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Uncovering the Atkins diet secret



 
 
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  #101  
Old January 29th, 2004, 08:17 PM
tcomeau
external usenet poster
 
Posts: n/a
Default What a bunch of clowns ( Uncovering the Atkins diet secret - for Moosh)

Ron Ritzman wrote in message . ..
On 27 Jan 2004 11:46:06 -0800, (tcomeau) wrote:

And what "other mechanisms"?


Your Google search term for today is "acylation stimulating
protein"

From Mr. "Ketogenic Diet" himself Lyle McDonald.

http://groups.google.com/groups?q=%2...onr.com&rnum=1

Or

http://tinyurl.com/2fbpf


Here is a recent study on acylation stimulating protein.

**
Acylation stimulating protein stimulates insulin secretion.

Ahren B, Havel PJ, Pacini G, Cianflone K.

Department of Medicine, Lund University, Lund, Sweden.


Acylation stimulating protein (ASP) is a hormone produced by
adipocytes and is of importance for the storage of energy as fat. We
examined whether ASP might also have effects on islet function. In
clonal INS-1 cells, ASP dose-dependently augmented glucose-stimulated
insulin secretion. The lowest effective dose of ASP at 10 mmol/l
glucose was 5 micro mol/l. The effect was glucose-dependent because
ASP did not increase insulin secretion at 1 mmol/l glucose but had
clear effect at 10 and 20 mmol/l glucose. Similarly, ASP augmented
glyceraldehyde-induced insulin secretion but the hormone did not
enhance insulin secretion in response to depolarization by 20 mmol/l
of KCl. ASP-induced insulin secretion was completely abolished by
competitive inhibition of glucose phosphorylation by glucokinase with
5-thio-glucose and was partially inhibited by the calcium channel
blocker, nifedipine, and by the protein kinase C inhibitor, GF109203.
Furthermore, thapsigargin, an inhibitor of Ca(2+)-ATPase in the
endoplasmic reticulum, did not affect ASP-induced insulin secretion.
ASP (5 micro mol/l) also augmented glucose-stimulated insulin
secretion from islets isolated from C57BL/6J mice, and intravenous
administration of ASP (50 nmol/kg) augmented the acute (1 and 5 min)
insulin response to intravenous glucose (1 g/kg) in C57BL/6J mice.
This was accompanied by an increased rate of glucose disposal. Minimal
model analyses of data derived from the intravenous glucose tolerance
test revealed that whereas ASP augmented insulin secretion, the
hormone did not affect insulin sensitivity (S(I)) or glucose
effectiveness (S(G)). We conclude that ASP augments glucose-stimulated
insulin secretion through a direct action on the islet beta cells. The
effect is dependent on glucose phosphorylation, calcium uptake and
protein kinase C. Stimulation of insulin secretion by ASP in vivo
results in augmented glucose disposal.

PMID: 12917708 [PubMed - indexed for MEDLINE]
**


Of interest:

"We conclude that ASP augments glucose-stimulated insulin secretion
through a direct action on the islet beta cells. The effect is
dependent on glucose phosphorylation, calcium uptake and protein
kinase C. Stimulation of insulin secretion by ASP in vivo results in
augmented glucose disposal."

These sentences:

"...ASP augments glucose-stimulated insulin secretion..."

"The effect is dependent on glucose phosphorylation..."

Can we conclude that without "glucose-stimulated insulin secretion"
and "glucose phosphorylation" the effects of ASP would be minimal if
anything at all.

TC
  #102  
Old January 30th, 2004, 05:07 AM
September
external usenet poster
 
Posts: n/a
Default What a bunch of clowns ( Uncovering the Atkins diet secret - for Moosh)

(tcomeau) wrote in message . com...
Ron Ritzman wrote in message . ..
On 27 Jan 2004 11:46:06 -0800,
(tcomeau) wrote:

And what "other mechanisms"?


Your Google search term for today is "acylation stimulating
protein"

From Mr. "Ketogenic Diet" himself Lyle McDonald.

http://groups.google.com/groups?q=%2...onr.com&rnum=1

Or

http://tinyurl.com/2fbpf


Here is a recent study on acylation stimulating protein.

**
Acylation stimulating protein stimulates insulin secretion.

Ahren B, Havel PJ, Pacini G, Cianflone K.

Department of Medicine, Lund University, Lund, Sweden.


Acylation stimulating protein (ASP) is a hormone produced by
adipocytes and is of importance for the storage of energy as fat. We
examined whether ASP might also have effects on islet function. In
clonal INS-1 cells, ASP dose-dependently augmented glucose-stimulated
insulin secretion. The lowest effective dose of ASP at 10 mmol/l
glucose was 5 micro mol/l. The effect was glucose-dependent because
ASP did not increase insulin secretion at 1 mmol/l glucose but had
clear effect at 10 and 20 mmol/l glucose. Similarly, ASP augmented
glyceraldehyde-induced insulin secretion but the hormone did not
enhance insulin secretion in response to depolarization by 20 mmol/l
of KCl. ASP-induced insulin secretion was completely abolished by
competitive inhibition of glucose phosphorylation by glucokinase with
5-thio-glucose and was partially inhibited by the calcium channel
blocker, nifedipine, and by the protein kinase C inhibitor, GF109203.
Furthermore, thapsigargin, an inhibitor of Ca(2+)-ATPase in the
endoplasmic reticulum, did not affect ASP-induced insulin secretion.
ASP (5 micro mol/l) also augmented glucose-stimulated insulin
secretion from islets isolated from C57BL/6J mice, and intravenous
administration of ASP (50 nmol/kg) augmented the acute (1 and 5 min)
insulin response to intravenous glucose (1 g/kg) in C57BL/6J mice.
This was accompanied by an increased rate of glucose disposal. Minimal
model analyses of data derived from the intravenous glucose tolerance
test revealed that whereas ASP augmented insulin secretion, the
hormone did not affect insulin sensitivity (S(I)) or glucose
effectiveness (S(G)). We conclude that ASP augments glucose-stimulated
insulin secretion through a direct action on the islet beta cells. The
effect is dependent on glucose phosphorylation, calcium uptake and
protein kinase C. Stimulation of insulin secretion by ASP in vivo
results in augmented glucose disposal.

PMID: 12917708 [PubMed - indexed for MEDLINE]
**


Of interest:

"We conclude that ASP augments glucose-stimulated insulin secretion
through a direct action on the islet beta cells. The effect is
dependent on glucose phosphorylation, calcium uptake and protein
kinase C. Stimulation of insulin secretion by ASP in vivo results in
augmented glucose disposal."

These sentences:

"...ASP augments glucose-stimulated insulin secretion..."

"The effect is dependent on glucose phosphorylation..."

Can we conclude that without "glucose-stimulated insulin secretion"
and "glucose phosphorylation" the effects of ASP would be minimal if
anything at all.

TC



No. What this study shows is that ASP enhances insulin secretion from
the pancreas only in the presence of glucose; in other words, ASP can
not stimulate insulin secretion on its own. However, the *primary*
lipogenic effect of ASP is independent of insulin. ASP increases
triglyceride synthesis in fat cells by stimulating the activity of the
enzyme diacylglycerol acyltransferase (DGAT). DGAT catalyzes the last
step in the making of a triglyceride molecule (when the third and
final fatty acid is attached to the glycerol backbone).

It's well known that insulin enhances fat-storage primarily by
preventing lipolysis (triglyceride breakdown). ASP, on the other
hand, promotes fat-storage primarily by stimulating lipogenesis
(triglyceride synthesis). Think about it -- eating carbs causes
insulin secretion; the insulin prevents fatty acid release from
adipose tissue so that the carbs are burned for energy first. Eating
fat causes ASP secretion; the ASP causes any extra fat to be stored in
adipose tissue. This doesn't mean the insulin does not directly
stimulate lipogenesis or that ASP doesn't directly prevent lipolysis,
because they do. However, these are secondary effects.
  #103  
Old January 30th, 2004, 05:46 PM
tcomeau
external usenet poster
 
Posts: n/a
Default What a bunch of clowns ( Uncovering the Atkins diet secret - for Moosh)

(September) wrote in message om...
(tcomeau) wrote in message . com...
Ron Ritzman wrote in message . ..
On 27 Jan 2004 11:46:06 -0800,
(tcomeau) wrote:

And what "other mechanisms"?

Your Google search term for today is "acylation stimulating
protein"

From Mr. "Ketogenic Diet" himself Lyle McDonald.

http://groups.google.com/groups?q=%2...onr.com&rnum=1

Or

http://tinyurl.com/2fbpf


Here is a recent study on acylation stimulating protein.

**
Acylation stimulating protein stimulates insulin secretion.

Ahren B, Havel PJ, Pacini G, Cianflone K.

Department of Medicine, Lund University, Lund, Sweden.


Acylation stimulating protein (ASP) is a hormone produced by
adipocytes and is of importance for the storage of energy as fat. We
examined whether ASP might also have effects on islet function. In
clonal INS-1 cells, ASP dose-dependently augmented glucose-stimulated
insulin secretion. The lowest effective dose of ASP at 10 mmol/l
glucose was 5 micro mol/l. The effect was glucose-dependent because
ASP did not increase insulin secretion at 1 mmol/l glucose but had
clear effect at 10 and 20 mmol/l glucose. Similarly, ASP augmented
glyceraldehyde-induced insulin secretion but the hormone did not
enhance insulin secretion in response to depolarization by 20 mmol/l
of KCl. ASP-induced insulin secretion was completely abolished by
competitive inhibition of glucose phosphorylation by glucokinase with
5-thio-glucose and was partially inhibited by the calcium channel
blocker, nifedipine, and by the protein kinase C inhibitor, GF109203.
Furthermore, thapsigargin, an inhibitor of Ca(2+)-ATPase in the
endoplasmic reticulum, did not affect ASP-induced insulin secretion.
ASP (5 micro mol/l) also augmented glucose-stimulated insulin
secretion from islets isolated from C57BL/6J mice, and intravenous
administration of ASP (50 nmol/kg) augmented the acute (1 and 5 min)
insulin response to intravenous glucose (1 g/kg) in C57BL/6J mice.
This was accompanied by an increased rate of glucose disposal. Minimal
model analyses of data derived from the intravenous glucose tolerance
test revealed that whereas ASP augmented insulin secretion, the
hormone did not affect insulin sensitivity (S(I)) or glucose
effectiveness (S(G)). We conclude that ASP augments glucose-stimulated
insulin secretion through a direct action on the islet beta cells. The
effect is dependent on glucose phosphorylation, calcium uptake and
protein kinase C. Stimulation of insulin secretion by ASP in vivo
results in augmented glucose disposal.

PMID: 12917708 [PubMed - indexed for MEDLINE]
**


Of interest:

"We conclude that ASP augments glucose-stimulated insulin secretion
through a direct action on the islet beta cells. The effect is
dependent on glucose phosphorylation, calcium uptake and protein
kinase C. Stimulation of insulin secretion by ASP in vivo results in
augmented glucose disposal."

These sentences:

"...ASP augments glucose-stimulated insulin secretion..."

"The effect is dependent on glucose phosphorylation..."

Can we conclude that without "glucose-stimulated insulin secretion"
and "glucose phosphorylation" the effects of ASP would be minimal if
anything at all.

TC



No. What this study shows is that ASP enhances insulin secretion from
the pancreas only in the presence of glucose; in other words, ASP can
not stimulate insulin secretion on its own. However, the *primary*
lipogenic effect of ASP is independent of insulin. ASP increases
triglyceride synthesis in fat cells by stimulating the activity of the
enzyme diacylglycerol acyltransferase (DGAT). DGAT catalyzes the last
step in the making of a triglyceride molecule (when the third and
final fatty acid is attached to the glycerol backbone).

It's well known that insulin enhances fat-storage primarily by
preventing lipolysis (triglyceride breakdown). ASP, on the other
hand, promotes fat-storage primarily by stimulating lipogenesis
(triglyceride synthesis). Think about it -- eating carbs causes
insulin secretion; the insulin prevents fatty acid release from
adipose tissue so that the carbs are burned for energy first. Eating
fat causes ASP secretion; the ASP causes any extra fat to be stored in
adipose tissue. This doesn't mean the insulin does not directly
stimulate lipogenesis or that ASP doesn't directly prevent lipolysis,
because they do. However, these are secondary effects.


Thanks for the info. One or two questions...

"Acylation stimulating protein (ASP) is a hormone produced by
adipocytes and is of importance for the storage of energy as fat."

Under what circumstances do the adipocytes produce ASP? What triggers
the fat cells to increase or decrease production of ASP?

TC
  #105  
Old January 31st, 2004, 03:34 AM
September
external usenet poster
 
Posts: n/a
Default What a bunch of clowns ( Uncovering the Atkins diet secret - for Moosh)

(tcomeau) wrote in message . com...
(September) wrote in message om...
(tcomeau) wrote in message . com...
Ron Ritzman wrote in message . ..
On 27 Jan 2004 11:46:06 -0800,
(tcomeau) wrote:

And what "other mechanisms"?

Your Google search term for today is "acylation stimulating
protein"

From Mr. "Ketogenic Diet" himself Lyle McDonald.

http://groups.google.com/groups?q=%2...onr.com&rnum=1

Or

http://tinyurl.com/2fbpf

Here is a recent study on acylation stimulating protein.

**
Acylation stimulating protein stimulates insulin secretion.

Ahren B, Havel PJ, Pacini G, Cianflone K.

Department of Medicine, Lund University, Lund, Sweden.


Acylation stimulating protein (ASP) is a hormone produced by
adipocytes and is of importance for the storage of energy as fat. We
examined whether ASP might also have effects on islet function. In
clonal INS-1 cells, ASP dose-dependently augmented glucose-stimulated
insulin secretion. The lowest effective dose of ASP at 10 mmol/l
glucose was 5 micro mol/l. The effect was glucose-dependent because
ASP did not increase insulin secretion at 1 mmol/l glucose but had
clear effect at 10 and 20 mmol/l glucose. Similarly, ASP augmented
glyceraldehyde-induced insulin secretion but the hormone did not
enhance insulin secretion in response to depolarization by 20 mmol/l
of KCl. ASP-induced insulin secretion was completely abolished by
competitive inhibition of glucose phosphorylation by glucokinase with
5-thio-glucose and was partially inhibited by the calcium channel
blocker, nifedipine, and by the protein kinase C inhibitor, GF109203.
Furthermore, thapsigargin, an inhibitor of Ca(2+)-ATPase in the
endoplasmic reticulum, did not affect ASP-induced insulin secretion.
ASP (5 micro mol/l) also augmented glucose-stimulated insulin
secretion from islets isolated from C57BL/6J mice, and intravenous
administration of ASP (50 nmol/kg) augmented the acute (1 and 5 min)
insulin response to intravenous glucose (1 g/kg) in C57BL/6J mice.
This was accompanied by an increased rate of glucose disposal. Minimal
model analyses of data derived from the intravenous glucose tolerance
test revealed that whereas ASP augmented insulin secretion, the
hormone did not affect insulin sensitivity (S(I)) or glucose
effectiveness (S(G)). We conclude that ASP augments glucose-stimulated
insulin secretion through a direct action on the islet beta cells. The
effect is dependent on glucose phosphorylation, calcium uptake and
protein kinase C. Stimulation of insulin secretion by ASP in vivo
results in augmented glucose disposal.

PMID: 12917708 [PubMed - indexed for MEDLINE]
**


Of interest:

"We conclude that ASP augments glucose-stimulated insulin secretion
through a direct action on the islet beta cells. The effect is
dependent on glucose phosphorylation, calcium uptake and protein
kinase C. Stimulation of insulin secretion by ASP in vivo results in
augmented glucose disposal."

These sentences:

"...ASP augments glucose-stimulated insulin secretion..."

"The effect is dependent on glucose phosphorylation..."

Can we conclude that without "glucose-stimulated insulin secretion"
and "glucose phosphorylation" the effects of ASP would be minimal if
anything at all.

TC



No. What this study shows is that ASP enhances insulin secretion from
the pancreas only in the presence of glucose; in other words, ASP can
not stimulate insulin secretion on its own. However, the *primary*
lipogenic effect of ASP is independent of insulin. ASP increases
triglyceride synthesis in fat cells by stimulating the activity of the
enzyme diacylglycerol acyltransferase (DGAT). DGAT catalyzes the last
step in the making of a triglyceride molecule (when the third and
final fatty acid is attached to the glycerol backbone).

It's well known that insulin enhances fat-storage primarily by
preventing lipolysis (triglyceride breakdown). ASP, on the other
hand, promotes fat-storage primarily by stimulating lipogenesis
(triglyceride synthesis). Think about it -- eating carbs causes
insulin secretion; the insulin prevents fatty acid release from
adipose tissue so that the carbs are burned for energy first. Eating
fat causes ASP secretion; the ASP causes any extra fat to be stored in
adipose tissue. This doesn't mean the insulin does not directly
stimulate lipogenesis or that ASP doesn't directly prevent lipolysis,
because they do. However, these are secondary effects.


Thanks for the info. One or two questions...

"Acylation stimulating protein (ASP) is a hormone produced by
adipocytes and is of importance for the storage of energy as fat."

Under what circumstances do the adipocytes produce ASP? What triggers
the fat cells to increase or decrease production of ASP?

TC


Insulin causes a modest increase in ASP - about 2 times basal levels.
Chylomicrons, lipoproteins produced by the intestines containing
ingested fat, cause a much larger increase - about 10 times basal
levels. Glucose, fatty acids, and VLDL don't stimulate ASP production
directly at all. After eating a mixed meal, ASP levels in adipose
tissue peak in 3 to 5 hours and decrease to baseline levels by 6
hours. ASP in plasma, however, doesn't necessarily rise after eating.
ASP works locally in adipose tissue. I'm not sure how it's degraded
or disposed of, but it doesn't seem to make its way into the general
circulation in a predictable way AFAIK.
  #107  
Old February 11th, 2004, 05:38 AM
PCBiker
external usenet poster
 
Posts: n/a
Default Uncovering the Atkins diet secret

eat about 4 or 5 malitol based chocolate candy bars each day, (lo carb) and
watch the weight drop off ...
diarrhia so bad it blows you out. Assures Outgo = Input


"talkback" wrote in message
...
wrote:

In sci.med.nutrition tcomeau wrote:
: Maybe the lesson to be learned is that calories really have little
: bearing when it comes to weight gain or loss in humans.

1) Please learn to trim quotes
2) Have you somehow forgotten the laws of thermodynamics? It is quite
simple: if energy in energy out, the body will gain mass. If
energy out energy in, the body will lose mass.


Do as I preach, not as I do.

(The Late) Dr. Atkins
Stroked out, fat & dead



  #108  
Old February 12th, 2004, 03:06 PM
J Stutzmann
external usenet poster
 
Posts: n/a
Default Uncovering the Atkins diet secret

Thermodynamics --- a law we can't live without! [grin]


wrote in message
news:[email protected]_s53...
In sci.med.nutrition tcomeau wrote:
: Maybe the lesson to be learned is that calories really have little
: bearing when it comes to weight gain or loss in humans.

1) Please learn to trim quotes
2) Have you somehow forgotten the laws of thermodynamics? It is quite
simple: if energy in energy out, the body will gain mass. If
energy out energy in, the body will lose mass.



  #109  
Old February 12th, 2004, 03:18 PM
Bob in CT
external usenet poster
 
Posts: n/a
Default Uncovering the Atkins diet secret

On Thu, 12 Feb 2004 14:06:29 GMT, J Stutzmann
wrote:

Thermodynamics --- a law we can't live without! [grin]


wrote in message
news:[email protected]_s53...
In sci.med.nutrition tcomeau wrote:
: Maybe the lesson to be learned is that calories really have little
: bearing when it comes to weight gain or loss in humans.

1) Please learn to trim quotes
2) Have you somehow forgotten the laws of thermodynamics? It is quite
simple: if energy in energy out, the body will gain mass. If
energy out energy in, the body will lose mass.




Let's say that eating fiber caries a certain amount of calories through
your body so that you don't digest them. Then, while calories in might
not change, eating more fiber would change the amount of calories out.

These "laws" are based on ideal situations. For instance, "an object in
motion tends to stay in motion" works great IN A VACUUM. It doesn't work
nearly as well in atmosphere.

People aren't closed systems. While these "laws" can help to describe
what happens to people, they aren't 100% accurate.


--------
Bob in CT
Remove ".x" to reply
  #110  
Old February 12th, 2004, 04:11 PM
Carol Frilegh
external usenet poster
 
Posts: n/a
Default Uncovering the Atkins diet secret

In article , Bob in CT
wrote:

On Thu, 12 Feb 2004 14:06:29 GMT, J Stutzmann
wrote:

Thermodynamics --- a law we can't live without! [grin]


wrote in message
news:[email protected]_s53...
In sci.med.nutrition tcomeau wrote:
: Maybe the lesson to be learned is that calories really have little
: bearing when it comes to weight gain or loss in humans.

1) Please learn to trim quotes
2) Have you somehow forgotten the laws of thermodynamics? It is quite
simple: if energy in energy out, the body will gain mass. If
energy out energy in, the body will lose mass.




Let's say that eating fiber caries a certain amount of calories through
your body so that you don't digest them. Then, while calories in might
not change, eating more fiber would change the amount of calories out.

These "laws" are based on ideal situations. For instance, "an object in
motion tends to stay in motion" works great IN A VACUUM. It doesn't work
nearly as well in atmosphere.

People aren't closed systems. While these "laws" can help to describe
what happens to people, they aren't 100% accurate.


And they don't matter in the long run because people can't give
everlasting microscopic attention to every bite for a lifetime.

They have to develop an eating "cruise control" that they can use
without negative calorie theories and this fiber concept, Fiber is
important for good bowel function. Eating less, exercising more and
doing it ongoing is what will yield results. The one thing that stands
out IMO is this has to be a lifetime committment, not annual, seasonal
or now and then, not let's splurge weekends and start over Monday.

--
Diva
******
There is no substitute for the right food
 




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