Glucose better?

"Cubit" <[email hidden]> wrote in
:"]news:[email hidden]:

Quoted message said:

I've read about fructose causing obesity and insulin
resistance. I gather fructose is found in both sugar and
corn syrup. Might it be better to sweeten foods with
glucose?

Glucose is substantially less sweet than fructose, so any
possible benefits would almost certainly be negated by the
need to use larger amounts.

I'm aware this is off-topic to this discussion, nevertheless
I ask -- what are your thoughts on the use of artificial
sweeteners in lieu of fructose and glucose? Do you use them?

-Chad

"Cubit" <[email hidden]> wrote in message
"]news:[email hidden]...

Quoted message said:

I've read about fructose causing obesity and insulin
resistance. I gather fructose is found in both sugar and
corn syrup. Might it be better to sweeten foods with
glucose?

Commercial fructose and glucose are both predigested,
therefore it would not be useful to use either of them as
sweeteners. Your best bet is to use a natural sweetener in
combination with whatever it comes with naturally.

Ora

Cubit said:

I've read about fructose causing obesity and insulin
resistance. I gather fructose is found in both sugar
and corn syrup. Might it be better to sweeten foods
with glucose?

Some of the artificial sweeteners can cause diarrhea so if
you want to use them, use them sparingly.

Ora

Chad C. said:

I'm aware this is off-topic to this discussion,
nevertheless I ask -- what are your thoughts on the use of
artificial sweeteners in lieu of fructose and glucose? Do
you use them?

-Chad

"Cubit" <[email hidden]> wrote in message
"]news:[email hidden]...

Quoted message said:

I've read about fructose causing obesity and insulin
resistance. I gather fructose is found in both sugar and
corn syrup. Might it be better to sweeten foods with
glucose?

"Cubit" <[email hidden]> wrote in message news:<[email hidden]>...

Quoted message said:

I've read about fructose causing obesity and insulin
resistance. I gather fructose is found in both sugar and
corn syrup. Might it be better to sweeten foods with
glucose?

If your concern is development of insulin resistance/obesity
etc. you might want to entertain the notion of simply not
sweetening your foods (and avoiding those that are
manufactured with refined sugars)!

Fructose from its natural sources (fruits!) is not going to
contribute to ill health......rather they will contribute to
improved health. Focus on eating real food in its natural
form and you won't to worry so much!!

and finally, I'd would love to know if it was an actual
research article that linked fructose with obesity and
insulin resistance. As a researcher, it would be a daunting
task to narrow an exposure to such a small fraction of
overall diet let alone attribute causality to that small
fraction. But thats a whole other topic!

Cheers, Lisa

Er, I think you've got that exactly backwards. Fructose
enters the bloodstream quite slowly and is associated with
steadier blood sugar levels, while glucose enters more
quickly and leads to spikes in blood sugar. Fructose is
found mainly in fruits and vegetables, I would be very
surprised if it were in standard table sugar. Search google
on "glycemic index" and you'll get a lot of info. -- M9

"Cubit" <[email hidden]> wrote in message
"]news:[email hidden]...

Quoted message said:

I've read about fructose causing obesity and insulin
resistance. I gather fructose is found in both sugar and
corn syrup. Might it be better to sweeten foods with
glucose?

"Chad C." <[email hidden]> wrote in message news:<[email hidden]>...

Quoted message said:

I'm aware this is off-topic to this discussion,
nevertheless I ask -- what are your thoughts on the use of
artificial sweeteners in lieu of fructose and glucose? Do
you use them?

-Chad

"Cubit" <[email hidden]> wrote in message
"]news:[email hidden]...

Quoted message said:

I've read about fructose causing obesity and insulin
resistance. I gather fructose is found in both sugar and
corn syrup. Might it be better to sweeten foods with
glucose?

I think that any and all of these are okay if they are
easten in moderate amounts... If you go overboard with any
of these things you will get negative results, but in
suggested amounts, these are not that bad... People need to
develop some personal responsibility. Why are we making
such a big deal out of this type of thing? Don't eat or
drink ridiculous amounts of anything, get exercise, and you
will be fine.

"Lisa" <[email hidden]> wrote in message
"]news:[email hidden]...

Quoted message said:

"Cubit" <[email hidden]> wrote in message

news:<[email hidden]>...

Quoted message said:

Quoted message said:

I've read about fructose causing obesity and insulin
resistance. I

gather

Quoted message said:

Quoted message said:

fructose is found in both sugar and corn syrup. Might it
be better to sweeten foods with glucose?

If your concern is development of insulin
resistance/obesity etc. you might want to entertain the
notion of simply not sweetening your foods (and avoiding
those that are manufactured with refined sugars)!

Fructose from its natural sources (fruits!) is not going
to contribute to ill health......rather they will
contribute to improved health. Focus on eating real food
in its natural form and you won't to worry so much!!

and finally, I'd would love to know if it was an actual
research article that linked fructose with obesity and
insulin resistance. As a researcher, it would be a
daunting task to narrow an exposure to such a small
fraction of overall diet let alone attribute causality to
that small fraction. But thats a whole other topic!

Cheers, Lisa

FYI: tinyurl.comys8ljOpen ↗

MikeV

Interesting article. I'm no dietary scientist, but I can't
reconcile in my mind the low g.i. profile of fructose (as
compared to glucose) along with the preliminary data
suggesting a connection between fructose and insulin
resistance. To me, it seems like it would work just the
opposite -- i.e., a lower g.i. = slower insulin response =
less risk of insulin syndrome. What am I missing here? -- M9

"Mike V" <[email hidden]> wrote in message news:ww-
[email hidden]...

Quoted message said:

"Lisa" <[email hidden]> wrote in message
"]news:[email hidden]...

Quoted message said:

"Cubit" <[email hidden]> wrote in message

news:<[email hidden]>...

Quoted message said:

Quoted message said:

I've read about fructose causing obesity and insulin
resistance. I

gather

Quoted message said:

Quoted message said:

fructose is found in both sugar and corn syrup. Might
it be better to sweeten foods with glucose?

If your concern is development of insulin
resistance/obesity etc. you might want to entertain the
notion of simply not sweetening your foods (and avoiding
those that are manufactured with refined sugars)!

Fructose from its natural sources (fruits!) is not going
to contribute to ill health......rather they will
contribute to improved health. Focus on eating real food
in its natural form and you won't to worry so much!!

and finally, I'd would love to know if it was an actual
research article that linked fructose with obesity and
insulin resistance. As a researcher, it would be a
daunting task to narrow an exposure to such a small
fraction of overall diet let alone attribute causality
to that small fraction. But thats a whole other topic!

Cheers, Lisa

FYI: tinyurl.comys8ljOpen ↗

MikeV

"minerva nine" <[email hidden]> wrote in message
"]news:[email hidden]...

Quoted message said:

Interesting article. I'm no dietary scientist, but I can't
reconcile in

my

Quoted message said:

mind the low g.i. profile of fructose (as compared to
glucose) along with the preliminary data suggesting a
connection between fructose and insulin resistance. To me,
it seems like it would work just the opposite -- i.e.,

a

Quoted message said:

lower g.i. = slower insulin response = less risk of
insulin syndrome.

What

Quoted message said:

am I missing here? -- M9

"Mike V" <[email hidden]> wrote in message news:-
[email hidden]...

Quoted message said:

Quoted message said:

> > Lisa

FYI: tinyurl.comys8ljOpen ↗

MikeV

M9:Fructose is tricky in that although it is a refined
sugar, it does not invoke much insulin response, satiety
etc. It is said to bypass normal glucose regulatory
response and to be processed mainly by the liver directly
into fats. Read nature.com040510Open ↗
5.html

See also the recent thread "Corn Syrup Linked to Diabetes,
Diarmid Logan, May 13" See refs to IRS-1, IRS-2 in earlier
posts by HUA KUL for more insight in how IR arises. MikeV

This also may be of interest.

ncbi.nlm.nih.govquery.fcgiOpen ↗
db=PubMed&list_uids=12627878&dopt=Abstract

Hypertens Res. 2003 Feb;26(2):169-76. Related
Articles, Links

*Tissue-specific impairment of insulin signaling in
vasculature and skeletal muscle of fructose-fed rats.*

Hyakukoku M, Higashiura K, Ura N, Murakami H, Yamaguchi K,
[censored] L, Furuhashi M, Togashi N, Shimamoto K.

Second Department of Internal Medicine, Sapporo Medical
University School of Medicine, Sapporo, Japan. hyakoku-masaya@nshp-
muroran.or.jp

The relation between insulin resistance/hyperinsulinemia and
cardiovascular diseases has attracted much attention.
Insulin affects not only glucose metabolism, but also
protein synthesis and cell growth. Insulin stimulates both
the phosphatidylinositol 3-kinase (PI3-K) and mitogen-
activated protein kinase (MAPK) pathways, but the
relationship between cardiovascular disease and selective
insulin signal pathways is unclear. We investigated the
tissue specificity and intracellular signal transduction
selectivity of insulin resistance in the vasculature and
skeletal muscle of fructose-fed rats (FFR). Sprague-Dawley
rats were fed either normal rat chow (control rats) or fructose-
rich chow. Normal saline with or without 1,000 (microg/kg)
insulin was injected, and then the thoracic aorta or soleus
muscle was removed under anesthetization. Insulin-induced
tyrosine phosphorylation of insulin receptor beta subunit
(IRbeta) and insulin receptor substrate-1 (IRS-1) and
tyrosine/threonine phosphorylation of p44/42 MAPK (ERK-1/2)
were evaluated. There were no significant differences in the
degree of phosphorylation of IRbeta or ERK-1/2 in the
thoracic aorta or in the soleus muscle between FFR and
controls. However, tyrosine phosphorylation of IRS-1 in the
soleus muscle of FFR was significantly reduced to 80%
(p<0.001) of that in controls. The results suggest that PI3-
K pathway in skeletal muscle is selectively impaired in FFR,
and this impairment may induce hyperinsulinemia, which in
turn may stimulate the MAPK pathway and lead to
atherosclerosis. Thus PI3-K pathway may be one of the
factors underlying the onset of cardiovascular disease in
patients with insulin resistance.

PMID: 12627878 [PubMed - indexed for MEDLINE]

Quoted message said:

M9:Fructose is tricky in that although it is a refined
sugar, it does not invoke much insulin response,
satiety etc. It is said to bypass normal glucose
regulatory response and to be processed mainly by the
liver

directly

Quoted message said:

into fats.

OK, if it doesn't invoke much insulin response, how does it
contribute to insulin resistance? I've read the articles,
but they're pretty technical, so a "for dummies" explanation
would be appreciated. Thanks -- M9

thanks for the article! there is a lot of talk these days
about the ol' high fructose corn syrup being to blame for
the rise in obesity.....this may be true but its hard to
tell from environmental studies that use consumption data
from food/industry sales or food disappearance data. While
it is a good start and may give a foundation for more direct
research in human subjects, it still cant be taken as a true
association. Also, the term high fructose corn syrup is a
bit of a misnomer....processing does convert some of the
sugars of corn syrup to fructose (hence higher fructose than
normal corn syrup) however, it still is about half glucose.
It will be interested to see results of longitudinal studies
on this topic in actual people!

Cheers, Lisa

Mike V" <[email hidden]> wrote in message news:<40-
[email hidden]>...

Quoted message said:

"minerva nine" <[email hidden]> wrote in message
"]news:[email hidden]...

Quoted message said:

Interesting article. I'm no dietary scientist, but I
can't reconcile in

my

Quoted message said:

mind the low g.i. profile of fructose (as compared to
glucose) along with the preliminary data suggesting a
connection between fructose and insulin resistance.
To me, it seems like it would work just the opposite
-- i.e.,

a

Quoted message said:

lower g.i. = slower insulin response = less risk of
insulin syndrome.

What

Quoted message said:

am I missing here? -- M9

"Mike V" <[email hidden]> wrote in message
-"]news:[email hidden]-
k.net...

Quoted message said:

> > > Lisa

FYI: tinyurl.comys8ljOpen ↗

MikeV

M9:Fructose is tricky in that although it is a refined
sugar, it does not invoke much insulin response,
satiety etc. It is said to bypass normal glucose
regulatory response and to be processed mainly by the
liver directly into fats. Read nature.com040510Open ↗
5.html

See also the recent thread "Corn Syrup Linked to Diabetes,
Diarmid Logan, May 13" See refs to IRS-1, IRS-2 in earlier
posts by HUA KUL for more insight in how IR arises. MikeV

This also may be of interest.

ncbi.nlm.nih.govquery.fcgiOpen ↗
e&db=PubMed&list_uids=12627878&dopt=Abstract

Hypertens Res. 2003 Feb;26(2):169-76. Related
Articles, Links

*Tissue-specific impairment of insulin signaling in
vasculature and skeletal muscle of fructose-fed rats.*

Hyakukoku M, Higashiura K, Ura N, Murakami H, Yamaguchi K,
[censored] L, Furuhashi M, Togashi N, Shimamoto K.

Second Department of Internal Medicine, Sapporo Medical
University School of Medicine, Sapporo, Japan. hyakoku-masaya@nshp-
muroran.or.jp

The relation between insulin resistance/hyperinsulinemia
and cardiovascular diseases has attracted much attention.
Insulin affects not only glucose metabolism, but also
protein synthesis and cell growth. Insulin stimulates both
the phosphatidylinositol 3-kinase (PI3-K) and mitogen-
activated protein kinase (MAPK) pathways, but the
relationship between cardiovascular disease and selective
insulin signal pathways is unclear. We investigated the
tissue specificity and intracellular signal transduction
selectivity of insulin resistance in the vasculature and
skeletal muscle of fructose-fed rats (FFR). Sprague-Dawley
rats were fed either normal rat chow (control rats) or fructose-
rich chow. Normal saline with or without 1,000 (microg/kg)
insulin was injected, and then the thoracic aorta or
soleus muscle was removed under anesthetization. Insulin-
induced tyrosine phosphorylation of insulin receptor beta
subunit (IRbeta) and insulin receptor substrate-1 (IRS-1)
and tyrosine/threonine phosphorylation of p44/42 MAPK (ERK-
1/2) were evaluated. There were no significant differences
in the degree of phosphorylation of IRbeta or ERK-1/2 in
the thoracic aorta or in the soleus muscle between FFR and
controls. However, tyrosine phosphorylation of IRS-1 in
the soleus muscle of FFR was significantly reduced to 80%
(p<0.001) of that in controls. The results suggest that
PI3-K pathway in skeletal muscle is selectively impaired
in FFR, and this impairment may induce hyperinsulinemia,
which in turn may stimulate the MAPK pathway and lead to
atherosclerosis. Thus PI3-K pathway may be one of the
factors underlying the onset of cardiovascular disease in
patients with insulin resistance.

PMID: 12627878 [PubMed - indexed for MEDLINE]

Hmmm, it doesn't really specify in the abstracts what form
of fructose they used -- I wonder if the form makes any
difference? I've been using granulated fructose as a
sweetener in my tea in the morning instead of table sugar,
because of it's low g.i., which is why I've been following
this topic. I don't have any of the markers for insulin
syndrome cited in the studies (obesity, bad blood lipid
profile, family history of diabetes, etc.), so I'm not gonna
sweat over a teaspoon of granulated fructose a day, but
still, it's sort of a "well, damn!" situation.

- M9

"Lisa" <[email hidden]> wrote in message
"]news:[email hidden]...

Quoted message said:

thanks for the article! there is a lot of talk these days
about the ol' high fructose corn syrup being to blame for
the rise in obesity.....this may be true but its hard to
tell from environmental studies that use consumption data
from food/industry sales or food disappearance data. While
it is a good start and may give a foundation for more
direct research in human subjects, it still cant be taken
as a true association. Also, the term high fructose corn
syrup is a bit of a misnomer....processing does convert
some of the sugars of corn syrup to fructose (hence higher
fructose than normal corn syrup) however, it still is
about half glucose. It will be interested to see results
of longitudinal studies on this topic in actual people!

Cheers, Lisa

"minerva nine" <[email hidden]> wrote in message news:<[email hidden]>...

Quoted message said:

Quoted message said:

M9:Fructose is tricky in that although it is a refined
sugar, it does not invoke much insulin response,
satiety etc. It is said to bypass normal glucose
regulatory response and to be processed mainly by the
liver

directly

Quoted message said:

into fats.

OK, if it doesn't invoke much insulin response, how does
it contribute to insulin resistance? I've read the
articles, but they're pretty technical, so a "for dummies"
explanation would be appreciated. Thanks -- M9

Hi M9. At the risk of seeming repetitive I'll repost the
following information from a previous post, to which Mike V
referred. I hope it helps.

====================================================================

groups.google.comgroupsOpen ↗
8&selm=3da4c6e5.0405140508.31ecee46%40posting.google.c-
om&rnum=19

Thank you all for posting and reposting this information. I
would like to add a little bit more that I have discovered.
Ever since I started reading about fructose and IRS-2 I have
been puzzled about the results of one study (1st one below)
that showed children singly deficient in either IRS-1 or IRS-
2 did not become significantly insulin resistant, but those
deficient in both "showed a 25-35% decrease in sensitivity."
If fructose inhibits IRS-2 but not IRS-1, how could it be
the cause of such a huge increase in juvenile obesity and
diabetes? Then I discovered (thanks to poster "kofi"😉 the
2nd study posted below, which shows that an increase in
osmotic stress caused by hyperglycemia reduces levels of IRS-
1, "prolonged osmotic stress alters IRS-1 function by
inducing its degradation, which could contribute to the down-
regulation of insulin action." Thus it would appear that a
combination diet of high fructose intake and high
carbohydrate intake (anything that raises blood glucose
levels significantly, which fructose does not do), would
reduce insulin sensitivity significantly. This is exactly a
large component of the typical teen diet, high carb snack
foods and high fructose soda. It might also indicate that
injections of IRS-1/IRS-2 could be an extremely powerful
weight reduction treatment, as well as a treatment for
symptoms of PCOS, but I don't know if these proteins are
available for medical use.

===================================================================

Diabetes. 2002 Dec;51 Suppl 3:S304-7.

Increased insulin resistance in obese children who have
both 972 IRS-1 and 1057 IRS-2 polymorphisms. Le Fur S, Le
Stunff C, Bougneres P. Department of Pediatric
Endocrinology, Hopital Saint-Vincent de Paul, Universite
Paris V, Paris, France.

In two cohorts of 174 and 165 obese Caucasian children, we
measured insulin sensitivity and genotyped insulin receptor
substrate IRS-1 and IRS-2 genes for the Arg972Gly and the
Asp1057Gly variants, respectively. Because IRS-1 and IRS-2
have complementary roles in insulin signaling, we classified
the genotypes in three categories: those with none of the
variants in IRS-1 or IRS-2, those with one variant in IRS-1
or IRS-2, and those with variants in both IRS-1 and 2
proteins. The obese children with either the IRS-1 or IRS-2
variant had a mean insulin sensitivity index (2.9 +/- 0.2 in
cohort 1, 2.7 +/- .1 in cohort 2) only slightly lower than
the children having no variant in either gene (3.1 +/- 0.2
and 3.5 +/- 0.3, respectively). However, patients having
variant alleles in both IRS-1 and IRS-2 genes showed a 25-
35% decrease in sensitivity (2.3 +/- 0.2 and 2.0 +/- 0.2,
respectively) when compared with nonvariant homozygotes (P <
0.001). These observations are reminiscent of the insulin
sensitivity phenotypes in double IRS-1(+/-) IRS-2(+/-)
heterozygous knockout mice. Our results stress the need for
combined genotype analysis when candidate genes are
functionally involved in the same pathway.

PMID: 12475767 [PubMed - indexed for MEDLINE]
=======================================================================

=======================================================================

J Biol Chem. 2003 Jul 18;278(29):26550-7. Epub 2003 May 01.

Hyperosmotic stress inhibits insulin receptor substrate-1
function by distinct mechanisms in 3T3-L1 adipocytes. Gual
P, Gonzalez T, Gremeaux T, Barres R, Le Marchand-Brustel Y,
Tanti JF. INSERM U 568 and l'Institut Federatif de
Recherches 50, Faculte de Medecine, Avenue de Valombrose,
06107 Nice Cedex 02, France.

In 3T3-L1 adipocytes, hyperosmotic stress was found to
inhibit insulin signaling, leading to an insulin-resistant
state. We show here that, despite normal activation of
insulin receptor, hyperosmotic stress inhibits both tyrosine
phosphorylation of insulin receptor substrate-1 (IRS-1) and
IRS-1-associated phosphoinositide 3 (PI 3)-kinase activity
in response to physiological insulin concentrations. Insulin-
induced membrane ruffling, which is dependent on PI 3-kinase
activation, was also markedly reduced. These inhibitory
effects were associated with an increase in IRS-1 Ser307
phosphorylation. Furthermore, the mammalian target of
rapamycin (mTOR) inhibitor rapamycin prevented the osmotic
shock-induced phosphorylation of IRS-1 on Ser307. The
inhibition of mTOR completely reversed the inhibitory effect
of hyperosmotic stress on insulin-induced IRS-1 tyrosine
phosphorylation and PI 3-kinase activation. In addition,
prolonged osmotic stress enhanced the degradation of IRS
proteins through a rapamycin-insensitive pathway and a proteasome-
independent process. These data support evidence of new
mechanisms involved in osmotic stress-induced cellular
insulin resistance. Short-term osmotic stress induces the
phosphorylation of IRS-1 on Ser307 by an mTOR-dependent
pathway. This, in turn, leads to a decrease in early
proximal signaling events induced by physiological insulin
concentrations. On the other hand, prolonged osmotic stress
alters IRS-1 function by inducing its degradation, which
could contribute to the down-regulation of insulin action.

PMID: 12730242 [PubMed - indexed for MEDLINE]
=================================================================

--Hua Kul [email hidden]

[email hidden] (Lisa) wrote in message news:<[email hidden]>...

Quoted message said:

thanks for the article! there is a lot of talk these days
about the ol' high fructose corn syrup being to blame for
the rise in obesity.....this may be true but its hard to
tell from environmental studies that use consumption data
from food/industry sales or food disappearance data. While
it is a good start and may give a foundation for more
direct research in human subjects, it still cant be taken
as a true association. Also, the term high fructose corn
syrup is a bit of a misnomer....processing does convert
some of the sugars of corn syrup to fructose (hence higher
fructose than normal corn syrup) however, it still is
about half glucose. It will be interested to see results
of longitudinal studies on this topic in actual people!

Cheers, Lisa

Hi Lisa. I'm reposting below an earlier post I made
concerning HFCS in the soft drink industry. It may answer
some of your questions.

===================================================================

groups.google.comgroupsOpen ↗
google.com&rnum=3&prev=/groups%3Fhl%3Den%26lr%3D%26ie%3DUTF-
8%26scoring%3Dd%26q%3D%2522hua%2Bkul%2522%2Bfructose%2Bcorn-
%2Bsyrup%26btnG%3DSearch

Quoted message said:

Quoted message said:

"Werner" <[email hidden]> wrote in message news:<MWo8b.2$2a3.592@psinet-eu-

Quoted message said:

> nl ...

Certainly, fructose corn syrup or soda pop is doing
irreparable?

harm to

Quoted message said:

Quoted message said:

people today, because it is a fabricated fructose
which is

completely

Quoted message said:

Quoted message said:

isolated from isoflavones which you find in apples or
oranges.

That´s the

Quoted message said:

Quoted message said:

difference. Apples also contain fructose, natural
fructose, and

there will

Quoted message said:

Quoted message said:

be no harm at all, the contrary is right.

There is no difference chemically between what you call
"industrial fructose" and "natural fructose", they are the
same thing. It's not fabricated, it's extracted. If soda
pops contained fructose from apples instead of corn it
would be just as damaging. If the only source of fructose
in our diets were from eating fruit I don't think we would
have such a problem, but in the U.S. people consume far
more fructose than used to be in a "natural" diet. The
food industries use a liquid mix extracted from corn. The
sugar content of commercial HFCS is a mix of glucose and
fructose but varies between 42% fructose and 90% fructose
based on what the food company wants. The soft drink
industry (at least in the US) uses a mix with 42% glucose
and 55% fructose, meaning it has 1/3 more fructose than
glucose, far more than the mix in the sucrose that was
used prior to 1976.

Fructose is used in virtually every processed food product
in the US, probably because the U.S. government kept the
price of sucrose artificially high (about 4 times as
expensive as the global market, if I remember correctly) to
protect domestic sugar beet farmers. Wouldn't it just be
incredibly stupid if government protectionism led to our
current obesity and diabetes "epidemic"? Part of the problem
is eating habits, but if children drank pure fruit juices
instead of soda pop, in the same quantities, they would
still be getting way too much fructose.

====================================================================

"For many purposes a 42% fructose syrup is perfectly
satisfactory for use but it does not match the exacting
criteria of the quality soft drink manufacturers as a
replacement for sucrose in acidic soft drinks. For use in
the better colas, 55% fructose is required. This is produced
by using vast chromatographic columns of zeolites or the
calcium salts of cation exchange resins to adsorb and
separate the fructose from the other components. The
fractionation process, although basically very simple, is
only economic if run continuously. The fructose stream (90%
(w/w) fructose, 9% glucose) is blended with 42% fructose
syrups to give the 55% fructose (42% glucose) product
required."

sbu.ac.ukhfcs.htmlOpen ↗
eden.rutgers.eduHFCSpresentation.pptOpen ↗
=====================================================================

--Hua Kul [email hidden]

"minerva nine" <[email hidden]> wrote in message
"]news:[email hidden]...

Quoted message said:

Quoted message said:

M9:Fructose is tricky in that although it is a refined
sugar, it does not invoke much insulin response,
satiety etc. It is said to bypass normal glucose
regulatory response and to be processed mainly by the
liver

directly

Quoted message said:

into fats.

OK, if it doesn't invoke much insulin response, how does
it contribute to insulin resistance? I've read the
articles, but they're pretty technical, so a "for dummies"
explanation would be appreciated. Thanks -- M9

As a recognized non-expert, my opinion is worth what you pay
for it. It is constantly in a state of revision. With Hua
Kul's posts some of this is redundant. Maybe it will serve
as a sort of summary.

Insulin resistance is known to be complex and
multifactorial; research has been very animal dependent, and
much more remains to be done. Persistent insulin resistance
does not necessarily imply that you will eventually become
diabetic. It probably does imply that you will become
overweight or obese. (some still suggest that gluttony and
obesity come before IR) After genetics, current evidence
tends to point to influences which affect or bypass appetite
regulation. As an example, triaglycerides (which may be
derived from either dietary fats or sugars) are said to
block leptin (a regulatory hormone) from reaching the brain.
Excessive fatty particles have also been implicated in cells
which are insulin resistant. A direct relationship has been
shown between excessive fructose consumption and elevated
triaglycerides. (low levels of frucose from whole fruit are
not a problem, and are probably advantageous).

IRS-1 and IRS-2 Insulin Receptor Substrates are proteins
involved in inducting glucose into cells for proper use
according to the cell's needs. There is evidence that IRS-2
may be compromised by excessive fructose. IRS-1 also
appears to be compromised by hyperglycemic 'osmotic
pressure'. I understand this to be excessive pressure
differences across cellular membranes caused by excessive
blood sugar. Hua Kul suggests that this condition requires
excessive BG possibly with high BF. The production of
insulin by pancreatic beta cells are understood to be under
the control of pathways via IRS-1.

**Coordination of Insulin Action and Secretion by IRS
Proteins** Morris F. White, Ph.D.
hhmi.orgwhite.htmlOpen ↗

There are far more knowledgeable people than me who read
smn. Contributions to correct my understanding most welcome.

Mike
Note: I am not diabetic, IR or obese, so what do I know?

Misc. excerpts from studies/articles referenced earlier.

"IRS-2 is like a switchboard that coordinates appetite, fat
storage, and blood glucose together with energy demanding
processes like reproduction, development, and tissue
repair," says Morris F. White, Ph.D., of the Joslin Diabetes
Center and the Howard Hughes Medical Institute.
**************
"Fructose is worse than just an added sugar. The following
article shows that rats deficient in a protein called
insulin receptor substrate-2 become obese and diabetic. The
abstract summary that follows shows that IRS-2 is
significantly reduced by fructose, more than sucrose. In
1976 the US soft drink companies started using high fructose
corn sweetener because it was cheaper than using sucrose,
and by 1980 the switch was complete. Other processed food
manufacturers followed suit, and now fructose is ubiquitous.
One almost can't find a processed food without fructose;
soda pop, salad dressings, baked goods, even some fruit
juices are sweetened with fructose"

Braz J Med Biol Res 2000 Dec;33(12):1421-7 A high-fructose
diet induces changes in pp185 phosphorylation in muscle and
liver of rats. Ueno M, Bezerra RM, Silva MS, Tavares DQ,
Carvalho CR, Saad MJ Departamento de Planejamento Alimentar
e Nutricao, Faculdade de Engenharia de Alimentos,
Universidade Estadual de Campinas, Campinas, SP, Brasil.
*************

"Ever since I started reading about fructose and IRS-2 I
have been puzzled about the results of one study (1st one
below) that showed children singly deficient in either IRS-1
or IRS-2 did not become significantly insulin resistant, but
those deficient in both "showed a 25-35% decrease in
sensitivity." If fructose inhibits IRS-2 but not IRS-1, how
could it be the cause of such a huge increase in juvenile
obesity and diabetes? Then I discovered (thanks to poster
"kofi"😉 the 2nd study posted below, which shows that an
increase in osmotic stress caused by hyperglycemia reduces
levels of IRS-1, "prolonged osmotic stress alters IRS-1
function by inducing its degradation, which could contribute
to the down-regulation of insulin action." Thus it would
appear that a combination diet of high fructose intake and
high carbohydrate intake (anything that raises blood glucose
levels significantly, which fructose does not do), would
reduce insulin sensitivity significantly. This is exactly a
large component of the typical teen diet, high carb snack
foods and high fructose soda. It might also indicate that
injections of IRS-1/IRS-2 could be an extremely powerful
weight reduction treatment, as well as a treatment for
symptoms of PCOS, but I don't know if these proteins are
available for medical use. from Hua Kul's post.

*************
Scientists and clinicians have known for a long time that
obesity and chronic insulin resistance go hand-in-hand, but
they usually say that obesity causes insulin resistance.
That's one of the reasons why obesity is said to be a risk
factor for type 2 diabetes. But evidence in this study
suggests that it could be the other way around, with insulin
resistance initially dysregulating appetite that contributes
to obesity. The developing obesity exacerbates the insulin
resistance, which further burdens the pancreatic beta cells.
"It appears that IRS-2 helps coordinates insulin production
and nutrient metabolism to promote important biological
processes that reflect our health and fitness such as
appetite and fertility," Dr. Burks says.

************
"Type 2 diabetes is more than a problem with blood glucose,"
Dr. White says. "High blood glucose is the easiest thing to
measure, but the underlying cause might reside in the IRS-2
branch of the insulin-signaling pathway. You can live with
reduced IRS-2 function, but you might be glucose intolerant,
over-eat and gain weight; have a difficult time becoming
pregnant and when you do, develop gestational diabetes; and
worst of all, face life with pancreatic beta cells that
eventually fail to make enough insulin to avoid the life-
threatening consequences of type 2 diabetes."

************
The researchers, led by Howard Hughes Medical Institute
investigator Gerald
I. Shulman, who is also professor of medicine and physiology
at Yale, published their findings in the February 12,
2004, issue of the New England Journal of Medicine.

"Prior to this work, it was pretty clear that insulin
resistance was the best predictor for the development of
type 2 diabetes; and that accumulation of lipid in muscle
correlated very strongly with insulin resistance," said
Shulman. This correlation has been observed in cross-
sectional studies, as well as in young people with a family
history of type 2 diabetes, he said.

"We found that these lean insulin-resistant offspring - who
have a high probability of later developing type 2 diabetes
- had muscle insulin resistance, but no detectable
abnormalities in their fat cells compared to the insulin-
sensitive subjects," said Shulman
************
Triglycerides block leptin from brain.
slu.edu4263Open ↗

************
"We now understand that IRS1 and IRS2 play unique roles in
mediating the effects of insulin and IGF1 on embryonic
development, postnatal somatic growth, and glucose
homeostasis: No embryos (16.5 days or older) lacking both
genes have been detected in our studies, suggesting that
signals coordinated by these IRS proteins are essential for
embryonic development. However, deletion of Irs1 alone
causes insulin resistance and growth retardation, but
diabetes never occurs."

"By contrast, mice without Irs2 grow into normal-size adults
that develop type 2 diabetes. Without IRS2, neonates are
insulin resistant but display appropriate compensatory
insulin secretion; as they age, however, the peripheral
insulin resistance is exacerbated by failure of the
pancreatic b cells." Morris F White.