x-no-achive: yes
Alan Moorman wrote:
> And, there is a question about this:
>
> is a fast, high spike which comes and goes quickly better or
> worse for you than...
>
> a long, slow rise in your bG?
>
> Does ANYONE really know if 45 minutes of high is worse for
> you than 3 hours of medium?
>
> I doubt it.
>
> Someone, undoubtedly will respond saying something like: "It
> stands to reason that......"
>
> Or: "Common sense says.........."
>
> But, has ANYONE ever researched this?????
>
>
> Alan Moorman
From phlaunt.com/diabetes
Prolonged Exposure to Blood Sugars Over 140 mg/dl (7.8 mmol/L) Kills
Human Beta Cells
Another series of experiments on beta cells grown in culture showed that
there is a threshold over which the damage to beta cells caused by
exposure to elevated blood sugars becomes irreversible. It found that
amount of damage cells sustained in genes that produced insulin depended
on the concentration of glucose they were exposed to. The effect was
continuous, not a threshold effect--meaning that the more glucose the
cell was grown in, the more function it lost.
In a second experiment, the same researchers took cells damaged by
exposure to high blood sugars and moved them to media that had a lower
concentration of blood sugar. They found the cells could survive and
recover after being moved to a growth medium containing a much lower
concentration of glucose, but only if the switch was made before a
certain amount of time had passed. Once the cells had been exposed to
glucose for that fatal time period, they could no longer be revived.
In an email to me, R. Paul Robertson, one of authors of this study
wrote, "I think the glucose toxic effects begin when blood glucose gets
above 140 and probably earlier." However, he also explained that while
studies with diabetic rats could better quantify the blood sugar levels
at which this irreversible damage occurs, these rats cost $200 apiece
and a lot of rats would be required. So such a project is not planned
for any time soon.
Catherine E. Gleason, Michael Gonzalez, Jamie S. Harmon, and R. Paul
Robertson. Determinants of glucose toxicity and its reversibility in
pancreatic islet Beta-cell line, HIT-T15. Am J Physiol Endocrinol Metab
279: E997-E1002, 2000
http://ajpendo.physiology.org/cgi/co...act/279/5/E997
******
Original Article
The postprandial state and risk of cardiovascular disease
P.J. Lefèbvre *, A.J. Scheen
Division of Diabetes, Nutrition and Metabolic Disorders, Department of
Medicine, University of Liège, Belgium
*Correspondence to P.J. Lefèbvre, Division of Diabetes, Nutrition and
Metabolic Disorders, Department of Medicine, University of Liège, Belgium
Conference: 5th International Symposium on Type 2 Diabetes Mellitus:
Breaking the Barriers for Improved Glycaemic Control, Copenhagen, 7
December 1998 to 8 December 1998. Novo Nordisk.
Keywords
postprandial state • hyperglycaemia • impaired glucose tolerance •
lipidaemia • cardiovascular disease • diabetes mellitus
Abstract
Metabolism in man is regulated by complex hormonal signals and substrate
interactions, and for many years the clinical focus has centred on the
metabolic and hormonal picture after an overnight fast. More recently,
the postprandial state, i.e. the period that comprises and follows a
meal, has received more attention. The oral glucose tolerance test
(OGTT), although highly non-physiological, has been used largely as a
model of the postprandial state. Epidemiological studies have shown
that, when impaired, oral glucose tolerance is associated with an
increased risk of cardiovascular disease. Postprandial hyperlipidaemia
has been investigated more recently in epidemiological, mechanistical
and intervention studies, most of which indicate that high postprandial
triglyceride levels, and particularly postprandial rich triglyceride
remnants, constitute an increased risk for cardiovascular disease.
Recent studies have shown that excessive postprandial glucose excursions
are accompanied by oxidative stress and, less well known, activation of
blood coagulation (increase in circulating D-dimers and prothrombin
fragments). The mechanisms through which increased postprandial glucose
levels and lipid concentrations may damage endothelial cells on blood
vessel walls appear to be complex. These mechanisms include the
activation of protein kinase C, increased expression of adhesion
molecules, increased adhesion and uptake of leucocytes, increased
production of proliferative substances such as endothelin, increased
proliferation of endothelial cells, increased synthesis of collagen IV
and fibronectin, and decreased production of nitric oxide (NO). In
conclusion, the postprandial state cumulatively covers almost half of
the nycthemeral (*DAILY*) period, and its physiology involves numerous
finely regulated motor, secretory, hormonal and metabolic events.
Epidemiological and mechanistical studies have suggested that
perturbations of the postprandial state are involved in cardiovascular
disease. Correcting the abnormalities of the postprandial state must
form part of the strategy for the prevention and management of
cardiovascular diseases, particularly those that are associated with
diabetes mellitus. Copyright © 1998 John Wiley & Sons, Ltd.
--------------------------------------------------------------------------------
Received: 3 September 1998; Accepted: 7 September 1998
Digital Object Identifier (DOI)
10.1002/(SICI)1096-9136(1998120)15:4+<S63::AID-DIA737>3.0.CO;2-7 About DOI