The RAPID Method for Blood Processing Yields New Insight in Plasma Concentrations and Molecular Forms of Circulating Gut Peptides

Stengel, Andreas; Keire, David A.; Goebel, Miriam; Evilevitch, Lena; Wiggins, Brian; Taché, Yvette; Reeve, Joseph R.

doi:10.1210/edrv.30.6.9989

Cited by 2 publications

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“…CCK circulates predominantly in a 58-amino acid form (CCK-58) (243,431,612,722). Importantly, many CCK assays that involve plasma formation recover Ͻ20% of endogenous CCK, so they provide accurate relative, but not absolute, levels (243,431,722). Additionally, most tests of exogenous CCK use CCK-8, which is rare or absent in the plasma.…”

Section: A Introductionmentioning

confidence: 99%

Ghrelin, CCK, GLP-1, and PYY(3–36): Secretory Controls and Physiological Roles in Eating and Glycemia in Health, Obesity, and After RYGB

Steinert

Feinle‐Bisset

Asarian

et al. 2017

Physiological Reviews

462

415

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The efficacy of Roux-en-Y gastric-bypass (RYGB) and other bariatric surgeries in the management of obesity and type 2 diabetes mellitus and novel developments in gastrointestinal (GI) endocrinology have renewed interest in the roles of GI hormones in the control of eating, meal-related glycemia, and obesity. Here we review the nutrient-sensing mechanisms that control the secretion of four of these hormones, ghrelin, cholecystokinin (CCK), glucagon-like peptide-1 (GLP-1), and peptide tyrosine tyrosine [PYY(3-36)], and their contributions to the controls of GI motor function, food intake, and meal-related increases in glycemia in healthy-weight and obese persons, as well as in RYGB patients. Their physiological roles as classical endocrine and as locally acting signals are discussed. Gastric emptying, the detection of specific digestive products by small intestinal enteroendocrine cells, and synergistic interactions among different GI loci all contribute to the secretion of ghrelin, CCK, GLP-1, and PYY(3-36). While CCK has been fully established as an endogenous endocrine control of eating in healthy-weight persons, the roles of all four hormones in eating in obese persons and following RYGB are uncertain. Similarly, only GLP-1 clearly contributes to the endocrine control of meal-related glycemia. It is likely that local signaling is involved in these hormones' actions, but methods to determine the physiological status of local signaling effects are lacking. Further research and fresh approaches are required to better understand ghrelin, CCK, GLP-1, and PYY(3-36) physiology; their roles in obesity and bariatric surgery; and their therapeutic potentials.

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Section: A Introductionmentioning

confidence: 99%

Ghrelin, CCK, GLP-1, and PYY(3–36): Secretory Controls and Physiological Roles in Eating and Glycemia in Health, Obesity, and After RYGB

Steinert

Feinle‐Bisset

Asarian

et al. 2017

Physiological Reviews

462

415

View full text Add to dashboard Cite

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“…The lack of acetylation leads to desacyl ghrelin which renders ghrelin unable to bind to its receptor, growth hormone secretagogue receptor type 1a (GHSR1a). The ratio of plasma acylated ghrelin/total ghrelin is 1:5 [6] and the receptor for desacyl ghrelin is yet to be identified. Interestingly, a mass spectrometry analysis of human plasma acyl ghrelin suggests that all ghrelin in circulation is acylated and that des-acyl perhaps is an artefact owing to sample handling [7].…”

Section: Ghrelin Structuresmentioning

confidence: 99%

Biased signaling: A viable strategy to drug ghrelin receptors for the treatment of obesity

Nagi

Habib

2021

Cellular Signalling

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Obesity is a global burden and a chronic ailment with damaging overall health effects. Ghrelin, an octanoylated 28 amino acid peptide hormone, is secreted from the oxyntic mucosa of the stomach. Ghrelin acts on regions of the hypothalamus to regulate feeding behavior and glucose homeostasis through its G protein-coupled receptor. Recently, several central pathways modulating the metabolic actions of ghrelin have been reported. While these signaling pathways can be inhibited or activated by antagonists or agonists, they can also be discriminatingly activated in a "biased" response to impart different degrees of activation in distinct pathways downstream of the receptor. Here, we review recent ghrelin biased signaling findings as well as characteristics of ghrelin hormone and its receptors pertinent for biased signaling. We then evaluate the feasibility for ghrelin receptor biased signaling as a strategy for the development of effective pharmacotherapy in obesity treatment.

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The RAPID Method for Blood Processing Yields New Insight in Plasma Concentrations and Molecular Forms of Circulating Gut Peptides

Cited by 2 publications

References 0 publications

Ghrelin, CCK, GLP-1, and PYY(3–36): Secretory Controls and Physiological Roles in Eating and Glycemia in Health, Obesity, and After RYGB

Ghrelin, CCK, GLP-1, and PYY(3–36): Secretory Controls and Physiological Roles in Eating and Glycemia in Health, Obesity, and After RYGB

Biased signaling: A viable strategy to drug ghrelin receptors for the treatment of obesity

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