Re: Is the Pancreas restorable?

On Sun, 5 Oct 2008 17:26:40 +0200, "GysdeJongh"
<jongh711@xxxxxxxxx> wrote:

"hermie" <hermie@xxxxxxxxxxxxx> wrote in message
news:gc8tbj$uva$2@xxxxxxxxxxxxxxxxxxxx
I have read in various places that those who are developing type 2
diabetes can restore their pancreas by exercise and diet. Is this true;
are there any supplements or other things that can be done to promote
growth of new insulin producing cells? Thanks.

Hi hermie,
your question seems to imply that you think that we just have a pancreas
which we may loose...

Here is the current scientific picture (which may- and will chance over time
of course) :
each second cells in the pancreas die, each second new cells are born in the
pancreas.The total number of cells in the pancreas is tightly regulated.This
is called a dynamic equilibrium, homeostasis.

This is nothing new, your skin works exactly in the same way.From this model
it is clear that the total number of cells in the pancreas decreases if the
rate at which existing cells die is increased, while the rate at which new
cells are generated stays the same.


Gys, it's not a matter of popularity.

I'm sure you will have papers to support some of the
statements in this post. Possibly I have missed these
support papers over time, so I would appreciate specific
cites for each of the statements in this post that I feel
need that support. I'll note the ones I mean with a couple
of question marks.

This is what happens in T2.Cells die faster due to inflamation.The
inflamation is caused by eating too much.

?? Too much of a specific macronutrient or too much
absolutely?

I know that what follows is not
very popular here, to say the least.....The way to reverse this is stop
eating.

?? Seems drastic. Or do you mean stop over-eating? If so, do
you mean a specific macronutrient or over-eating generally?

This will upregulate master switches like Sirtuins and PPAR's.Which
in turn will upregulate the protectors like GLP-1 etc.Here is a very new
review.It is not yet in Pubmed, but will appear there in a few weeks { I
inserted a few translations to increase readability } :

Beta-cell failure as a complication of diabetes

K. J. Chang-Chen & R. Mullur & E. Bernal-Mizrachi



Rev Endocr Metab Disord

DOI 10.1007/s11154-008-9101-5



Abstract

Type 2 diabetes mellitus is a complex disease characterized by b-cell
failure in the setting of insulin resistance. In early stages of the
disease, pancreatic b-cells adapt to insulin resistance by increasing mass
and function. As nutrient excess persists, hyperglycemia {to high blood
glucose} and elevated free fatty acids negatively impact b-cell function.
This happens by numerous mechanisms, including the generation of reactive
oxygen species {is prevented by anti oxidants like alpha lipoic acid and
fresh fruits}, alterations in metabolic pathways, increases in intracellular
calcium and the activation of endoplasmic reticulum stress. These processes
adversely affect b-cells by impairing insulin secretion, decreasing insulin
gene expression and ultimately causing apoptosis {a nifty word for
death....}.



Type 2 diabetes mellitus is a multifactorial disease that has greatly risen
in prevalence in part due to the obesity {too high body weight} and
inactivity {too low exercise}that characterize the modern Western lifestyle.

?? That definitely needs support. There is a possible
confusion of cause and effect there.

The following was very intersting, but does not appear to
support those queried statements.

Pancreatic b-cells possess the potential to greatly expand their function
and mass in both physiologic and pathologic states of nutrient excess {too
much food} and increased insulin demand.


Transient {peak} increases in glucose levels within physiological {normal}
range induce insulin secretion and potentially beneficial signals.In
contrast, glucotoxicity { toxic high blood glucose} induced by prolonged
hyperglycemia causes b-cell dysfunction and altered b-cell mass.In humans,
chronic hyperglycemia is associated with alterations in b-cell mass and
function. The b-cell has an incredible ability to adapt and compensate for
chronic hyperglycemia, but ultimately, obesity, chronic hyperglycemia, and
worsening insulin resistance lead to increased b-cell apoptosis. Similarly,
postmortem studies in human type 2 diabetic patients reveal low frequency of
replication and reduced b-cell mass, mainly by increased apoptosis



That this model may hold promise for the cure of T2 can be seen from phase
III clinical trials where they use blockers of inflamation signals, the same
blockers that are currently in use for rheumatism.I hope you will see what
happens here : the inflamation signal is taken away, I think it may be a
better strategy to take the cause of this warning signal away.....





N Engl J Med. 2007 Apr 12;356(15):1517-26.
Interleukin-1-receptor antagonist in type 2 diabetes mellitus.

BACKGROUND: The expression of interleukin-1-receptor antagonist is reduced
in pancreatic islets of patients with type 2 diabetes mellitus, and high
glucose concentrations induce the production of interleukin-1beta in human
pancreatic beta cells, leading to impaired insulin secretion, decreased cell
proliferation, and apoptosis. METHODS: In this double-blind, parallel-group
trial involving 70 patients with type 2 diabetes, we randomly assigned 34
patients to receive 100 mg of anakinra (a recombinant human
interleukin-1-receptor antagonist) subcutaneously once daily for 13 weeks
and 36 patients to receive placebo. At baseline and at 13 weeks, all
patients underwent an oral glucose-tolerance test, followed by an
intravenous bolus of 0.3 g of glucose per kilogram of body weight, 0.5 mg of
glucagon, and 5 g of arginine. In addition, 35 patients underwent a
hyperinsulinemic-euglycemic clamp study. The primary end point was a change
in the level of glycated hemoglobin, and secondary end points were changes
in beta-cell function, insulin sensitivity, and inflammatory markers.
RESULTS: At 13 weeks, in the anakinra group, the glycated hemoglobin level
was 0.46 percentage point lower than in the placebo group (P=0.03);
C-peptide secretion was enhanced (P=0.05), and there were reductions in the
ratio of proinsulin to insulin (P=0.005) and in levels of interleukin-6
(P<0.001) and C-reactive protein (P=0.002). Insulin resistance,
insulin-regulated gene expression in skeletal muscle, serum adipokine
levels, and the body-mass index were similar in the two study groups.
Symptomatic hypoglycemia was not observed, and there were no apparent
drug-related serious adverse events. CONCLUSIONS: The blockade of
interleukin-1 with anakinra improved glycemia and beta-cell secretory
function and reduced markers of systemic inflammation. (ClinicalTrials.gov
number, NCT00303394 [ClinicalTrials.gov].). Copyright 2007 Massachusetts
Medical Society.

PMID: 17429083



hth

Gys


Cheers, Alan, T2, Australia.
--
d&e, metformin 2000 mg
Everything in Moderation - Except Laughter.
http://loraldiabetes.blogspot.com (Be Smart, Be Skeptical)
dLife http://tinyurl.com/54get5 (Diabetes Diet Wars)
.

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