essential role of dietary carbohydrate in beta cell destruction

[Jim Chinnis]

This is interesting! I hope I haven't missed this already being posted and
discussed...

Note the conclusion: "These data indicate that the combination of obesity,
insulin resistance and the inflammatory response of adipose tissue are
insufficient to cause beta cell destruction in the absence of dietary
carbohydrate."

Development of diabetes in obese, insulin-resistant mice: essential role of
dietary carbohydrate in beta cell destruction

Abstract
Aims/hypothesis The role of dietary carbohydrate in the pathogenesis of
type 2 diabetes is still a subject of controversial debate. Here we analysed
the effects of diets with and without carbohydrate on obesity, insulin
resistance and development of beta cell failure in the obese, diabetes-prone
New Zealand Obese (NZO) mouse.

Materials and methods NZO mice were kept on a standard diet (4% [w/w] fat,
51% carbohydrate, 19% protein), a high-fat diet (15, 47 and 17%,
respectively) and a carbohydrate-free diet in which carbohydrate was
exchanged for fat (68 and 20%, respectively). Body composition and blood
glucose were measured over a period of 22 weeks. Glucose tolerance tests and
euglycaemic-hyperinsulinaemic clamps were performed to analyse insulin
sensitivity. Islet morphology was assessed by immunohistochemistry.

Results Mice on carbohydrate-containing standard or high-fat diets
developed severe diabetes (blood glucose >16.6 mmol/l, glucosuria) due to
selective destruction of pancreatic beta cells associated with severe loss
of immunoreactivity of insulin, glucose transporter 2 (GLUT2) and
musculoaponeurotic fibrosarcoma oncogene homologue A (MafA). In contrast,
mice on the carbohydrate-free diet remained normoglycaemic and exhibited
hyperplastic islets in spite of a morbid obesity associated with severe
insulin resistance and a massive accumulation of macrophages in adipose
tissue.

Conclusions/interpretation These data indicate that the combination of
obesity, insulin resistance and the inflammatory response of adipose tissue
are insufficient to cause beta cell destruction in the absence of dietary
carbohydrate.

http://tinyurl.com/37mcpl
--
Jim Chinnis Warrenton, Virginia, USA

[Ricavito]

On Jul 8, 8:13 am, Jim Chinnis <jchin...@SPAMalum.mit.edu> wrote:
> This is interesting! I hope I haven't missed this already being posted and
> discussed...
>
> Note the conclusion: "These data indicate that the combination of obesity,
> insulin resistance and the inflammatory response of adipose tissue are
> insufficient to cause beta cell destruction in the absence of dietary
> carbohydrate."
>
> Development of diabetes in obese, insulin-resistant mice: essential role of
> dietary carbohydrate in beta cell destruction
>
> Abstract
> Aims/hypothesis The role of dietary carbohydrate in the pathogenesis of
> type 2 diabetes is still a subject of controversial debate. Here we analysed
> the effects of diets with and without carbohydrate on obesity, insulin
> resistance and development of beta cell failure in the obese, diabetes-prone
> New Zealand Obese (NZO) mouse.
>
> Materials and methods NZO mice were kept on a standard diet (4% [w/w] fat,
> 51% carbohydrate, 19% protein), a high-fat diet (15, 47 and 17%,
> respectively) and a carbohydrate-free diet in which carbohydrate was
> exchanged for fat (68 and 20%, respectively). Body composition and blood
> glucose were measured over a period of 22 weeks. Glucose tolerance tests and
> euglycaemic-hyperinsulinaemic clamps were performed to analyse insulin
> sensitivity. Islet morphology was assessed by immunohistochemistry.
>
> Results Mice on carbohydrate-containing standard or high-fat diets
> developed severe diabetes (blood glucose >16.6 mmol/l, glucosuria) due to
> selective destruction of pancreatic beta cells associated with severe loss
> of immunoreactivity of insulin, glucose transporter 2 (GLUT2) and
> musculoaponeurotic fibrosarcoma oncogene homologue A (MafA). In contrast,
> mice on the carbohydrate-free diet remained normoglycaemic and exhibited
> hyperplastic islets in spite of a morbid obesity associated with severe
> insulin resistance and a massive accumulation of macrophages in adipose
> tissue.
>
> Conclusions/interpretation These data indicate that the combination of
> obesity, insulin resistance and the inflammatory response of adipose tissue
> are insufficient to cause beta cell destruction in the absence of dietary
> carbohydrate.
>
> http://tinyurl.com/37mcpl
> --
> Jim Chinnis Warrenton, Virginia, USA

Jim, I'm confused by the percentage targets for fat; what does "[w/w]
fat" mean? A "standard" diet can't mean only 4% fat content.

[Susan]

x-no-archive: yes

Jim Chinnis wrote:
> This is interesting! I hope I haven't missed this already being posted and
> discussed...

You did! But it bears repetition!

Susan
>
> Note the conclusion: "These data indicate that the combination of obesity,
> insulin resistance and the inflammatory response of adipose tissue are
> insufficient to cause beta cell destruction in the absence of dietary
> carbohydrate."
>
> Development of diabetes in obese, insulin-resistant mice: essential role of
> dietary carbohydrate in beta cell destruction
>
> Abstract
> Aims/hypothesis The role of dietary carbohydrate in the pathogenesis of
> type 2 diabetes is still a subject of controversial debate. Here we analysed
> the effects of diets with and without carbohydrate on obesity, insulin
> resistance and development of beta cell failure in the obese, diabetes-prone
> New Zealand Obese (NZO) mouse.
>
> Materials and methods NZO mice were kept on a standard diet (4% [w/w] fat,
> 51% carbohydrate, 19% protein), a high-fat diet (15, 47 and 17%,
> respectively) and a carbohydrate-free diet in which carbohydrate was
> exchanged for fat (68 and 20%, respectively). Body composition and blood
> glucose were measured over a period of 22 weeks. Glucose tolerance tests and
> euglycaemic-hyperinsulinaemic clamps were performed to analyse insulin
> sensitivity. Islet morphology was assessed by immunohistochemistry.
>
> Results Mice on carbohydrate-containing standard or high-fat diets
> developed severe diabetes (blood glucose >16.6 mmol/l, glucosuria) due to
> selective destruction of pancreatic beta cells associated with severe loss
> of immunoreactivity of insulin, glucose transporter 2 (GLUT2) and
> musculoaponeurotic fibrosarcoma oncogene homologue A (MafA). In contrast,
> mice on the carbohydrate-free diet remained normoglycaemic and exhibited
> hyperplastic islets in spite of a morbid obesity associated with severe
> insulin resistance and a massive accumulation of macrophages in adipose
> tissue.
>
> Conclusions/interpretation These data indicate that the combination of
> obesity, insulin resistance and the inflammatory response of adipose tissue
> are insufficient to cause beta cell destruction in the absence of dietary
> carbohydrate.
>
> http://tinyurl.com/37mcpl
> --
> Jim Chinnis Warrenton, Virginia, USA

[Andrew B. Chung, MD/PhD]

neighbor Jim Chinnis wrote:
>
> This is interesting!

It is.

> I hope I haven't missed this already being posted and
> discussed...

Not here on either ASD or SMC.

> Note the conclusion: "These data indicate that the combination of obesity,
> insulin resistance and the inflammatory response of adipose tissue are
> insufficient to cause beta cell destruction in the absence of dietary
> carbohydrate."

Beta cell destruction here would be apoptosis.

The presence of carbohydrates has long been understood to be a
condition that this permissive for beta cell apoptosis rather than the
cause of it.

This understanding logically follows from the fact that the purpose of
beta cells is to make and secrete insulin which is needed for
carbohydrate metabolism.

No carbohydrates --> Beta cells are dormant (non-active).

As a general rule, it is not possible for dormant cells to go into
apoptosis (also known a programmed cells death).

> Development of diabetes in obese, insulin-resistant mice: essential role of
> dietary carbohydrate in beta cell destruction
>
> Abstract
> Aims/hypothesis The role of dietary carbohydrate in the pathogenesis of
> type 2 diabetes is still a subject of controversial debate. Here we analysed
> the effects of diets with and without carbohydrate on obesity, insulin
> resistance and development of beta cell failure in the obese, diabetes-prone
> New Zealand Obese (NZO) mouse.
>
> Materials and methods NZO mice were kept on a standard diet (4% [w/w] fat,
> 51% carbohydrate, 19% protein), a high-fat diet (15, 47 and 17%,
> respectively) and a carbohydrate-free diet in which carbohydrate was
> exchanged for fat (68 and 20%, respectively). Body composition and blood
> glucose were measured over a period of 22 weeks. Glucose tolerance tests and
> euglycaemic-hyperinsulinaemic clamps were performed to analyse insulin
> sensitivity. Islet morphology was assessed by immunohistochemistry.
>
> Results Mice on carbohydrate-containing standard or high-fat diets
> developed severe diabetes (blood glucose >16.6 mmol/l, glucosuria) due to
> selective destruction of pancreatic beta cells associated with severe loss
> of immunoreactivity of insulin, glucose transporter 2 (GLUT2) and
> musculoaponeurotic fibrosarcoma oncogene homologue A (MafA). In contrast,
> mice on the carbohydrate-free diet remained normoglycaemic and exhibited
> hyperplastic islets in spite of a morbid obesity associated with severe
> insulin resistance and a massive accumulation of macrophages in adipose
> tissue.

This latter observation is key to understanding that insulin
resistance (IR/MetS/PCOS) arises from VAT and not from a diet
containing carbohydrates ! ! !

While it appears to be possible for rats to survive on a no-carb
diet, this would typically not be tolerated by humans so that
preventing type-2 diabetes with a no-carb diet would not be feasible.

However, the good news is that it is actually the VAT that is causing
the IR/MetS/PCOS which becomes type-2 diabetes in the presence of
carbohydrates.

overeating --> VAT --> IR/MetS/PCOS --> CVD and T2DM (in the presence
of dietary carbs)

Now if folks wisely choose to eat less down to the optimal amount,
they will lose the VAT thereby curing their MetS and possibly curing
their T2DM:

http://HeartMDPhD.com/HolySpirit/Healing

http://HeartMDPhD.com/press.asp

> Conclusions/interpretation These data indicate that the combination of
> obesity, insulin resistance and the inflammatory response of adipose tissue
> are insufficient to cause beta cell destruction in the absence of dietary
> carbohydrate.
>
> http://tinyurl.com/37mcpl

Many thanks, much praise, and all the glory to GOD for HIS compelling
you to post the abstract of this interesting study.

Be hungry... be healthy (less VAT) ... be blessed.

Prayerfully in Jesus' awesome love,

Andrew <><
--
Andrew B. Chung, MD/PhD
Cardiologist

[Andy is Evil]

"Andrew B. Chung, MD/PhD" <[email protected]> wrote in
news:[email protected] ps.com:

Sock Notice: "andrew" active. "Socks of Satan"tm heartdoc(s)9-15 on
standby.

> neighbor Jim Chinnis wrote:
>>
>> This is interesting!
>
Andrew's medical expertise would be worth something if he hadn't been
driven by his personal unholy demon to SPAM his SCAM SITE. Even if we
didn't have the email he provided himself demon-strating his incompetence,
the evidence on Google that his posts have dubious medical value renders
his contributions useless.
>
> http://HeawtMDPhD.com/HowySpirit/Heawing
SPAM SITE
SPAM
SPAM
SPAM
>
> http://HeawtMDPhD.com/pwess.asp
SCAM SITE
SPAM
SPAM
SPAM
>
>> Conclusions/interpretation These data indicate that the combination of
>> obesity, insulin resistance and the inflammatory response of adipose
>> tissue are insufficient to cause beta cell destruction in the absence
>> of dietary carbohydrate.
>>
>> http://tinyurl.com/37mcpl
>
> Many thanks, much praise, and all the glory to GOD for HIS compelling
> you to post the abstract of this interesting study.
All praise to the The Flying Spaghetti Monster for compelling Andrew to
demon-strate his rudeness in sci.med froups.


Our Spaghetti
Which art upon our plate
Hallowed be Thy Name.


Thy Juicy Sauce
Fresh Bolognese
Is great with Meatballs or Plain


Give us this day
our daily bread
to dunk in Thy Juicy Excess
as we dunk those who dunk against us


Lead us not into temptation
but deliver us from tinned sauces
For Thine is the Best
Fresh Prepared and The Organic


Forever and Ever
Slurp

>
> Be hungwy... be heawthy (wess VAT)... be bwessed... be fwustwated (wess
SEX)... be woony... B.Chung
>
> Pwayerfuwwy in Jesus' awesome wove,
>
> Andwew <><
> --
> Andwew B. Chung, MD/PhD/NJ/WOKA
> Ex-Cawdiowogist
>
>

This is what Andrew did with his PhD:
http://groups.google.co.uk/group/sci...c912979fa3b5b?
hl=en&

Andy is Evil

**NJ-->Nut Job,WOKA-->Winner Of K00K Awards

[Jim Chinnis]

Susan <[email protected]> wrote in part:

>Jim Chinnis wrote:
>> This is interesting! I hope I haven't missed this already being posted and
>> discussed...
>
>You did! But it bears repetition!

I figured. I've been away and outta touch.
--
Jim Chinnis Warrenton, Virginia, USA

[Susan]

x-no-archive: yes

Jim Chinnis wrote:

>
> I figured. I've been away and outta touch.
> --

Don't let that happen again!

Susan

[Jim Chinnis]

Ricavito <[email protected]> wrote in part:

>Jim, I'm confused by the percentage targets for fat; what does "[w/w]
>fat" mean? A "standard" diet can't mean only 4% fat content.

w/w means weight divided by weight. For instance, a 4% fat (w/w), 51%
carbohydrate, 19% protein diet translates into roughly 12% fat (kcal/kcal),
when treated according to calories. Caloric % is the way nutritionists
usually refer to macronutrient proportions.

Remember that these are mice, not humans! Note also that--if I did the math
right--the no-carb diet is 88% fat by calories...

Interesting that on an 88% fat diet, diabetes did not develop... :-)
--
Jim Chinnis Warrenton, Virginia, USA

[Andrew B. Chung, MD/PhD]

Jim Chinnis wrote:
> Ricavito <[email protected]> wrote in part:
>
> >Jim, I'm confused by the percentage targets for fat; what does "[w/w]
> >fat" mean? A "standard" diet can't mean only 4% fat content.
>
> w/w means weight divided by weight. For instance, a 4% fat (w/w), 51%
> carbohydrate, 19% protein diet translates into roughly 12% fat (kcal/kcal),
> when treated according to calories. Caloric % is the way nutritionists
> usually refer to macronutrient proportions.
>
> Remember that these are mice, not humans! Note also that--if I did the math
> right--the no-carb diet is 88% fat by calories...
>
> Interesting that on an 88% fat diet, diabetes did not develop... :-)

However, IR/MetS did develop and we know that IR/MetS -->
cardiovascular disease.

See additional comments here:

http://groups.google.com/group/alt.s...8714fc98babb0?

Be hungry... be healthy... be blessed.

Prayerfully in Jesus' awesome love,

Andrew <><
--
Andrew B. Chung, MD/PhD
Cardiologist

[W. Baker]

Ricavito <[email protected]> wrote:
: On Jul 8, 8:13 am, Jim Chinnis <jchin...@SPAMalum.mit.edu> wrote:
: > This is interesting! I hope I haven't missed this already being posted and
: > discussed...
: >
: > Note the conclusion: "These data indicate that the combination of obesity,
: > insulin resistance and the inflammatory response of adipose tissue are
: > insufficient to cause beta cell destruction in the absence of dietary
: > carbohydrate."
: >
: > Development of diabetes in obese, insulin-resistant mice: essential role of
: > dietary carbohydrate in beta cell destruction
: >
: > Abstract
: > Aims/hypothesis The role of dietary carbohydrate in the pathogenesis of
: > type 2 diabetes is still a subject of controversial debate. Here we analysed
: > the effects of diets with and without carbohydrate on obesity, insulin
: > resistance and development of beta cell failure in the obese, diabetes-prone
: > New Zealand Obese (NZO) mouse.
: >
: > Materials and methods NZO mice were kept on a standard diet (4% [w/w] fat,
: > 51% carbohydrate, 19% protein), a high-fat diet (15, 47 and 17%,
: > respectively) and a carbohydrate-free diet in which carbohydrate was
: > exchanged for fat (68 and 20%, respectively). Body composition and blood
: > glucose were measured over a period of 22 weeks. Glucose tolerance tests and
: > euglycaemic-hyperinsulinaemic clamps were performed to analyse insulin
: > sensitivity. Islet morphology was assessed by immunohistochemistry.

Jim,

shouldn't these diets add up to 100%? None of them do. Other
than fat, protein and carbohydrate, what makes up the rest of the diets?

Wendy

[TC]

On Jul 8, 11:43 am, "Andrew B. Chung, MD/PhD"
<and...@emorycardiology.com> wrote:
> neighbor Jim Chinnis wrote:
>
> > This is interesting!
>
> It is.
>
> > I hope I haven't missed this already being posted and
> > discussed...
>
> Not here on either ASD or SMC.
>
> > Note the conclusion: "These data indicate that the combination of obesity,
> > insulin resistance and the inflammatory response of adipose tissue are
> > insufficient to cause beta cell destruction in the absence of dietary
> > carbohydrate."
>
> Beta cell destruction here would be apoptosis.
>
> The presence of carbohydrates has long been understood to be a
> condition that this permissive for beta cell apoptosis rather than the
> cause of it.
>
> This understanding logically follows from the fact that the purpose of
> beta cells is to make and secrete insulin which is needed for
> carbohydrate metabolism.
>
> No carbohydrates --> Beta cells are dormant (non-active).
>
> As a general rule, it is not possible for dormant cells to go into
> apoptosis (also known a programmed cells death).
>
>
>
>
>
> > Development of diabetes in obese, insulin-resistant mice: essential role of
> > dietary carbohydrate in beta cell destruction
>
> > Abstract
> > Aims/hypothesis The role of dietary carbohydrate in the pathogenesis of
> > type 2 diabetes is still a subject of controversial debate. Here we analysed
> > the effects of diets with and without carbohydrate on obesity, insulin
> > resistance and development of beta cell failure in the obese, diabetes-prone
> > New Zealand Obese (NZO) mouse.
>
> > Materials and methods NZO mice were kept on a standard diet (4% [w/w] fat,
> > 51% carbohydrate, 19% protein), a high-fat diet (15, 47 and 17%,
> > respectively) and a carbohydrate-free diet in which carbohydrate was
> > exchanged for fat (68 and 20%, respectively). Body composition and blood
> > glucose were measured over a period of 22 weeks. Glucose tolerance tests and
> > euglycaemic-hyperinsulinaemic clamps were performed to analyse insulin
> > sensitivity. Islet morphology was assessed by immunohistochemistry.
>
> > Results Mice on carbohydrate-containing standard or high-fat diets
> > developed severe diabetes (blood glucose >16.6 mmol/l, glucosuria) due to
> > selective destruction of pancreatic beta cells associated with severe loss
> > of immunoreactivity of insulin, glucose transporter 2 (GLUT2) and
> > musculoaponeurotic fibrosarcoma oncogene homologue A (MafA). In contrast,
> > mice on the carbohydrate-free diet remained normoglycaemic and exhibited
> > hyperplastic islets in spite of a morbid obesity associated with severe
> > insulin resistance and a massive accumulation of macrophages in adipose
> > tissue.
>
> This latter observation is key to understanding that insulin
> resistance (IR/MetS/PCOS) arises from VAT and not from a diet
> containing carbohydrates ! ! !
>
> While it appears to be possible for rats to survive on a no-carb
> diet, this would typically not be tolerated by humans so that
> preventing type-2 diabetes with a no-carb diet would not be feasible.
>
> However, the good news is that it is actually the VAT that is causing
> the IR/MetS/PCOS which becomes type-2 diabetes in the presence of
> carbohydrates.
>
> overeating --> VAT --> IR/MetS/PCOS --> CVD and T2DM (in the presence
> of dietary carbs)
>
> Now if folks wisely choose to eat less down to the optimal amount,
> they will lose the VAT thereby curing their MetS and possibly curing
> their T2DM:
>
> http://HeartMDPhD.com/HolySpirit/Healing
>
> http://HeartMDPhD.com/press.asp
>
> > Conclusions/interpretation These data indicate that the combination of
> > obesity, insulin resistance and the inflammatory response of adipose tissue
> > are insufficient to cause beta cell destruction in the absence of dietary
> > carbohydrate.
>
> >http://tinyurl.com/37mcpl
>
> Many thanks, much praise, and all the glory to GOD for HIS compelling
> you to post the abstract of this interesting study.
>
> Be hungry... be healthy (less VAT) ... be blessed.
>
> Prayerfully in Jesus' awesome love,
>
> Andrew <><
> --
> Andrew B. Chung, MD/PhD
> Cardiologist- Hide quoted text -
>
> - Show quoted text -

You are an unemployed idiot.

Refined carbs = elevated blood sugar levels = dead b cells. It is that
bloody simple you unemployed board certified moron.