The MOTHER of all GUT Posts? GPR43 (FFAR2) TLR's B-vits = LONG LIFE
randall
Hi,
What's the biggest thing today right now in your yin/yang?
That's right.
The uroborus BM of them ALL... :)
What?
What are you talking about?
Elementary or in this case "Alimentary MY DEAR WATSON".....
This is another randallific uroboric moment?
U said it...
As in that snake who doesn't want you to eat the fiber rich aPPle in
eden?
What?
OK, then.
That snake who wants you to eat your tail, or his tail?
http://en.wikipedia.org/wiki/Ouroboros
So how does this alimenatarian Adam and Eve live forever east of EDEN?
EASY as aPPle Pie...
Did any of you read about GPR43 in a recent thread or two?
GPR43 really is almost as big as some others recently, like SFB & L.
Plantarum come to mind.
So what is it?
From wikipedia?
Yes make it short and sweet, like your whey.
OK...
http://en.wikipedia.org/wiki/Free_fatty_acid_receptor
The free fatty acid receptor is a G-protein coupled receptor which
binds free fatty acids.[1] There are four variants of the receptor,
each encoded by a separate gene (FFAR1, FFAR2, FFAR3, GPR42).
Huh?
GPR43 is really FFAR2?
How about that? LOL
http://www.genenames.org/data/hgnc_data.php?match=FFAR2
So ok already let's see what's what with FFAR2 which is GPR43.
The science (pubmed--abstract) answer contains words like ileum. LOL
So Susan don't read this and skip to the articles. :)
http://www.ncbi.nlm.nih.gov/pubmed/16453106
Short-chain fatty acid receptor, GPR43, is expressed by
enteroendocrine cells and mucosal mast cells in rat intestine.
Karaki S, Mitsui R, Hayashi H, Kato I, Sugiya H, Iwanaga T, Furness
JB, Kuwahara A.
Laboratory of Physiology, Institute for Environmental Sciences,
University of Shizuoka, 52-1 Yada, Shizuoka, 422-8526, Japan.
Short-chain fatty acids (SCFAs), such as acetate, propionate, and
butyrate, are the major anions in the large intestinal lumen. They are
produced from dietary fiber by bacterial fermentation and are known to
have a variety of physiological and pathophysiological effects on the
intestine. In the present study, we investigated the expression of the
SCFA receptor, GPR43, in the rat distal ileum and colon. Expression of
GPR43 was detected by reverse transcriptase/polymerase chain reaction
(RT-PCR), Western blotting, and immunohistochemistry. mRNA for GPR43
was detected, by RT-PCR, in extracts of the whole wall and separated
mucosa from the ileum and colon and from muscle plus submucosa from
the ileum, but not from muscle plus submucosa preparations from the
colon. We raised a rabbit antiserum against a synthesized fragment of
rat GPR43; this was specific for rat GPR43. GPR43 protein was detected
by Western blot analysis in extracts of whole wall and separated
mucosa, but not in muscle plus submucosa extracts. By
immunohistochemistry, GPR43 immunoreactivity was localized to
enteroendocrine cells expressing peptide YY (PYY), whereas 5-
hydroxytryptamine (5-HT)-immunoreactive (IR) enteroendocrine cells
were not immunoreactive for GPR43. Mast cells of the lamina propria
expressing 5-HT were also GPR43-IR. The results of the present study
suggest that the PYY-containing enteroendocrine cells and 5-HT-
containing mucosal mast cells sense SCFAs via the GPR43 receptor. This
is consistent with physiological data showing that SCFAs stimulate the
release of PYY and 5-HT from the ____ileum____ and colon.
PMID: 16453106
Why is it, that your ileum is important? Not to long ago JRSTERN was
posting
stuff for your appendix and eight years ago JR posted the GOOD ARTICLE
link
from XOMA that no longer works but was posted in full in this group.
The GOOD ARTICLE clued some of in to LPS and what it does in your
colon.
Then we found out about TLR's (toll like receptors)
Since then I've never looked back. :)
I knew this was the right track. It had to be.
And if i waited the science would catch up to my trials
that cleared my skin with the wit kit and sweet whey diet.
OK, ok...
First lets see what this science and GPR43 in your colon and ileum is
all about.
I'll repost the recent links:
This was on oct 30 2009 or less then a week ago.
http://www.eurekalert.org/pub_releases/2009-10/ra-nfc102809.php
New findings connect diet and intestinal bacteria with healthier
immune systems
<sniP>
And from byron's article i posted yesterday:
http://www.wellnessresources.com/health/articles/how_fiber_friendly_flora_reduce_inflammation/
This one is so good you should read byrons notes:
http://www.wellnessresources.com/studies/entry/fiber_and_friendly_flora_reduce_inflammation
This looks like the same link. So go to the link in the article and in
blue
it says " dietary fiber and friendly GI tract flora" and click it
and you'll get byrons notes on this topic.
==========================================
This next B vitamin Article is for Susan and others who want to LIVE
long and prosPer.
Like a vulcan?
Sure or here on earth like Methuselah grand-father of Noah who
invented red wine. LOL
NO>?
Really?
Wiki says so. So it must be.
http://en.wikipedia.org/wiki/Methuselah
Methuselah was the grandfather of Noah and the oldest person whose age
is mentioned in the Hebrew Bible, given as 969 years
The name Methuselah has become a general synonym for any living
creature of great age.
http://en.wikipedia.org/wiki/Noah
[...]
"Noah was the first tiller of the soil. He planted a vineyard; and he
drank of the wine."[10]
Noah died 350 years after the Flood, at the age of 950,[11] the last
of the immensely long-lived antediluvian Patriarchs. The maximum human
lifespan, as depicted by the Bible, diminishes rapidly thereafter,
from as much as 900 years to the 120 years of Moses within twenty
generations. Another few generations later, lifespans were reported to
be less than 100 years on average.
<sniP>
http://en.wikipedia.org/wiki/Noah#Textual_criticism
[...]
Genesis seems to contain two accounts concerning Noah, the first
making him the hero of the Flood, the second representing him as a
husbandman who planted a vineyard. This has led some scholars to
believe that Noah was believed by the ancients to be the inventor of
wine, in keeping with the statement at Genesis 5:29 that Lamech
"called his name Noah, saying, 'Out of the ground which the Lord has
cursed this one shall bring us relief from our work and from the toil
of our hands.'"[18]
<sniP>
See third paragraph:
http://en.wikipedia.org/wiki/Noah#Connections_to_other_lore
Wow---> did Ham sodomize his dad while drunk on wine?
http://en.wikipedia.org/wiki/Ham,_son_of_Noah
read genesis 20-25
http://www.mechon-mamre.org/p/pt/pt0109.htm#20
&
http://en.wikipedia.org/wiki/Ham,_son_of_Noah#Curse_of_Canaan_also_known_as_the_Curse_of_Ham
I love this biblicow stuff.
Wine, and God, what's not to like?
Here's another:
This was a really fun read by Larry Williams in another Godly vein.
Moses and where did he park after leaving Town.
"The mountain of Moses discovery of mount sinai: (book) by larry
williams
You can buy one here:
http://www.alibris.com/booksearch?qwork=4484495&matches=21&author=Williams%2C+Larry&browse=1&cm_sp=works*listing*title
Larry had a blast doing this book and the RESEARCH for it.
In his __work__ life, he's found a great measure of success that he
shares:
http://www.ireallytrade.com/
While Larry Makes the big bucks your health is still your greatest
WEALTH.
================
How do we find it?
Wowser, take a tiP already.
It's a gut trip with red wine or those cool longevinex capsules.
Now---> red wine in a capsule can be had from www.longevinex.com
without
Ham pulling the BONE on you while skunk drunk. LOL
I never knew this Canaan curse. See fifth paragraph till end:
http://en.wikipedia.org/wiki/Canaan#Biblical_Canaanites
How do we avoid the curse in OUR bodies?
Easy....
Just take the alcohol free www.longevinex.com capsules and block
the sugar, sugar, honey, honey problems with B vits.
How amazing? Which ones?
http://www.vrp.com/articles.aspx
Can a Single Vitamin Prevent Premature Aging?
By VRP Staff
Believe it or not, your body is producing poisons at this very
moment. And while they may be a natural part of aging, they’re also
very, very damaging. In fact, advanced glycation end products (AGEs)—
toxic molecules formed through a series of haywire reactions between
sugar, proteins and lipids—are directly involved in just about every
disease of aging imaginable.1–11
Research shows that, among diabetics, AGEs are the main culprit behind
aging that’s accelerated a full 20 to 40 years faster than non–
diabetics—taking the form of conditions like arterial plaque and
hardening of arteries, kidney disease, retinopathy and peripheral
nerve damage.12 But even non–diabetics need to watch out for these
dangerous byproducts, as your levels only increase with age, and pave
the way to any number of other serious diseases—including Alzheimer’s
disease, arthritis and macular degeneration.
The good news is that there’s a way to block and even reverse the
damage these AGEs can cause—and a single B vitamin may be your secret
weapon.13
In recent years, scientists have discovered that benfotiamine—a
synthetic, fat–soluble form of thiamine, or vitamin B1—is a potent AGE
blocker. In fact, clinical studies show that this form of the vitamin
is as much as 430 percent more bioavailable than its water–soluble
counterpart, which has a modest absorption rate of only four to six
percent.14–16
This superior absorption rate offers one reason for the powerful
protection benfotiamine offers against AGEs—a benefit that’s been
borne out in a number of animal and human studies. In one study, for
example, researchers found that type 1 diabetics given 600 mg of
benfotiamine daily experienced a 40 to 62 percent drop in just four
weeks of levels of carboxymethyllysine (CML) and methylglyoxal — two
predominant AGEs implicated in Alzheimer’s disease, blood vessel
complications and atherosclerosis.17
Further trials show that supplementing with benfotiamine can also
significantly reduce pain associated with diabetic neuropathy (that
is, peripheral nerve damage), while helping to regulate heartbeat—
results that don’t correspond to standard B–complex supplementation.18–
19 And finally, animal studies suggest that benfotiamine offers
critical protection against diabetic retinopathy, too.
In a 36–week study of three groups of rats—two of which were diabetic
or hyperglycemic, along with one set of healthy controls—researchers
found that rats receiving benfotiamine had retinas as healthy as
controls by the end of the study. Those diabetic rats that did not
receive benfotiamine, however, suffered severely damaged retinal blood
vessels as a result.20
The bottom line: Even if you’re already taking a B–complex, adding an
additional daily dose of benfotiamine—readily available in capsule
form through Vitamin Research Products—can provide a critical extra
layer of protection against AGE damage at any age.
References:
<snip>
==================
Did you get the grp43 import above?
I hope so.
If not. For hard core types only.... :)
One more for GPR43 from science daily:
http://www.sciencedaily.com/releases/2009/10/091028142235.htm
Diet And Intestinal Bacteria Linked To Healthier Immune Systems
ScienceDaily (Oct. 28, 2009) — Insoluble dietary fibre, or roughage,
not only keeps you regular, say Australian scientists, it also plays a
vital role in the immune system, keeping certain diseases at bay
The indigestible part of all plant-based foods pushes its way through
most of the digestive tract unchanged, acting as a kind of internal
broom. When it arrives in the colon, bacteria convert it to energy and
compounds known as 'short chain fatty acids'. These are already known
to alleviate the symptoms of colitis, an inflammatory gut condition. 1
Similarly, probiotics and prebiotics, food supplements that affect the
balance of gut bacteria, reduce the symptoms of asthma and rheumatoid
arthritis, also inflammatory diseases. Until now no-one has understood
why.
Published October 28 in Nature, breakthrough research by a Sydney-
based team makes new sense of such known facts by describing a
mechanism that links diet, gut bacteria and the immune system.
PhD student Kendle Maslowski and Professor Charles Mackay from the
Garvan Institute of Medical Research, in collaboration with the Co-
operative Research Centre for Asthma and Airways, have demonstrated
that GPR43, a molecule expressed by immune cells and previously shown
to bind short chain fatty acids, functions as an anti-inflammatory
receptor.
"The notion that diet might have profound effects on immune responses
or inflammatory diseases has never been taken that seriously" said
Professor Mackay. "We believe that changes in diet, associated with
western lifestyles, contribute to the increasing incidences of asthma,
Type 1 diabetes and other autoimmune diseases. Now we have a new
molecular mechanism that might explain how diet is affecting our
immune systems."
"We're also now beginning to understand that from the moment you're
born, it's incredibly important to be colonised by the right kinds of
gut bacteria," added Kendle. "The kinds of foods you eat directly
determine the levels of certain bacteria in your gut."
"Changing diets are changing the kinds of gut bacteria we have, as
well as their by-products, particularly short chain fatty acids. If we
have low amounts of dietary fibre, then we're going to have low levels
of short chain fatty acids, which we have demonstrated are very
important in the immune systems of mice."
Mice that lack the GPR43 gene have increased inflammation, and poor
ability to resolve inflammation, because their immune cells can't bind
to short chain fatty acids.
There is plenty of evidence to suggest that bacteria and their by-
products play an important role in people. An American study published
in Nature in 2006 2 compared the bacteria in the guts of obese and
lean people. The obese people were put on a diet, and as they lost
weight their bacteria profile gradually came to match that of the lean
people.
Another study 3 looked at what diets might do to short chain fatty
acid levels. Obese people were put on three different diets over time
-- high, medium and low fibre -- and there was a direct correlation
between the level of carbohydrate, or fibre, in the diet and the level
of short chain fatty acids.
The conclusions drawn from the current research provide some of the
most compelling reasons yet for eating considerably more unprocessed
whole foods -- fruits, vegetables, grains, nuts and seeds. 4
Dietary fibre, of course, has many known health benefits in addition
to those discussed above, including reduced risk of cardiovascular
disease and certain cancers 5, and various health organizations around
the world recommend daily minimum levels. 6 It is certain that the
majority of people in countries like Australia, the United States and
Britain eat much less fibre than they need to stay healthy.
"The role of nutrition and gut intestinal bacteria in immune responses
is an exciting new topic in immunology, and recent findings including
our own open up new possibilities to explore causes as well as new
treatments for inflammatory diseases such as asthma," said Professor
Mackay.
1. In several trials, people with colitis have been given dietary
fibre, resulting in beneficial anti-inflammatory effects:
Harig, J. M., Soergel, K. H., Komorowski, R. A. & Wood, C. M.
Treatment of diversion colitis with short-chain-fatty acid irrigation.
N. Engl. J. Med. 320, 23-28 (1989). http://www.ncbi.nlm.nih.gov/pubmed/2909876?dopt=Abstract
Kanauchi, O. et al. Treatment of ulcerative colitis by feeding with
germinated barley foodstuff: first report of a multicenter open
control trial. J. Gastroenterol. 37 (suppl. 14), 67-72 (2002).
http://www.ncbi.nlm.nih.gov/pubmed/12572869?dopt=Abstract
Breuer, R. I. et al. Rectal irrigation with short-chain fatty acids
for distal ulcerative colitis. Preliminary report. Dig. Dis. Sci. 36,
185-187 (1991). http://www.ncbi.nlm.nih.gov/pubmed/1988261?dopt=Abstract
Scheppach, W. Treatment of distal ulcerative colitis with short-chain
fatty acid enemas. A placebo-controlled trial. German-Austrian SCFA
Study Group. Dig. Dis. Sci. 41, 2254-2259 (1996).
http://www.ncbi.nlm.nih.gov/pubmed/8943981?dopt=Abstract
Vernia, P. et al. Short-chain fatty acid topical treatment in distal
ulcerative colitis. Aliment. Pharmacol. Ther. 9, 309-313 (1995).
http://www.ncbi.nlm.nih.gov/pubmed/7654893?dopt=Abstract
2. Ley, R. Turnbaugh, P.J. Klein, S Gordon, J.I Human gut microbes
associated with obesity. Nature 444, 1022-1023 (2006).
http://www.nature.com/nature/journal/v444/n7122/abs/4441022a.html
3. Duncan, S.H Belenguer, A. Holtrop, G. Johnstone, A.M. Flint, H.J.
Lobley, G.E. Reduced Dietary Intake of Carbohydrates by Obese Subjects
Results in Decreased Concentrations of Butyrate and Butyrate-Producing
Bacteria in Feces. Applied and Environmental Microbiology, 1073-1078
(2007) http://aem.asm.org/cgi/content/abstract/73/4/1073
4. There are many online sources where information can be found about
foods and their levels of soluble and insoluble fibre -- the effects
of the latter investigated in this research. Some foods, such as wheat
bran, chick peas, dried fruits (apricots, peaches, figs and dates) and
berries (raspberries and blackberries) have particularly high levels
of insoluble fibre. CSIRO produces a useful fact sheet.
http://www.csiro.au/resources/DietaryFibre.html#1
5. O'Keefe, S Ou, J Aufreiter, S O'Connor, D Sharma, S Sepulveda, J
Fukuwatari, T Shibata, K Mawhinney, T. Products of the Colonic
Microbiota Mediate the Effects of Diet on Colon Cancer Risk. J. Nutr.
2009 139: 2044-2048. First published online November 1, 2009; doi:
10.3945/jn.109.104380 http://jn.nutrition.org/cgi/content/abstract/139/11/2044
6. Australian Dietary Guidelines, produced by the National Health and
Medical Research Council recommend a daily intake of 30-35 grams of
fibre. http://www.health.gov.au/internet/healthyactive/publishing.nsf/content/eating
================================
Let's run pubmed for the abstract that got this shiP of health a
float.
If Noah and his crew knew, why don't YOU?
www.ncbi.nlm.nih.gov/pubmed/19865172
Regulation of inflammatory responses by gut microbiota and
chemoattractant receptor GPR43.
Maslowski KM, Vieira AT, Ng A, Kranich J, Sierro F, Yu D, Schilter HC,
Rolph MS, Mackay F, Artis D, Xavier RJ, Teixeira MM, Mackay CR.
Garvan Institute of Medical Research, 384 Victoria Street,
Darlinghurst, New South Wales 2010, Australia.
The immune system responds to pathogens by a variety of pattern
recognition molecules such as the Toll-like receptors (TLRs), which
promote recognition of dangerous foreign pathogens. However, recent
evidence indicates that normal intestinal microbiota might also
positively influence immune responses, and protect against the
development of inflammatory diseases. One of these elements may be
short-chain fatty acids (SCFAs), which are produced by fermentation of
dietary fibre by intestinal microbiota. A feature of human ulcerative
colitis and other colitic diseases is a change in 'healthy' microbiota
such as Bifidobacterium and Bacteriodes, and a concurrent reduction in
SCFAs. Moreover, increased intake of fermentable dietary fibre, or
SCFAs, seems to be clinically beneficial in the treatment of colitis.
SCFAs bind the G-protein-coupled receptor 43 (GPR43, also known as
FFAR2), and here we show that SCFA-GPR43 interactions profoundly
affect inflammatory responses. Stimulation of GPR43 by SCFAs was
necessary for the normal resolution of certain inflammatory responses,
because GPR43-deficient (Gpr43(-/-)) mice showed exacerbated or
unresolving inflammation in models of colitis, arthritis and asthma.
This seemed to relate to increased production of inflammatory
mediators by Gpr43(-/-) immune cells, and increased immune cell
recruitment. Germ-free mice, which are devoid of bacteria and express
little or no SCFAs, showed a similar dysregulation of certain
inflammatory responses. GPR43 binding of SCFAs potentially provides a
molecular link between diet, gastrointestinal bacterial metabolism,
and immune and inflammatory responses.
PMID: 19865172
www.ncbi.nlm.nih.gov/pubmed/19817784
Lipid receptors and islet function: therapeutic implications?
Kebede MA, Alquier T, Latour MG, Poitout V.
Montréal Diabetes Research Center, CRCHUM, QC, Canada.
G-protein coupled receptors (GPCRs) are targets of approximately 30%
of currently marketed drugs. Over the last few years, a number of
GPCRs expressed in pancreatic beta-cells and activated by lipids have
been discovered. GPR40 was shown to be activated by medium- to long-
chain fatty acids (FAs). It has since been shown that GPR40
contributes to FA amplification of glucose-induced insulin secretion.
Although some controversy still exists as to whether GPR40 agonists or
antagonists should be designed as novel type 2 diabetes drugs, data
obtained in our laboratory and others strongly suggest that GPR40
agonism might represent a valuable therapeutic approach. GPR119 is
expressed in pancreatic beta-cells and enteroendocrine L-cells, and
augments circulating insulin levels both through its direct
insulinotropic action on beta-cells and through FA stimulation of
glucagon-like peptide 1 (GLP-1) secretion. GPR120 is expressed in L-
cells and was also shown to mediate FA-stimulated GLP-1 release.
Finally, GPR41 and GPR43 are receptors for short-chain FAs and may
indirectly regulate beta-cell function via adipokine secretion.
Although the discovery of these various lipid receptors opens new and
exciting avenues of research for drug development, a number of
questions regarding their mechanisms of action and physiological roles
remain to be answered.
PMID: 19817784
[Pre- and probiotics increase host-cell immunological competence,
improve bowel movement, and prevent the onset of colon cancer--an
analysis based on movements of intestinal microbiota]
[Article in Japanese]
Ohara T, Yoshino K, Kitajima M.
Department of Gastroenterology, International University of Health and
Welfare Hospital, Nasu-shiobara 329-2763, Japan. toh...@iuhw.ac.jp
The activation of host immunological competence through improvement of
the intestinal environment by pre and probiotics has been reported. NK
cell activity, the bactericidal phagocytic activities of neutrophils
in peripheral blood, and bowel movements and short chain fatty acids
(SCFAs) in intestinal microbiota increase after the administration of
pre- and probiotics. SCFAs shift to acidosis of the intestinal
environment and advance apoptosis. Furthermore, SCFAs promote
intestinal peristaltic movements through SCFA receptors such as GPT 41
and GPR43, located in the intestinal epithelium. It is known that the
acceleration of intestinal apoptosis prevents the onset of colon
cancer. Improvement of the intestinal environment leads to an increase
in host-cell immunological competence, bowel movements, and the
prevention of colon cancer.
PMID: 19621785
Here's all 29 hits on pubmed for : gpr43
http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=DetailsSearch&term=gpr43&log$=activity
This is odd. Only nine hits come up for FFAR2 on pubmed:
http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=DetailsSearch&term=ffar2&log$=activity
Here's one that only mentions FFAR's
www.ncbi.nlm.nih.gov/pubmed/19780758
Identification of transforming activity of free fatty acid receptor 2
by retroviral expression screening.
Hatanaka H, Tsukui M, Takada S, Kurashina K, Choi YL, Soda M,
Yamashita Y, Haruta H, Hamada T, Ueno T, Tamada K, Hosoya Y, Sata N,
Yasuda Y, Nagai H, Sugano K, Mano H.
Division of Functional Genomics, Jichi Medical University, Tochigi,
Japan.
Gallbladder cancer (GBC) is a highly fatal malignancy in humans.
Genetic alterations in KRAS or TP53 as well as overexpression of ERBB2
have been shown to contribute to the development of certain types of
GBC. However, many cases of GBC do not harbor such genetic changes,
with other transforming events awaiting discovery. We here tried to
identify novel cancer-promoting genes in GBC, with the use of a
retroviral cDNA expression library. A retroviral cDNA expression
library was constructed from a surgically resected clinical specimen
of GBC, and was used to infect 3T3 fibroblasts in a focus formation
assay. cDNA incorporated into the transformed foci was rescued by PCR.
One such cDNA was found to encode free fatty acid receptor 2 (FFAR2),
a G protein-coupled receptor for short-chain fatty acids. The
oncogenic potential of FFAR2 was confirmed both in vitro with the
focus formation assay and by evaluation of cell growth in soft agar as
well as in vivo with a tumorigenicity assay in nude mice. The isolated
FFAR2 cDNA had no sequence alterations, suggesting that upregulation
of FFAR2 expression may contribute to malignant transformation.
Indeed, all of quantitative RT-PCR, in situ hybridization, and
immunohistochemical analyses showed that the amount of FFAR2 mRNA and
its protein product was increased in digestive tract cancer specimens.
Furthermore, short-chain fatty acids potentiated the mitogenic action
of FFAR2 in 3T3 cells. Our data thus, for the first time, implicate
FFAR2 in carcinogenesis of the digestive tract. (Cancer Sci 2009).
PMID: 19780758
Wow... it says that FFAR2 (gpr43) is upregulated in Gi tract cancer?
Maybe not if you have an autoimmune condition? LOL
This one looks more optimistic.
www.ncbi.nlm.nih.gov/pubmed/19460454
Free fatty acid receptors act as nutrient sensors to regulate energy
homeostasis.
Ichimura A, Hirasawa A, Hara T, Tsujimoto G.
Department of Genomic Drug Discovery Science, Graduate School of
Pharmaceutical Sciences, Kyoto University, Sakyo-ku, Kyoto, Japan.
Free fatty acids (FFAs) have been demonstrated to act as ligands of
several G-protein-coupled receptors (GPCRs) (FFAR1, FFAR2, FFAR3,
GPR84, and GPR120). These fatty acid receptors are proposed to play
critical roles in a variety of types of physiological homeostasis.
FFAR1 and GPR120 are activated by medium- and long-chain FFAs. GPR84
is activated by medium-chain, but not long-chain, FFAs. In contrast,
FFAR2 and FFAR3 are activated by short-chain FFAs. FFAR1 is expressed
mainly in pancreatic beta-cells and mediates insulin secretion,
whereas GPR120 is expressed abundantly in the intestine and promotes
the secretion of glucagon-like peptide-1 (GLP-1). FFAR3 is expressed
in enteroendocrine cells and regulates host energy balance through
effects that are dependent upon the gut microbiota. In this review, we
summarize the identification, structure, and pharmacology of these
receptors and present an essential overview of the current
understanding of their physiological roles.
PMID: 19460454
===========================
randall.... isn't it all stunning? I think SO.. :)
JRStern
wrote:
>randall.... isn't it all stunning? I think SO.. :)
Yes, I think so too.
The GPR43 sounds hot ... but can't we just swallow some short chain
fatty acids and skip the flora? And I guess they mean *really* short
chain fatty acids ... acetate?
And maybe the benfotiamine is 400% more absorbable, but 2000%
B-complex pills are a penny each.
And maybe I should go get some.
Still, it is exciting to see some mainline research looking at these
things and finding results.
J.
randall
> On Fri, 6 Nov 2009 13:39:54 -0800 (PST), randall <ranhu...@aol.com>
J,
What do you think? I haven't done the work on fatty acids?
What about w3? How short is it compared to 6, 9, 12 hike?
How many omega-3 threads in our group?
716 hits for keyword: omega-3 [in the psor news group]
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?hl=en&group=alt.support.skin-diseases.psoriasis&q=omega-3
But why stop there?
I really REALLY like'd the benfotiamine (artificial B1) article.
We've had six hits TOTAL in the psor group for benfotiamine.
That;s it?
Yes...
AS opposed to way over 700 hits for omega-3's.
Why is that? We should really look at AGE's more.
And one of those may look rather familiar to YOU. <W>
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/msg/304ea7b113cf5e1c
That's right.
You hooked up with synthetic Vit B1 back on FEB 16 2003 in our group.
LOL
How prescient are you? <G> ;~/
And how prescient AM i?
Only as prescient as google allows me. LOL
Further down in the same thread to evetsm:
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/msg/9045336c07a26d54
Wow i'm reading me from six years ago and i'm smarter then then, NOW.
How can that be?
Easy... i need more B-1. LOL
And look at this anti pharma post in a similar B1 thread:
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/msg/598c37d3d9a5c960
Holy Ghost. This is so weird to revisit the ghost of fumaderm.
And how COME we're not privy to FAE;s right now?
I'll tell you why. Because big Pharma is not going to let us use
anything that will intrude on their bio illogical pot of gold....
Biologicals are simply so elementary compared to the places and genes
we've
seen in the last few weeks, it's UNreal...
And living longer for psoriatics is the single most important area
i'm now researching. :)
After SFB's and L. Plantarum and those genes in our pathways i'm
thinking living till mid 90's and doing it with my brain cells still
intact.
And all because of a benfotiamine group search:
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?hl=en&group=alt.support.skin-diseases.psoriasis&q=benfotiamine+&qt_g=Search+this+group
----------
What I ALSO liked i this thread was the biblical apple references,
besides the red wine cites.
Apples and red wine and living for over a 100 years. Yikes...
How much do i like it?
Tons..
I've posted way to much on resveratrol (from: www.longevinex.com --
red wine or japanese knot weed) and not enough on aPPles.
APPles are loaded with quercetin:
http://en.wikipedia.org/wiki/Quercetin
The only foods loaded with more are capers and lovage.
When are you gonna swill those two down, when you can easily nail a
few apples a day? LOL
I"m using capers in my sweet whey shakes NOW....
I'm gonna live AT THE VERY LEAST LONG ENOUGH FOR THE CURE OF
PSORIASIS.
And when we can muster the CD4+CD25+ regulatory T (Treg) cells and
attenuate Th17
in a timely manner to stay clear, i'll say hip hip hooray.
Why?
Because then i'll know i'm clear.
Why?
Just look stuPid.
156 hits for keywords: CD4+CD25+ regulatory T (Treg) cells [in our
psor support group]
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?hl=en&q=CD4%2BCD25%2B+regulatory+T+(Treg)+cells&start=0&scoring=d&hl=en&
Isn't that cool?
I think so.
With the most recent posts i'm so Jazzed it's not funny.
My OCD is paying off. LOL
And my Chargers beat the Giants in a less second thriller today.
21-20 with 20 seconds left on the clock.
Btw- sorry your LA team couldn't beat the New York team.
Now i'm worried my chargers may be coming back home
next year or shortly thereafter.
Those Spanos are money grubbing grubbers. LOL
So if YOU get to become a fan of MY team, what can i say?
EAT my SWEET WHEY and DIE.... LOL
---------------------
randall... gets down... kill death and hang around to root for the
home team...
JRStern
wrote:
>What about w3? How short is it compared to 6, 9, 12 hike?
That's a point.
>And one of those may look rather familiar to YOU. <W>
>
>http://groups.google.com/group/alt.support.skin-diseases.psoriasis/msg/304ea7b113cf5e1c
how about that.
>And look at this anti pharma post in a similar B1 thread:
>http://groups.google.com/group/alt.support.skin-diseases.psoriasis/msg/598c37d3d9a5c960
>
>Holy Ghost. This is so weird to revisit the ghost of fumaderm.
That's OK, Obama will fix it.
>What I ALSO liked i this thread was the biblical apple references,
>besides the red wine cites.
>
>Apples and red wine and living for over a 100 years. Yikes...
I've taken a lot of quercetin, back when I got some capsules and tried
those, but didn't see any major results, but I still consume mass
quantities of apples, onions, and tea, three good sources. Maybe it
helps. But I still think a mixed bag of such bioflavonids is probably
about the same effectiveness as mass quantities of any one, at least
short of having a custom DNA profile.
>Btw- sorry your LA team couldn't beat the New York team.
Lakers rool.
J.