enterostatin

Enterostatin has the sequence Val-Pro-Asp-Pro-Arg in most mammals, but Val-Pro-Gly-Pro-Arg or Val-Pro-Asp-Pro-Arg in rodents and Ala-Pro-Gly-Pro-Arg in humans.{{cite journal |last1=Erlanson-Albertsson |first1=C |title=Enterostatin: the pancreatic procolipase activation peptide--a signal for regulation of fat intake. |journal=Nutrition Reviews |date=October 1992 |volume=50 |issue=10 |pages=307–10 |doi=10.1111/j.1753-4887.1992.tb02473.x |pmid=1436769}} The sequence that it necessary for its anorexic effects is X-pro-Y-pro-arg and conserved among several vertebrate species.{{cite journal |last1=Lin |first1=L |last2=Okada |first2=S |last3=York |first3=DA |last4=Bray |first4=GA |title=Structural requirements for the biological activity of enterostatin. |journal=Peptides |date=1994 |volume=15 |issue=5 |pages=849–54 |doi=10.1016/0196-9781(94)90041-8 |pmid=7984504}}{{cite journal |last1=Lin |first1=L |last2=York |first2=DA |title=5-HT1B receptors modulate the feeding inhibitory effects of enterostatin. |journal=Brain Research |date=16 November 2005 |volume=1062 |issue=1–2 |pages=26–31 |doi=10.1016/j.brainres.2005.09.029 |pmid=16256085|pmc=2526559 }}

Enterostatin has been detected in gut endocrine cells.{{cite journal |last1=Sörhede |first1=M |last2=Erlanson-Albertsson |first2=C |last3=Mei |first3=J |last4=Nevalainen |first4=T |last5=Aho |first5=A |last6=Sundler |first6=F |title=Enterostatin in gut endocrine cells--immunocytochemical evidence. |journal=Peptides |date=1996 |volume=17 |issue=4 |pages=609–14 |doi=10.1016/0196-9781(96)00017-4 |pmid=8804069}} It is created in the intestine by pancreatic procolipase, the other colipase serving as an obligatory cofactor for pancreatic lipase during fat digestion. Enterostatin can be created in the gastric mucosa and the mucosal epithelia in the small intestine. A high fat diet will cause the procolipase gene transcription and enterostatin to release into the gastrointestinal lumen. Enterostatin appears in the lymph and circulation after a meal. Enterostatin has been shown to selectively reduce fat intake during a normal meal. The testing has been successful with different species.{{cite journal |last1=Jonaidi |first1=H |last2=Rasooli |first2=R |title=Effect of central enterostatin on fat intake in neonatal chicks. |journal=Neuroscience Letters |date=15 January 2013 |volume=533 |pages=60–4 |doi=10.1016/j.neulet.2012.11.021 |pmid=23178475}}

The signaling pathway of the peripheral mechanism uses afferent vagal to hypothalamic centers. The central responses are mediated through a pathway including serotonergic and opioidergic components.{{cite journal |last1=Berger |first1=K |last2=Winzell |first2=MS |last3=Mei |first3=J |last4=Erlanson-Albertsson |first4=C |title=Enterostatin and its target mechanisms during regulation of fat intake. |journal=Physiology & Behavior |date=30 December 2004 |volume=83 |issue=4 |pages=623–30 |doi=10.1016/j.physbeh.2004.08.040 |pmid=15621068|url=https://lup.lub.lu.se/record/133399 }} Enterostatin cuts fat intake, bodyweight, and body fat. This reaction may involve multiple metabolic effects of enterostatin, which include a decrease of insulin secretion,{{cite journal |vauthors=Park M, Farrell J, Lemmon K, York DA |title=Enterostatin alters protein trafficking to inhibit insulin secretion in Beta-TC6 cells |journal=Peptides |volume=30 |issue=10 |pages=1866–73 |date=October 2009 |pmid=19563849 |doi=10.1016/j.peptides.2009.06.021 |pmc=2755607}} a growth in sympathetic drive to brown adipose tissue, and the stimulation of adrenal corticosteroid secretion. It has been demonstrated that enterostatin stimulates neurons in the amygdala, the arcuate nucleus, the lateral and the ventromedial hypothalamus that have anatomic and functional projections to the paraventricular nucleus (PVN) of the hypothalamus.{{cite journal |last1=Lin |first1=L |last2=York |first2=DA |title=Amygdala enterostatin induces c-Fos expression in regions of hypothalamus that innervate the PVN. |journal=Brain Research |date=10 September 2004 |volume=1020 |issue=1–2 |pages=147–53 |doi=10.1016/j.brainres.2004.06.029 |pmid=15312796}} Additionally, enterostatin regulates the expression of Agouti-related peptide (AgRP) in a complex manner.{{cite journal |last1=Park |first1=M |last2=Oh |first2=H |last3=York |first3=DA |title=Enterostatin affects cyclic AMP and ERK signaling pathways to regulate Agouti-related protein (AgRP) expression. |journal=Peptides |date=February 2009 |volume=30 |issue=2 |pages=181–90 |doi=10.1016/j.peptides.2008.11.005 |pmid=19059445}}

A possible pathophysiological role is indicated by studies that have associated low enterostatin output and/or responsiveness to breeds of rat that become obese and prefer dietary fat. Humans with obesity also exhibit a lower secretion from pancreatic procolipase after a test meal, compared with persons of normal weight.{{Cite journal |last1=Erlanson-Albertsson |first1=C |last2=York |first2=D |date=July 1997 |title=Enterostatin--a peptide regulating fat intake |journal=Obesity Research |publisher=Nature Publishing Group |volume=5 |issue=4| pages=360–72 |issn=1930-7381 |pmid=9285845 |doi=10.1002/j.1550-8528.1997.tb00565.x|doi-access=free }}

Its effects include a reduction of insulin secretion, an increase in sympathetic drive to brown adipose tissue, and the stimulation of adrenal corticosteroid secretion. At the end level, it initiates a sensation of fullness of stomach which could be the reason for its role in regulation of fat intake and reduction of body weight. For enterostatin to be utilized it needs the presence of CCK A receptors. Studies based on rats who lack these receptors have found them to be un-responsive to enterostatin.{{cite book

|author=Jean-Pierre Montmayeur |author2=Johannes le Coutre

| title = Fat Detection: Taste, Texture, and Post Ingestive Effects

| publisher =CRC Press; 1 edition

| date =September 14, 2009

| url = https://books.google.com/books?id=jSb7aQxm9UEC&dq=Enterostatin&pg=PA359

| page =359

| isbn =978-1-4200-6775-0 }}

When rats have been injected with high doses of enterostatin into the brain the rats ate progressively less food as the dose was increased.{{cite book

| title =Handbook of biologically active peptides

| publisher = Academic Press

| year = 2006

| location =Londan

| url = https://books.google.com/books?id=n8SV9iM6kT0C&dq=Enterostatin&pg=PA969

| isbn =978-0-12-369442-3}}{{rp|969}}

In rats, examination of experiments involving the effects of peripheral or intracerebroventricular administration of enterostatin show this selectively slows down fat consumption.{{cite book

|author=George A. Bray |author2=Donna H. Ryan

| title = Overweight and the Metabolic Syndrome: From Bench to Bedside

| publisher = Springer; 1 edition

| year = 2006

| url = https://books.google.com/books?id=0BtMHOQebo4C&dq=Enterostatin&pg=PA7

| isbn = 978-0-387-32163-9}}{{rp|8}}

Although enterostatin-like immunoreactivities exist in blood, brain, and gut, and exogenous enterostatins decrease fat appetite and insulin secretion in rats, the roles of these peptides in human obesity remain to be examined.{{cite journal |last1=Prasad |first1=C |last2=Imamura |first2=M |last3=Debata |first3=C |last4=Svec |first4=F |last5=Sumar |first5=N |last6=Hermon-Taylor |first6=J |title=Hyperenterostatinemia in premenopausal obese women. |journal=The Journal of Clinical Endocrinology and Metabolism |date=March 1999 |volume=84 |issue=3 |pages=937–41 |doi=10.1210/jcem.84.3.5562 |pmid=10084574}} It has been hypothesized that resistance to enterostatin impairs its effects in obesity.

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Category:Digestive system

Category:Pentapeptides