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Re: [IP] Re: bolusing for high-protein meal

I'm not sure what you mean by the fat utilizing the glucose. Fat
cells don't utilize stored glucose (as, for example, a body cell
does). Excess dietary glucose gets converted and stored as fat
(and insulin is used to do this), is that what you meant?
The fat doesn't break down to glucose however, so no insulin
would be needed to cover it for that particular purpose.

Here is some info from Ellenberg & Rifkin's Diabetes Mellitus,
Chapter 1 (Integrated Fuel Metabolism):
pg 2:
"A hierarchy for energy interconversion also exists. It is
unidirectional in that amino acids can be converted to glucose
and fat, and glucose can be converted to fat, but fat, once
formed, can only be stored or oxidized."

same chapter, regarding protein, pg 6:
"It is noteworthy that some amino acids (such as arginine and
leucine) are strong insulin secretagogues, and in situations
where protein meals are ingested, insulin release is stimulated
even when carbohydrate in the meal may be lacking. Under these
conditions glucagon plays a critical biological role to prevent
potential hypoglycemia by maintaining hepatic glucose production
in the face of hyperinsulinemia."

and in same chapter, regarding fat metabolism, pgs 6-7:
"Finally, with regard to fat metabolism, insulin has three major
anabolic actions that combine to promote net triglyceride
accumulation in adipose tissue (Fig. 1-3). Following a
fat-containing meal, the triglyceride is hydrolyzed to free fatty
acids by lipases in the duodenum, absorbed in the small
intestine, and reesterified into chylomicron triglyceride, which
then enters the systemic circulation via the lymphatics. Insulin,
secreted in response to the carbohydrate and/or protein
components of the meal, stimulates lipoprotein lipase (LPL)
activity and promotes fat and muscle storage of both exogenously
derived triglyceride as well as that produced endogenously.(44)
LPL in the capillary endothelium hydrolyzes triglycerides in
chylomicrons and VLDL to free fatty acids, which are then
transferred to the adipocyte for reesterification into
triglyceride. This effect is complimented by insulin's potent
inhibitory effect on the hormone-sensitive lipase within the fat
cell. This lipase normally catalyzes the hydrolysis of stored
triglyceride. By this dual mechanism, insulin markedly decreases
plasma free fatty acid concentration and stores fat. Finally,
insulin stimulates glucose uptake into the adipocyte by
stimulating Glut-4 translocation from the cytoplasm to the plasma
membrane, in a similar fashion to that which occurs in the
myocyte. (alpha)-glycerol phosphate formed from glucose is
required for the reesterification of fatty acids into
triglyceride. Adipocytes lack glycerol kinase, and therefore,
unlike liver and kidney, are unable to phosphorylate glycerol
directly. Thus, following a meal, insulin is the primary hormonal
factor that controls storage and metabolism of ingested metabolic
fuels. Under conditions of mixed meal ingestion when substrate is
available in the form of glucose, amino acids, and free fatty
acids, an increase in plasma insulin concentration will augment
their net storage as glycogen, protein, and fat, respectively.
This is accomplished by glycogenolysis, proteolysis, and
lipolysis as well as by facilitating the incorporation of
substrates into storage depots. It is noteworthy that the
dose-response relationships are such that the processes involving
breakdown of energy stores are much more sensitive to insulin
than those involved with energy accumulation. Thus, small meals
(associated with smaller insulin responses) serve mainly to
conserve depots by affecting breakdown, whereas larger meals (and
concomitant greater insulin responses) are generally required for
the direct stimulation of storage mechanisms."

and pg 56 (B-Cell Function and Insulin Secretion):
"Fats. Triglycerides, free fatty acids, and ketones have
negligible effects on insulin release in humans.(49) Because fat
is usually ingested with carbohydrate, glucose-stimulaed insulin
release suppreses both lipolysis and free fatty acid
mobilization, which help conserve stored triglyceride for periods
of fasting. Although ingested fat has little direct effect on the
B cell, it is well known to slow the digestion and absorption of
other nutrients that do directly stimulate the B cell. Thus,
mixed meals of varying fat content are not ideal for assessing
B-cell function."

Take care, Kerri - MSN IM: maverickmom1965
Parents of Pumpers chat host, Saturdays 9:30pm EDT, Parents chat
room at www.insulin-pumpers.org
"I've seen and met angels wearing the disguise of ordinary people
leading ordinary lives, filled with love, compassion,
forgiveness, and sacrifice." - Tracy Chapman [Heaven's Here on
Earth, 1994]

Wayne said:
While this is true, Kerri, fat cells themselves do require
insulin to utilize glucose.  So when ever you eat anything that
gets fats cells up and running (no pun intended), you will
require more insulin. i've never seen any data that would allow
one to predict in advance, however, so this is, like many things,
a trial and error thing.  It's a whole lot easier to try on a
pump, though.
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