Month: August 2013

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Secretin acetate is a hormone that is responsible for controlling the environment of a duodenum by regulating pancreatic and stomach secretions while regulating the water homeostasis throughout an animal’s body. Specifically, it helps to regulate the duodenum’s pH by inhibiting the secretion of gastric acid from the parietal cells of the stomach and increasing stimulation of the bicarbonate production in the centroacinar cells from the pancreas.

More recent research has determined that this chemical may play a role in osmoregulation by helping to manage the kidneys pituitary and hypothalamus.

Secretin was one of the first hormones to be identified in 1902 by Ernest Starling and William Bayliss who were looking to understand more about how the nervous system works to control digestion.

The increased role of secretin acetate way discovered by performing autopsies on animals as this was the most advanced means of investigating the chemical makeup of a mammal’s body at the time. It was then discovered that it was not the nervous system but hormones that were impacting the controls Bayliss and Starling were hoping to discover.

In Vitro Inhibitory Effects of Somatostatin

Exocrien pancreatic function has been found to influence islet hormones and the existence of somatostatin receptors can shut down pancreatic acinar cells.

• Isolated pancreatic acini from rats were used to test the effects of somatostatin on the release of amylase, cyclic adenosine mono-phosphate and hormone binding.
• Somatostatin was found to inhibit the potentiating effects of the secretin on the amylase responses to cholecystokinin octapeptide. Similar molar basis reactions were observed when a vasoactive intestinal polypeptide was released instead of secretin.

Conclusions to this study revealed that somatostain will act directly upon acinar cells. This will inhibit the potentiation of secretin and the secretory response to this hormone. This is partially due to inhibiting cAMP production in vitro.

Protective Effects of Exogenous Secretin

Rats that were placed unconscious were given intravenous cerultide in large applications to develop acude pancreatitis to determine the effects of secretin on the body.

• Biochemical markets were used to monitor the pancreatitis symptoms and it was noted that these symptoms tended to be parallel to the severity of the damage done to the pancreas itself.
• In half of the rats a mesenteric fat necrosis was noted as well as free peritoneal fluid. This fluid contained large elevations of the trypsinogen as well as amylase.

Secretion of low doses along with ceruletide increases the protective effect of secretin. This produces a macroscopic, biochemical and microscopic effect on the pancreatitis. It redirected zymogen granules of the acini in the animals that were provided secretin applications which were shown to be quite beneficial in managing the condition.

Much of the research surrounding secretin acetate today revolves around further understanding the complex role of hormones in mammals and how they interact with other systems of the body to control essential functions. Much of how secretin acetate interacts with other hormones is still being learned, as is the effects of a deficit of this chemical on the body can affect an animal’s overall health.

Sources:

http://europepmc.org/abstract/MED/7681794
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1129276/

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Secretin acetate is a hormone that is made up of 120 amino acids which are a precursor to the prosecretin protein. It contains a spacer, N-terminal single peptide and secretin. Mature secretin peptides make up a linear hormone that has a molecular weight of 3055 with a helix formed from the amino acids at 13 and 5. These sequences are similar to vasoactive intestinal peptides, glucagon and gastric inhibitory peptide. Secretin may also amidate cerbodxyl- terminal amino acids in the body.

Secretin is synthesized by creasing cytoplasmic secretory granules of the S cells commonly found in the duodenum’s mucosa as well as the jujunum in the small intestine. These can be released into circulation within an animal to respond to low duodenal pH, about 2 to 4.5 depending on the type of animal that is being studied.

The hormone will target the pancreas causing it to release a bicarbonate fluid into the intestine that will neutralize excess acid so these tissues will not be burned.

Plasma Secretin as a Pancreatic Response

Dogs with gastric duodenal Thomas cannulas were investigated to determine the dose range that exogenous secretion for pancreatic bicarbonate secretion and an increase in plasma secretin concentrations would occur.

• Synthetic secretions of this chemical were dissolved in a saline solution and applied to the dogs without a background infusion.
• Minimal doses of secretin acetate were found to elicit a pancreatic bicarbonate response that was somewhat significant in addition to an increase in concentrations of plasma secretions.

Postpradinal secretion concentrations were measured and found that a meal consisting of meat would cause a larger spike in secretin acetate than spikes occurring during the infusion. Secretin and intraduodenal acid profusion would increase in larger doses but were unchanged by the concentrations added by a background caerulein infusion.

Synthesis of Gastrointestinal Peptides with Secretin

The REMA method was found ideal for creating a synthesis of secretin in animals that would be suitable for experimentation.

• This procedure is quite rapid because it is on a small scale and creates a synthesis of one amino acid each day to be attained and may yield an unambiguous product.
• After an ion-exchange chromoatography the REMA secretions were found to be chemically identical to the secretin acetate fragments that would be produced by an animal’s body.

These synthesized hormones showed similar biological activity to clinical units that are regularly compared to natural versions of this hormone. The yield of secretin acetate also produced a hepacosapeptide amide that was calculated to be the basis of a C-terminal residue. This made up approximately 5 percent of the final product.

Additional factors that may impact secretin release include the presence of fatty acids or bile salts which will act as‘bicarbonate’ when they reach the small intestine. This chemical is also inhibited by H2 antagonists which help the body to reduce gastric acid secretion as necessary. This results in any secretions of the duodenum above 4.5, being unaffected by secretin so it will not be released under these conditions.

Sources:

http://onlinelibrary.wiley.com/doi/10.1002/hlca.19760590415/abstract
http://ajpgi.physiology.org/content/246/5/G535.short

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HB EGF refers to the heparin binding form of the EGF-like growth factor that can be found in mammals. This chemical is also synthesized for use in medical research as a means of understanding how deficiencies or extreme amounts of this chemical might impact the way an animal reacts to different diseases.

This is commonly used as a means of developing a stress test for eating disorders, with scales used to determine the psychometric properties associated with varying amounts of HB EGF. This self-rating scale is commonly used to help track posttraumatic stress disorder, which has improved the effectiveness of research topics in animals within laboratory settings.

The expression of HB EGF was analyzed in rats to determine how this chemical packs a principal beta hairpin which can be expressed in a crystal structure or diphtheria toxin. Results indicate that HB EGF may act as a post-transcriptional mechanism that can be introduced in trophblasts that will amplify HB EGF, that is used by the animal’s body to inhibit apoptosis.

How HB EGF is Regulated

HB EGF cDNA was isolated in a library which focused on progesterone-induced transcripts in rat uterine stomal cells.

• This was performed to test the effects of estradiol and progesterone in the way that HB EGF is expressed in mature stomal and epithelial rat uterine cells.
• Progesterone treatment and estradiol injections were applied to each rat followed by a stimulation of HB EGF expression within the stomal cells.

The expression of HB EGF was linked as a primary response to mRNA in the stomal cells, revealing that epithelial or stomal cells in vivo that were exposed to similar hormonal conditions may induce cell proliferation. This holds true for both cell types which suggests that HB EGF could be used to mediate mitogenic effects that steroid hormones have on a rat uterus.

Post-Ischemic Administration

HB EGF has been found to be hypoxia inductible, acting as a neruoprotective protein that may stimulate proliferation of any neuronal precursor cells.

• This allows researchers to note that HB EGF could be used to aid in the recovery from cerebral injuries using direct neruoprotective effects such as enhancing enrogenesis.
• When HB EGF was administered to rats using intracerbroventricular for 103 days within the vertebral ischemia the HB EGF content of the rat’s body decreased the volume of infarcts and post-ischemic neurological deficits.

This delayed neruoprotective effect that is associated with HB EGF application in adult rats implies that this application process may aid in efforts that can prolong ‘therapeutic windows’ that could be used to intervene in the event of a stroke.

HB EGF has also been known to bind with EGFRs at a high affinity. It will also bind with sulfate proteogylcans that can result in mitogenic potential which helps to set this chemical apart from others in the same family. It has been concluded that HB EGF TM will synthesize exclusively with a luminal epithelium at blastocyst appositions. This is a juxtacrine adhesion factor that can help to mediate the adhesion of blastocysts to the uterus in some animals.

Sources:

http://endo.endojournals.org/content/134/3/1089.short
http://www.nature.com/jcbfm/journal/v24/n4/abs/9591541a.html

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