Synonym |
Gastrin-14 |
Species |
Human |
Protein Accession |
P01350 |
Purity |
Greater than 98% |
Endotoxin Level |
Less than 1 EU/μg |
Biological Activity |
Not determined |
Expression System |
E. coli |
Fusion Tag |
None |
Predicted Molecular Mass |
1579.8 Da |
Formulation |
Lyophilized from a 0.2 μm filtered solution of 20% acetonitrile and 0.1% TFA |
Reconstitution |
It is recommended to reconstitute the lyophilized Gastrin I (1-14) (human) in sterile 18MΩ-cm
H2O not less than 100μg/ml, which can then be further diluted to other aqueous solutions. |
Storage & Stability |
Lyophilized Gastrin I (1-14) (human) although stable at room temperature for 3 weeks, should be
stored desiccated below -18°C. Upon reconstitution Gastrin I (1-14) should be stored at 4°C
between 2-7 days and for future use below -18°C. |
FAQ
What is Gastrin I (1-14) (human), and what role does it play in the body?
Gastrin I (1-14)
(human) is a peptide fragment of the gastrin hormone, a crucial regulator of digestive processes.
Gastrin itself is primarily produced by G-cells located in the stomach lining and to some extent in the
duodenum. This hormone plays a vital role in the regulation of gastric acid secretion and
gastrointestinal motility. The Gastrin I (1-14) fragment represents the 14-amino-acid sequence within
the larger gastrin peptide that retains significant biological activity. This activity includes
stimulating the secretion of hydrochloric acid by parietal cells in the stomach, which is essential for
digestion and absorption of nutrients. In addition to acid secretion, gastrin also enhances gastric
mucosal growth and aids in the muscular contractions that propel food through the digestive
tract.
Moreover, gastrin interacts with receptors on the surface of gastric parietal cells,
specifically gastrin/CCK-B receptors, to exert its effects. By stimulating these receptors, gastrin
activates a cascade of intracellular signaling pathways that lead to the increased secretion of gastric
acid. This process helps maintain a pH suitable for enzymes like pepsin to digest proteins optimally.
Furthermore, recent research has implicated gastrin in various physiological and pathological contexts
beyond digestion. For instance, there is evidence suggesting its involvement in cellular proliferation
and differentiation, pointing to a potential role in cancer biology, particularly in gastrointestinal
malignancies. Understanding the molecular structure and function of Gastrin I (1-14) is vital for
developing therapeutic interventions targeting dysregulated gastrin levels, which are associated with
conditions like Zollinger-Ellison syndrome, peptic ulcers, and gastrinomas.
While vital for
maintaining optimal digestive function, abnormalities in gastrin levels can lead to medical
complications. Hypergastrinemia, for example, can result in excessive gastric acid production, leading
to ulcerative conditions and other digestive disorders. Research focused on Gastrin I (1-14) aims to
elucidate its specific roles and mechanisms within the broader context of gastrin hormone physiology.
Insights derived from such research continue to reveal its potential implications not only in digestive
health but also in various metabolic processes and disease states.
How does Gastrin I (1-14)
(human) influence gastric acid secretion?
Gastrin I (1-14) influences gastric acid secretion by
interacting with specific receptors on the gastric parietal cells. These cells, located in the lining of
the stomach, are primarily responsible for the secretion of hydrochloric acid (HCl), which is crucial
for the digestive process. Gastrin exerts its effect on acid secretion by binding to the gastrin/CCK-B
receptors on the surface of these parietal cells. This receptor-ligand interaction triggers a cascade of
intracellular events that eventually lead to the activation of the H+/K+ ATPase pump, also known as the
proton pump, situated in the apical membrane of parietal cells.
The activation of this proton
pump facilitates the exchange of hydrogen ions (protons) out of the cell for potassium ions into the
cell, driving the production and secretion of hydrochloric acid into the stomach lumen. This, in turn,
lowers the pH of the stomach contents, which is crucial for activating digestive enzymes such as
pepsinogen to pepsin, further aiding in protein digestion. Additionally, the acidic environment serves
as a barrier to pathogens and helps in the absorption of certain nutrients, including iron and vitamin
B12.
It is important to note that the secretion of gastric acid is a finely tuned process
regulated by neural, hormonal, and paracrine pathways. Gastrin I (1-14) operates within a complex
network involving other factors such as acetylcholine from parasympathetic nerve endings and histamine
from enterochromaffin-like (ECL) cells. These components work synergistically to optimize gastric
function. Overproduction of gastric acid due to excessive gastrin secretion can lead to conditions such
as gastroesophageal reflux disease (GERD) and peptic ulcers. Understanding the precise mechanisms by
which Gastrin I (1-14) impacts gastric acid secretion provides valuable insights for developing targeted
treatments for disorders resulting from imbalances in gastric acid production.
Can Gastrin I
(1-14) (human) be used in therapeutic applications?
Gastrin I (1-14), being a fundamental peptide
involved in digestive processes, holds potential for various therapeutic applications, particularly in
addressing disorders characterized by imbalances in gastrin levels. One area where this peptide could be
significant is in Zollinger-Ellison syndrome, a condition marked by tumors (gastrinomas) that secrete
excessive amounts of gastrin, leading to hypergastrinemia and subsequent gastric acid hypersecretion. In
such instances, understanding the precise role and mechanism of Gastrin I (1-14) could pave the way for
targeted therapies that modulate its activity, thereby alleviating symptoms associated with this
disorder.
Moreover, gastrin has been implicated in certain gastrointestinal malignancies,
suggesting that Gastrin I (1-14) or its analogs might be explored for therapeutic roles in cancer
treatment. For instance, certain anticancer strategies may involve the use of gastrin antagonists or
receptor blockers to inhibit the proliferative signaling pathways activated by gastrin in cancer cells.
While research is ongoing, the potential to manipulate gastrin activity or receptor interaction could
offer a novel approach to manage and possibly reduce tumor growth in gastrin-sensitive
cancers.
The intriguing aspect of Gastrin I (1-14) in therapy also extends to its role in gastric
mucosal health. Because gastrin not only stimulates acid secretion but also promotes gastric mucosal
growth and repair, there may be therapeutic applications in conditions requiring enhanced mucosal
protection or healing, such as in patients with gastric ulcers or following gastric surgery. Developing
analogs or modulators of Gastrin I (1-14) that can selectively enhance mucosal growth without
stimulating excessive acid secretion could indeed be a promising line of research.
Furthermore,
in experimental settings, the administration of gastrin and its derivatives has been utilized to study
its physiological and pathophysiological roles, allowing scientists to better understand its
contributions to gut health and disease. While much of this potential is still in the research phase,
the cumulative knowledge gained underscores the importance of Gastrin I (1-14) as not just a
physiological molecule but also a promising candidate for therapeutic innovation. Continued exploration
and understanding of its complex roles could unlock new possibilities in treating a variety of
gastrointestinal and systemic diseases.
Are there any known side effects or risks associated with
alterations in Gastrin I (1-14) (human) levels?
Alterations in levels of Gastrin I (1-14) can
manifest in several physiological and potential pathological consequences, which highlight both the
importance of this peptide in maintaining digestive homeostasis and the risks associated with its
dysregulation. One of the primary effects of altered gastrin levels is the change in gastric acid
secretion. Hypo- or hypersecretion of gastric acid can significantly impact digestive health, leading to
conditions such as gastroesophageal reflux disease (GERD), peptic ulcers, or achlorhydria, depending on
whether the secretion is elevated or reduced.
Excessive levels of gastrin, such as those observed
in conditions like Zollinger-Ellison syndrome, are associated with hypergastrinemia. The prolonged
hypersecretion of gastric acid in such circumstances can lead to the formation of peptic ulcers and
complications of the digestive tract. The risk extends to possible damage to the esophageal lining due
to acid reflux, which in turn can increase the risk of Barrett’s esophagus and even esophageal
adenocarcinoma. Thus, monitoring and managing gastrin levels are critical in patients susceptible to
these conditions.
Conversely, insufficient gastrin activity, though less commonly highlighted,
also poses health risks. Low levels of gastric acid secretion, or hypochlorhydria, can impair digestive
efficiency, leading to malabsorption of critical nutrients like vitamin B12, iron, calcium, and
magnesium. This malabsorption poses a particular risk for developing anemia, osteoporosis, and various
neurological disorders due to nutrient deficiencies.
Additionally, emerging research has
suggested a complex relationship between gastrin levels and cancer biology. Gastrin appears to possess
trophic effects on the gastric mucosa and other tissues, which under certain circumstances might
contribute to tumorigenesis, particularly in gastrointestinal cancers. The mechanistic pathways
underlying this relationship are still under investigation, but the potential for gastrin to influence
cellular proliferation and differentiation necessitates a careful approach in situations where gastrin
levels are manipulated therapeutically.
Thus, while Gastrin I (1-14) is essential for normal
digestive physiology, both its excess and deficiency present substantial risks that must be considered
in clinical contexts. Careful management and understanding of gastrin levels, perhaps through the
development of specific inhibitors or enhancers, can mitigate these risks, promoting better gastric
health and potentially reducing the incidence of gastrin-related disease states. Ongoing research
continues to refine our understanding of these dynamics, helping to improve therapeutic strategies aimed
at managing gastrin-related disorders.
How is Gastrin I (1-14) (human) studied in research, and
what are the implications of these studies?
Gastrin I (1-14) is a subject of intense research,
primarily because of its fundamental role in digestive physiology and its broader implications in health
and disease. Research efforts focus on understanding its molecular structure, its interaction with
receptors, and the subsequent downstream effects that drive gastric functions. Techniques such as
peptide synthesis and structural analysis using NMR spectroscopy or X-ray crystallography provide
detailed insights into the conformation of Gastrin I (1-14) and its active sites essential for receptor
binding and activation.
Functional studies often involve in vitro experiments using isolated
gastric cell cultures to observe the physiological responses to Gastrin I (1-14). Researchers assess
parameters such as changes in acid secretion, cell proliferation rates, and receptor activation
profiles. In vivo studies, usually conducted in animal models, provide critical insights into
whole-organism effects and how alterations in gastrin levels impact systemic physiology. These studies
help in elucidating the peptide’s role not only in acid secretion but also in gastric mucosa repair
mechanisms and its potential mitogenic effects.
The implications of these studies are sweeping
and deeply impactful. By delineating the physiological roles of Gastrin I (1-14), researchers can better
understand pathologies associated with its dysregulation, such as Zollinger-Ellison syndrome, GERD, and
peptic ulcer disease. Furthermore, this understanding supports the development of novel pharmacological
approaches, with researchers investigating gastrin receptor antagonists or agonists to treat conditions
stemming from excessive or insufficient gastrin activity.
In the realm of oncology, understanding
Gastrin I (1-14) has implications for developing cancer therapies, particularly for gastrin-sensitive
tumors. Since gastrin can influence cell proliferation, deciphering its pathways can indicate potential
intervention points for inhibiting tumor growth. Clinical trials are exploring gastrin antagonists as
potential treatments for certain gastrointestinal cancers, highlighting the translational aspect of
gastrin research from bench to bedside.
The diverse methods and technologies used in studying
Gastrin I (1-14) continue to expand, driven by advancements in molecular biology and bioinformatics.
These studies are not only unraveling the complex biological roles of this peptide but are also
identifying its potential as a biomarker for certain diseases. Overall, the research on Gastrin I (1-14)
is paving the way for therapeutic innovations, advancing our ability to address gastric disorders and
contributing to a broader understanding of peptide hormone regulation and its implications for human
health.