Talk:Ghrelin

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[edit] Merge?

There is mention on the Obestatin page that Obestatin be merged with Ghrelin. I strongly disagree. It is true that they are both coded on the same gene, but they are distinct in their action. I see nothing that justifies their being merged. —Preceding unsigned comment added by 71.15.92.103 (talk) 17:22, 6 June 2008 (UTC)

Agreed —Preceding unsigned comment added by 59.101.89.179 (talk) 12:29, 8 June 2008 (UTC)

[edit] Contradiction?

it is my understanding the levels of ghrelin present in the plasma of obese individuals is low ccompared to the amount present in lean individuals.

Ghrelin levels in the plasma of obese individuals are lower than those in leaner individuals. Ghrelin levels low -> low stimulation of appetite -> individual eats less -> individual tends to be leaner than comparable group... I too must say it seems illogical that persons with low Ghrelin levels tend to be obese. --Abdull 15:52, 25 May 2006 (UTC)

That section absolutely needs to be improved, there's either something wrong or some complex mechanism is involved which needs to be explained better in the article.--C39 13:34, 17 June 2007 (UTC)

Explanation: Ghrelin levels are low in obesity (except in Prader Willi snydrome). In fact most people with obesity don't get hungry (the growling stomach hunger caused by ghrelin). However the arcuate nucleus in obesity is oversensitive to ghrelin from chronically low levels of ghrelin and high levels of leptin. As a result the output from the NPY/AGRP cell is increased (more NPY and AGRP) and the output from the POMC cell (alpha MSH) is decreased. The result is increased cravings, decreased metabolic rate in the setting of low "hunger" levels. Ghrelin is also responsible for sleep progression which maybe why obese people have such a high rate of sleep disturbance.

Prader Willi is different. They have a genetic block of ghrelin stimulating the growth hormone releasing hormone receptor and as a result get very high ghrelin levels. These patients are obese because they overeat because they are always hungery ("the growling stomach hunger"). Todd Burstain, MD Associate Professor of Medicine, University of Iowa. todd-burstain@uiowa.edu —Preceding unsigned comment added by 129.255.246.56 (talk) 18:49, 21 September 2007 (UTC)

Just a thought; deep sleep is linked to HGH production, and Ghrelin increases HGH production. HGH increases metabolism and reduces fat. --76.175.199.3 (talk) 06:39, 15 January 2008 (UTC)

"What is known is that ghrelin promotes weight gain and fat storage through its metabolic actions, decreasing the breakdown of stored fat for energy as well as curbing energy expenditure itself." - from the source article about an anti-ghrelin vaccine. But ghrelin increases HGH? This seems contradictory. --76.175.199.3 (talk) 08:08, 15 January 2008 (UTC)

"the novel stomach hormone ghrelin ... is an endogenous agonist at the growth hormone secretagogne [sic, s.b. secretagogue -dsws] receptor and is the motilin-related family of regulatory peptides" Abstract[1] full text[2]
dsws 20:02, 29 July 2005 (UTC) GHRELINWASORIGINALLY isolated from human and rat stomach as a cognate endogenous ligand for the GH secretagogue receptor. This 28-aminoacid peptide has a posttranslational n-octanoyl modification indispensable for its activity. Ghrelin stimulates GH release when peripherally or centrally administered to rats and when applied directly to rat primary pituitary cells. In addition, ghrelin administration increases food intake and body weight gain. Whereas ghrelin secretion is upregulated under negative energy balance conditions, including starvation, insulin-induced hypoglycemia, cachexia, and anorexia nervosa, it is down-regulated under conditions of positive energy balance, such as feeding, hyperglycemia, and obesity. Gastric ghrelin enters the brain across the blood-brain barrier . Recently, stomach-derived ghrelin’s signals for starvation has been reported to be relayed to the hindbrain via the vagus afferent nerve.Ateeq Muhammed Khaliq

Ghrelin, the endogenous ligand of the GH secretagogue receptor (GHS-R), is a newly identified, ubiquitously expressed molecule that has been involved in a wide array of endocrine and nonendocrine functions, including cell proliferation. In this context, the GHS-R type 1a, in the human ovary and testis as well as several testicular tumors. Ovarian malignancies, however, remain unexplored. Notably, a vast majority of ovarian tumors derive from the surface epithelium, which originates from the celomic epithelium. Considering the proven expression of ghrelin in the human ovary, and its reported effects in the proliferative activity of different cancer cell lines, we aimed at evaluating whether the ovarian surface epithelium as well as related reproductive structures and tumors are potential targets of ghrelin. To this end, expression of GHS-R1a was analyzed by immunohistochemistry in a panel of normal, metaplastic, and neoplastic tissues. Uniform GHS-R1a immunostaining was detected throughout the ovarian surface epithelium. Likewise, ciliated cells within the fallopian tube epithelium showed strong GHS-R1a expression. In contrast, other celomic derivatives, such as endometrium and endocervix, were negative for GHS-R1a immunoreactivity. In keeping with data from normal tissues, inclusion cysts from the surface epithelium expressed GHS-R1a. Similarly, benign serous tumors resembling fallopian tube epithelium were also positive, whereas serous cystadenocarcinomas showed GHS-R1a expression only in highly differentiated specimens. In contrast, other neoplasms, such as mucinous cystadenomas and cystadenocarcinomas, endometrioid tumors, clear cell carcinomas, and Brenner tumors, did not express GHS-R1a. In conclusion, our results demonstrate that the ovarian surface epithelium and related tumors are potential targets for systemic or locally produced ghrelin because they express the functional type 1a GHS-R. Considering the relevant role of the ovarian surface epithelium in key physiological events (such as ovulation) and neoplastic transformation of the ovary, the potential actions of ghrelin in those phenomena merit further investigation.--Ateeq 3:15, 23 of june 2006 (UTC)

"Ghrelin levels increase before meals and decrease after meals" I can understand that it decreases after meals but what specifically prompts the increase? Tremello22 (talk) 21:13, 22 March 2008 (UTC)

[edit] Another Contradiction

In the opening paragraph, it is stated that "Ghrelin is a hormone produced mainly by P/D1 cells lining the fundus of the human stomach" and then a few sentences later it says "Ghrelin is also produced in the hypothalamic arcuate nucleus ". The "also" in the sentence that i just quoted refers to leptin. From my understanding, ghrelin is not produced in the hypothalamic arcuate nucleus (it is produced in the stomach), but it is received by specific receptors in the hypothalamic arcuate nucleus. Would someone care to either say that i am wrong or fix the article? Thanks. —Preceding unsigned comment added by 59.101.124.76 (talk) 10:44, 22 May 2008 (UTC)

I retract this contradiction. http://www.wisegeek.com/what-is-ghrelin.htm - that explains it all. Maybe this article should be made a little clearer then? —Preceding unsigned comment added by 59.101.124.76 (talk) 11:49, 22 May 2008 (UTC)