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Iron levels / insulin secretion / insulin action
Iron levels / insulin secretion / insulin action
<<snip>>
We conclude that tissue iron levels are an important determinant of
insulin secretion and insulin action
<<snip>>
Diabetologia. 2006 Nov ;49:2546-51 17019598
Increased insulin secretory capacity but decreased insulin sensitivity
after correction of iron overload by phlebotomy in hereditary
haemochromatosis.
[My paper] D Abraham , J Rogers , P Gault , J P Kushner , D A McClain
AIMS/HYPOTHESIS:
We recently demonstrated that humans with hereditary haemochromatosis
have decreased insulin secretory capacity with a compensatory increase
in insulin sensitivity. We therefore determined how these measures
change after correction of tissue iron overload.
SUBJECTS AND METHODS:
Five non-diabetic subjects who had been studied previously at the time
of initial diagnosis by means of the OGTT and frequently sampled
intravenous glucose tolerance tests (FSIVGTT) underwent phlebotomy to
normalise their serum ferritin. After normalisation of ferritin they
were studied again (33+/-4 months after the initial studies) by OGTT
and FSIVGTT. RESULTS: Normalisation of tissue iron stores resulted in
an average 1.8-fold increase in the integrated area under the insulin
curve during OGTT (p<0.0001), but no significant change in the area
under the glucose curve (10% decrease, p=0.32). After phlebotomy, there
was a 2.2-fold increase in insulin secretory capacity as determined by
FSIVGTT (acute insulin response to glucose [AIRg], p<0.02) but a
concomitant 70% fall in insulin sensitivity (Si, p<0.05). The
disposition index (AIRgxSi) was unchanged (5% increase, p=0.90). BMI
and fasting glucose were unchanged. At the time of diagnosis of
haemochromatosis, four of the subjects had IGT. After normalisation of
ferritin, two achieved NGT and two remained with IGT, despite 2.5- and
3.7-fold increases in insulin secretory capacity.
CONCLUSIONS/INTERPRETATION:
Insulin secretory capacity improves after normalisation of iron stores
in subjects with hereditary haemochromatosis. Glucose tolerance status
improves incompletely because of decreased insulin sensitivity after
phlebotomy. We conclude that tissue iron levels are an important
determinant of insulin secretion and insulin action.
Who loves ya.
Tom
Jesus Was A Vegetarian!
* jesuswasavegetarian.7h . com
Man Is A Herbivore!
* tinyurl . com /a3cc3
DEAD PEOPLE WALKING
* tinyurl . com /zk9fk
<<snip>>
We conclude that tissue iron levels are an important determinant of
insulin secretion and insulin action
<<snip>>
Diabetologia. 2006 Nov ;49:2546-51 17019598
Increased insulin secretory capacity but decreased insulin sensitivity
after correction of iron overload by phlebotomy in hereditary
haemochromatosis.
[My paper] D Abraham , J Rogers , P Gault , J P Kushner , D A McClain
AIMS/HYPOTHESIS:
We recently demonstrated that humans with hereditary haemochromatosis
have decreased insulin secretory capacity with a compensatory increase
in insulin sensitivity. We therefore determined how these measures
change after correction of tissue iron overload.
SUBJECTS AND METHODS:
Five non-diabetic subjects who had been studied previously at the time
of initial diagnosis by means of the OGTT and frequently sampled
intravenous glucose tolerance tests (FSIVGTT) underwent phlebotomy to
normalise their serum ferritin. After normalisation of ferritin they
were studied again (33+/-4 months after the initial studies) by OGTT
and FSIVGTT. RESULTS: Normalisation of tissue iron stores resulted in
an average 1.8-fold increase in the integrated area under the insulin
curve during OGTT (p<0.0001), but no significant change in the area
under the glucose curve (10% decrease, p=0.32). After phlebotomy, there
was a 2.2-fold increase in insulin secretory capacity as determined by
FSIVGTT (acute insulin response to glucose [AIRg], p<0.02) but a
concomitant 70% fall in insulin sensitivity (Si, p<0.05). The
disposition index (AIRgxSi) was unchanged (5% increase, p=0.90). BMI
and fasting glucose were unchanged. At the time of diagnosis of
haemochromatosis, four of the subjects had IGT. After normalisation of
ferritin, two achieved NGT and two remained with IGT, despite 2.5- and
3.7-fold increases in insulin secretory capacity.
CONCLUSIONS/INTERPRETATION:
Insulin secretory capacity improves after normalisation of iron stores
in subjects with hereditary haemochromatosis. Glucose tolerance status
improves incompletely because of decreased insulin sensitivity after
phlebotomy. We conclude that tissue iron levels are an important
determinant of insulin secretion and insulin action.
Who loves ya.
Tom
Jesus Was A Vegetarian!
* jesuswasavegetarian.7h . com
Man Is A Herbivore!
* tinyurl . com /a3cc3
DEAD PEOPLE WALKING
* tinyurl . com /zk9fk
Re: Iron levels / insulin secretion / insulin action
"Increased insulin secretory capacity but decreased insulin sensitivity
after correction of iron overload by phlebotomy in hereditary
haemochromatosis."
Ho hum, another post about a rare genetic disorder not related to most
folk, lower iron did not improve insulin resistence.
"Increased insulin secretory capacity but decreased insulin sensitivity
after correction of iron overload by phlebotomy in hereditary
haemochromatosis."
Ho hum, another post about a rare genetic disorder not related to most
folk, lower iron did not improve insulin resistence.
Re: Iron levels / insulin secretion / insulin action
>>capmack@shipper . com wrote: Ho hum, snore, another use of a rare genetic disorder to make a
non-point about most people.<<
Actually .. ya braindeadmoron .. the study was SPECIFICALLY .. done ..
TO .. assess .. **IRON **..
It was SPECIFICALLY done to assess .. iron REACTIONS .. in the body ..
You say the iron will 'react differently' .. IN .. genetic
hemochromatosis .. ?
BUT .. that wasn't the study .. was it ..
The study was conducted to see WHAT .. reactions .. different levels of
tissue iron HAVE .. on the body .. and it 'just so happens' .. in THIS
**specific** article .. the study group was .. genetic .. iron overload
..
And the .. reaction .. ?
Decreased .. diabetes .. symptoms ..
Now .. you .. for whatever .. reason .. seem to have found some ..
FAULT .. in the study .. ?
What was the .. FAULT .. again .. ?
EXPLAIN .. it .. again ..
Tissue iron 'levels' .. were .. measured ..
Now .. if you got a problem with .. the study .. why don't you place a
medical study to show .. HOW .. you believe iron reacts ..
**differently** .. IN .. those with genetic iron overload .. as opposed
to .. acquired / secondary .. iron overload ..
These ARE .. after all .. medical newsgroups .. and I am sure ..
EVERYONE .. will be VERY glad if you .. share .. your valued .. opinion
.. accompanied by at least ONE medical study as to WHY you would ..
attempt .. to demean these .. researchers .. work ..
The researchers .. 'noticed' .. iron and diabetes .. ARE linked.
They specifically took their time and got the funding and did the study
.. and got the .. **results** ..
What .. ? faults .. did you find in the study .. ?
>>Lower iron did not correct insulin
resistance.<<
Oh ..
Of course .. you mean the "normalization" .. of tissue iron levels did
not correct insulin resistance ..
Well .. if you recall .. the 'normal'.. according to PREVIOUS ..
studies .. has been shown to be .. **TOO high** ..
Because .. ?
Because .. ?
Oh yeah I remember .. you won't be able to recall .. because you are ..
stupid ..
NID/near-iron deficiency .. corrects .. diabetic .. symptoms ..
Sooo .. according to THIS .. study .. if 'they' are .. ALLOWED to ..
decide .. WHAT .. normal .. IS .. they will NEVER assess .. the
treatment modality OF .. iron reduction BECAUSE .. ?
They NEVER lower the iron levels DOWN .. into .. 'normal' ..
The REAL .. normal ..
Skewed .. from the beginning ..
<<snip>>
However, at NID, there was a
40%-55%
improvement of both fasting and glucose-stimulated
plasma
insulin concentrations, and near-normalization of serum alanine
aminotransferase activity
<<snip>>
But then .. YOU and your ilk should be very happy ..
Because .. ? .. diabetics will forever REMAIN to BE diabetics.. because
they TRUSTED .. you / 'they' / your ilk / medical professionals to DO
the studies .. correctly..
They will TRUST .. 'them' to DO the study .. **correctly** when in fact
.. they as .. evidenced above .. 'they' will NOT ..
They will not go past what they consider / ACCEPT as 'normal' .. iron
tissue levels.
EVEN THOUGH previous work has SHOWN .. directly .. improvement BY going
PAST this .. 'normal' .. into near-iron deficiency ..
"improvement of both fasting and glucose-stimulated
plasma insulin concentrations, and near-normalization of serum alanine
aminotransferase activity"
Diabetics should learn NOT to .. trust .. those who make money off ..
them ..
Isn't that .. right ..
You work for 'them' .. don't ya ..
Heh .. heh ..
Try some more underhanded .. stuff ..
Prove me to be .. right ..
Comeon .. you can do it ..
Gastroenterology 2002 Apr;122(4):931-9 Related Articles, Links
Effect of iron depletion in carbohydrate-intolerant patients with
clinical
evidence of nonalcoholic fatty liver disease.
Facchini FS, Hua NW, Stoohs RA.
Department of Medicine, University of California San Francisco and San
Francisco General Hospital, San Francisco, California, USA.
ffacch...@ecnea.org
BACKGROUND & AIMS: Increased body iron, genetic hemochromatosis (GH)
mutations,
and nonalcoholic fatty liver disease (NAFLD) tend to cluster in
carbohydrate-intolerant patients. In an attempt to further clarify the
interrelationships among these conditions, we studied 42
carbohydrate-intolerant patients who were free of the common GH
mutations C282Y
and H63D, and had a serum iron saturation lower than 50%. METHODS: We
measured
body iron stores, and induced iron depletion to a level of near-iron
deficiency
(NID) by quantitative phlebotomy. RESULTS: In the 17 patients with
clinical
evidence of NAFLD, we could not demonstrate supranormal levels of body
iron
(1.6 +/- 0.2 vs. 1.4 +/- 0.2 g; P = 0.06). However, at NID, there was a
40%-55%
improvement (P = 0.05-0.0001) of both fasting and glucose-stimulated
plasma
insulin concentrations, and near-normalization of serum alanine
aminotransferase activity (from 61 +/- 5 to 32 +/- 2 IU/L; P < 0.001).
CONCLUSIONS: These results reflect the insulin-sparing effect of iron
depletion
and indicate a key role of iron and hyperinsulinemia in the
pathogenesis of
NAFLD.
PMID: 11910345 [PubMed - indexed for MEDLINE]
--------------------------------------------------------------------------
Who loves ya.
Tom
Jesus Was A Vegetarian!
* jesuswasavegetarian.7h . com
Man Is A Herbivore!
* tinyurl . com /a3cc3
DEAD PEOPLE WALKING
* tinyurl . com /zk9fk
>>capmack@shipper . com wrote: Ho hum, snore, another use of a rare genetic disorder to make a
non-point about most people.<<
Actually .. ya braindeadmoron .. the study was SPECIFICALLY .. done ..
TO .. assess .. **IRON **..
It was SPECIFICALLY done to assess .. iron REACTIONS .. in the body ..
You say the iron will 'react differently' .. IN .. genetic
hemochromatosis .. ?
BUT .. that wasn't the study .. was it ..
The study was conducted to see WHAT .. reactions .. different levels of
tissue iron HAVE .. on the body .. and it 'just so happens' .. in THIS
**specific** article .. the study group was .. genetic .. iron overload
..
And the .. reaction .. ?
Decreased .. diabetes .. symptoms ..
Now .. you .. for whatever .. reason .. seem to have found some ..
FAULT .. in the study .. ?
What was the .. FAULT .. again .. ?
EXPLAIN .. it .. again ..
Tissue iron 'levels' .. were .. measured ..
Now .. if you got a problem with .. the study .. why don't you place a
medical study to show .. HOW .. you believe iron reacts ..
**differently** .. IN .. those with genetic iron overload .. as opposed
to .. acquired / secondary .. iron overload ..
These ARE .. after all .. medical newsgroups .. and I am sure ..
EVERYONE .. will be VERY glad if you .. share .. your valued .. opinion
.. accompanied by at least ONE medical study as to WHY you would ..
attempt .. to demean these .. researchers .. work ..
The researchers .. 'noticed' .. iron and diabetes .. ARE linked.
They specifically took their time and got the funding and did the study
.. and got the .. **results** ..
What .. ? faults .. did you find in the study .. ?
>>Lower iron did not correct insulin
resistance.<<
Oh ..
Of course .. you mean the "normalization" .. of tissue iron levels did
not correct insulin resistance ..
Well .. if you recall .. the 'normal'.. according to PREVIOUS ..
studies .. has been shown to be .. **TOO high** ..
Because .. ?
Because .. ?
Oh yeah I remember .. you won't be able to recall .. because you are ..
stupid ..
NID/near-iron deficiency .. corrects .. diabetic .. symptoms ..
Sooo .. according to THIS .. study .. if 'they' are .. ALLOWED to ..
decide .. WHAT .. normal .. IS .. they will NEVER assess .. the
treatment modality OF .. iron reduction BECAUSE .. ?
They NEVER lower the iron levels DOWN .. into .. 'normal' ..
The REAL .. normal ..
Skewed .. from the beginning ..
<<snip>>
However, at NID, there was a
40%-55%
improvement of both fasting and glucose-stimulated
plasma
insulin concentrations, and near-normalization of serum alanine
aminotransferase activity
<<snip>>
But then .. YOU and your ilk should be very happy ..
Because .. ? .. diabetics will forever REMAIN to BE diabetics.. because
they TRUSTED .. you / 'they' / your ilk / medical professionals to DO
the studies .. correctly..
They will TRUST .. 'them' to DO the study .. **correctly** when in fact
.. they as .. evidenced above .. 'they' will NOT ..
They will not go past what they consider / ACCEPT as 'normal' .. iron
tissue levels.
EVEN THOUGH previous work has SHOWN .. directly .. improvement BY going
PAST this .. 'normal' .. into near-iron deficiency ..
"improvement of both fasting and glucose-stimulated
plasma insulin concentrations, and near-normalization of serum alanine
aminotransferase activity"
Diabetics should learn NOT to .. trust .. those who make money off ..
them ..
Isn't that .. right ..
You work for 'them' .. don't ya ..
Heh .. heh ..
Try some more underhanded .. stuff ..
Prove me to be .. right ..
Comeon .. you can do it ..
Gastroenterology 2002 Apr;122(4):931-9 Related Articles, Links
Effect of iron depletion in carbohydrate-intolerant patients with
clinical
evidence of nonalcoholic fatty liver disease.
Facchini FS, Hua NW, Stoohs RA.
Department of Medicine, University of California San Francisco and San
Francisco General Hospital, San Francisco, California, USA.
ffacch...@ecnea.org
BACKGROUND & AIMS: Increased body iron, genetic hemochromatosis (GH)
mutations,
and nonalcoholic fatty liver disease (NAFLD) tend to cluster in
carbohydrate-intolerant patients. In an attempt to further clarify the
interrelationships among these conditions, we studied 42
carbohydrate-intolerant patients who were free of the common GH
mutations C282Y
and H63D, and had a serum iron saturation lower than 50%. METHODS: We
measured
body iron stores, and induced iron depletion to a level of near-iron
deficiency
(NID) by quantitative phlebotomy. RESULTS: In the 17 patients with
clinical
evidence of NAFLD, we could not demonstrate supranormal levels of body
iron
(1.6 +/- 0.2 vs. 1.4 +/- 0.2 g; P = 0.06). However, at NID, there was a
40%-55%
improvement (P = 0.05-0.0001) of both fasting and glucose-stimulated
plasma
insulin concentrations, and near-normalization of serum alanine
aminotransferase activity (from 61 +/- 5 to 32 +/- 2 IU/L; P < 0.001).
CONCLUSIONS: These results reflect the insulin-sparing effect of iron
depletion
and indicate a key role of iron and hyperinsulinemia in the
pathogenesis of
NAFLD.
PMID: 11910345 [PubMed - indexed for MEDLINE]
--------------------------------------------------------------------------
Who loves ya.
Tom
Jesus Was A Vegetarian!
* jesuswasavegetarian.7h . com
Man Is A Herbivore!
* tinyurl . com /a3cc3
DEAD PEOPLE WALKING
* tinyurl . com /zk9fk
