulated to regulate blood glucose and satiety, but the biological importance of GLP1 as an incretin and neuropeptide remains controversal. The regulation of nutrient-induced insulin secretion is dependent on the secretion of incretins, gut-derived peptides that potentiate insulin secretion from the pancreatic islets. To ascertain the relative physiological importance of GLP1 as a regulator of feeding behavior and insulin secretion, we have generated mice with a targeted disruption of the GLP1 receptor gene (GLP1R). These GLP1R-/- mice are viable, develop normally but exhibit increased levels of blood glucose following oral glucose challenge in association with diminished levels of circulating insulin. It is surprising that they also exhibit abnormal levels of blood glucose following intraperitoneal glucose challenge. Intracerebroventricular administration of GLP1 inhibited feeding in wild-type mice but not in GLP1R-/- mice; however, no evidence for abnormal body weight or feeding behavior was observed in GLP1R-/- mice. These observations demonstrate that GLP1 plays a central role in the regulation of glycemia; however, disruption of GLP1/GLP1R signaling in the central nervous system is not associated with perturbation of feeding behavior or obesity in vivo.

Glucose intolerance but normal satiety in mice with a null mutation in the glucagon-like peptide 1 receptor gene.

A complementary DNA for a glucagon-like peptide-1 receptor was isolated from a human pancreatics islet cDNA library. The isolated clone encoded a protein with 90% identity to the rat receptor. In stably transfected fibroblasts, the receptor bound [125I]GLP-1 with high affinity ( K d = 0.5 nM) and was coupled to adenylate cyclase as detected by a GLP-1-dependent increase in cAMP production (EC50 = 93 pM). Two peptides from the venom of the lizard Heloderma suspectum, exendin-4 and exendin-(9–39), displayed similar ligand binding affinities to the human GLP-1 receptor. Whereas exendin-4 acted as an agonist of the receptor, inducing cAMP formation, exendin-(9–39) was an antagonist of the receptor, inhibiting GLP-1–induced cAMP production. Because GLP-1 has been proposed as a potential agent for treatment of NIDDM, our present data will contribute to the characterization of the receptor binding site and the development of new agonists of this receptor.

https://diabetes.diabetesjournals.org/content/diabetes/42/11/1678.full.pdf

Cloning and functional expression of the human islet GLP-1 receptor. Demonstration that exendin-4 is an agonist and exendin-(9-39) an antagonist of the receptor.

Islets isolated from human cadaver pancreas were pulse-labeled (10 min with [3H]leucine) and then incubated for a 180-min chase Islets and chase medium were collected every 15 min and analyzed by reversed-phase HPLC to quantify the percentage of radioactively labeled proinsulin, conversion intermediates, and fully processed insulin Release of proinsulin-related labeled products into the chase medium was < 10% of total Whereas 50% of labeled proinsulin had been lost by conversion within 45 min, fully processed insulin only appeared with a half-time of 100 min This discrepancy is attributable to accumulation of radioactive conversion intermediates Des 6465 split proinsulin was a minor component, reaching a maximum of 52 +/- 17% (n = 4) at 60 min of chase By contrast, des 3132 split proinsulin--and a truncated form lacking the first three residues of C-peptide--rose progressively to 293 +/- 14% by 75 min, and declined thereafter The accumulation of des 3132 split proinsulin rather than the des 6465 split form during the conversion of human proinsulin reflects slower conversion at the C-peptide/A-chain than at the B-chain/C-peptide junction, and is consistent with the appearance of this particular conversion intermediate in the circulation

https://diabetes.diabetesjournals.org/content/diabetes/42/6/933.full.pdf

Kinetics of Proinsulin Conversion in Human Islets

https://aasldpubs.onlinelibrary.wiley.com/doi/pdf/10.1002/hep.510270326

Inhibition of leukocyte adherence and transendothelial migration in cultured human liver vascular endothelial cells by prostaglandin E1

Originated from Wuhan and expanded throughout China and the world, the 2019 novel coronavirus (COVID-19), has caused worldwide attention As of March 21, the overall confirmed cases reached to 0 2 million in 172 countries In all Chinese Medical Centers, elective surgery and the living donor transplantation has been suspended due to the rapid spread of the coronavirus In contrast, the cadaveric donor transplantations were mostly performed Therefore, strategies to interrupt transmission within transplantation wards were essential To date, we have performed at our center ten cases of kidney, four liver and two lung transplants (from deceased organ donors) during the coronavirus outbreak in China (from January 24th to March 11th, 2020) Based on our experience in combating the coronavirus while performing these organ transplants, we comprehensively address here the strategies for the prevention of the virus spread within the transplantation wards Donor management The potential organ donors were cleared for epidemiology history and should not have traveled from or have contact with people from epidemic areas Virus nucleic acid from pharyngeal swab specimens was determined, and chest CT was performed Only when they were confirmed negative for coronavirus, related laboratory tests as HLA typing of donor, antibody detection of the receptor and complement dependent cytotoxicity test could be performed Recipient management The potential recipients were screened for coronavirus (nucleic acid determination and chest CT scanning) on admission day Further, additional information was collected from the recipient such as travel history, close contacts, daily body temperature and respiratory symptoms During the hospitalization period, recipients received COVID-19 related education Meanwhile, they were given new surgical masks every six hours We also collaborated with psychologists to provide consultations Post-transplant immunosuppression was maintained at usual doses If the recipient had fever, cough, diarrhea or pulmonary infection manifestations, the patient was considered as suspected for contamination and was quarantined within an isolation ward Accompanying family members of recipients also received COVID-19 related screening as mentioned above In addition, regular visits were not allowed Prevention of hospitalacquired infections We implemented strict protocols in preventions of HAIs, including training of HCPs and providing personal protective equipment Outcome of the organ transplant recipients From January 24th to March 11th, we successfully performed 16 organ transplant operations (10 kidney, 4 liver and 2 lung transplants)

Strategies to HALT 2019 novel coronavirus (COVID-19) spread for organ transplantation programs at the Sichuan academy of medical science and Sichuan Provincial People's Hospital, China

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Cloning and functional expression of the human islet GLP-1 receptor. Demonstration that exendin-4 is an agonist and exendin-(9-39) an antagonist of the receptor.

Kinetics of Proinsulin Conversion in Human Islets

Inhibition of leukocyte adherence and transendothelial migration in cultured human liver vascular endothelial cells by prostaglandin E1

Strategies to HALT 2019 novel coronavirus (COVID-19) spread for organ transplantation programs at the Sichuan academy of medical science and Sichuan Provincial People's Hospital, China