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Photo: My
girlfriend, Joy, stealing food from strangers at Disney Land.
Check out her
sternocleidomastoids. What’s up with that?
THE 'UNIFIED THEORY' OF DIETING?
© 2003.
Rob Thoburn. All rights reserved.
IMPORTANT
(i.e., please read this):
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content of The Glucose Economy, in whole or in part, except as otherwise
expressly permitted, in writing, by Rob Thoburn.
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I've
said it a million times before (okay, maybe not a million), as have many others
before me:
There
is no one 'best' diet for losing body fat (getting ‘lean’, 'cut', 'shredded',
‘rock hard’, etc.), just as there is no one 'best' workout for building muscle.
I much prefer to understand what it is about
effective diets that make them...well...effective.
Why is it that some diets work better than
others as far as body fat management is concerned? What's the common thread?
Why can you get very lean on either a high-
or a low-carbohydrate diet? Why might some people find it easier to get that
‘granite hard’ look with one or the other?
Aren’t these the kinds of questions you should be
asking? Arming yourself with the answers, after all, will allow you to truly
master the art of eating to look good. 'Dieting', in the conventional sense of
the word, will become unnecessary –archaic, in fact.
The ‘common thread’ referred to above is something
I've coined 'The Glucose Economy'. The Glucose Economy concept explains
why so many different diets can effectively remove body fat, but why some may
work better than others. That's why I often refer to it as the 'Unified Theory
of Dieting'. To the extent that any eating approach satisfies the Glucose
Economy concept, it will enable you to stay exceptionally lean as you build
muscle.
What's the purpose of eating?
Eating
performs numerous biological functions. But there’s one that tops the charts:
Food provides energy, something physicists define as ‘the capacity to
perform work’.
In
particular, food provides you with energy in the form of carbon (C), one
of nature’s most common elements. Your body’s favorite source of it is a
6-carbon molecule known as glucose (a.k.a. ‘blood sugar’; molecular
formula: C6H12O6).
The ‘Glucose Economy’ –your body’s total supply of
glucose— largely determines whether you are getting leaner or fatter at any
given moment, and whether you're dragging your ass through the gym, or hurdling
it over other members. This concept is as
simple as it is powerful. Use it wisely and your body will always stick head,
neck and shoulders above the maddening crowd!
Your body has an economy, of sorts. This economy is
based not on finances, but on fuel -glucose, in particular. Strict
management of the Glucose Economy is its top priority, as running out of this
preferred energy source could have dire consequences.
Yes, as much as we blame glucose and other dietary
carbohydrate (i.e., sugars and starches) for our body fat woes, glucose is
‘high-man’ on the totem pole of fuels ‘burned’, or oxidized, by your body. The
more glucose you consume --typically in the form of sugars and starches found
in the foods you eat-- the more glucose your body burns. Simultaneously, it
burns less in the way of fat and protein.
Conversely, as your Glucose Economy shrinks (e.g.,
between meals, overnight, during exercise), the fuel mixture shifts: you burn
progressively less glucose and more fat. This
spares the small amount of glucose that is available for those tissues that
really need it (see DETAILS, below). You can take advantage of this
metabolic ‘see-saw’ to design meals that allow you to consume more calories
while burning more fat and promoting faster muscle growth!
Your brain isn’t the only part of your body that
relies heavily on glucose. The lens of your eye, your kidneys, the red blood
cells that feed you with oxygen --these and other tissues are also dependent on
glucose.
Are you pregnant? Then you’re carrying another
heavy consumer of glucose: the developing fetus. During lactation, the mammary
glands will also be using a lot of glucose (Butte et al., 1999).
This is an important question. Compared to the
amount of fat you carry on your body (even if you’re very lean), your Glucose
Economy is quite small (Cahill, 1971).
Normally only about 4 grams (g) of glucose –not
even a teaspoonful-- floats around in your blood (~ 5 mmol/L). Much more
glucose is efficiently stored in the form of highly branched chains, termed
glycogen, found most abundantly in your liver and skeletal muscle. Yet your
glycogen storage capacity is very limited, unlike your virtually infinite
capacity to store fat. It sucks, I know…
Rarely will your fasting blood glucose level
increase by more than a ½ teaspoon (1.5 to 2 g), and even then, only very
briefly (Acheson et al., 1982). Within an hour of eating, it will usually have
returned to normal. This fairly tight control becomes even more evident when
you realize that a typical meal can easily dump 50 g to 150 g or more of
glucose into your body.
END OF DETAILS
Management of your Glucose Economy is achieved in
part by the hormone known as insulin. We may not worship it much, but insulin
is the ‘King’ of energy storage (Morand et al., 1993; Hussain et al., 1995). In
addition to its roles in vitamin and mineral traffic, insulin promotes the
storage of the carbohydrate, fat and protein calories you consume. Insulin is
released from your pancreas in response to meal ingestion and the detection of
blood-borne nutrients (most notably, glucose) obtained following their
digestion.
You can think of insulin as a harbinger of glucose,
a messenger sent ahead to arrange this fuel’s use and storage. Reaching your
body’s tissues via the bloodstream, insulin molecules dock themselves onto
insulin receptors embedded within the outer layer of insulin-sensitive cells.
These insulin-receptor, or ‘key-fits-lock’, interactions trigger a cascade of
events that continue deep inside the cell. In regards to carbohydrate calories,
this results in an increase in glucose transport.
Insulin also stimulates the oxidation of glucose
and its storage as glycogen. Simultaneously, the oxidation of fat (fatty acids,
specifically) is suppressed. A vast majority of the glucose provided by the
food you eat is transported into your skeletal muscle cells (Baron et al.,
1988) (a.k.a. ‘muscle fibers’), perhaps the most important insulin-sensitive
cell type (fat cells, or adipocytes, are another).
Whereas blood glucose levels come down fairly
quickly after a meal, insulin is a little more sluggish. Even after eating only
a small portion of carbohydrate, with blood glucose levels increasing very
slightly, insulin levels can rise dramatically. It can take more than 2 hours
for the latter to fall back to normal. To a point, the more carbohydrate
ingested, the greater tends to be this effect (Jenkins et al., 1981).
When healthy people ate a meal providing just under
300 g of carbohydrate, insulin levels were still 300% above normal 7 hours
later (Taylor et al., 1993). Their blood glucose levels increased by only about
1.5 g, in contrast, and rapidly returned to normal (Taylor et al., 1982). The
lesson to be learned is that even small increments in blood glucose can cause
marked, long lasting increments in your insulin level. The implications this
can have for your physical appearance will become apparent in a few moments.
This is a widespread belief. Indeed, many people
believe that carbohydrate can be turned into fat. Hence the popular, albeit
overly simplistic, perception that sugars and starches (the form of
carbohydrate most commonly eaten) are fattening.
But this isn’t entirely true. Let’s set the record
straight. Practically all of the carbohydrate you eat ends up going down two
roads: (1) the glucose it provides is burned, or oxidized, as fuel and; (2) the
glucose is stored for later as glycogen (Acheson et al., 1982; Hellerstein,
2001).
Even when healthy people consume a meal containing
an unusually large serving of carbohydrate –nearly 500 grams- most of it
gets stored as glycogen and the rest is burned as fuel (oxidized) (Acheson et al., 1982; Flatt et al., 1985; Taylor
et al., 1993).
In fact, the more carbohydrate you eat, the greater
tends to be the rate at which you oxidize glucose and store it as glycogen
(Flatt et al., 1985). Again, this occurs mostly in your muscle cells (fibers)
(Baron et al., 1988) under the influence of insulin.
Contrary to popular belief, dietary carbohydrate
tends not to be converted into fat (Acheson et al., 1982; Flatt et al., 1985).
Why not?
For one thing, converting carbohydrate into fat
requires a great deal of energy (Flatt et al., 1985); for another, it’s a waste
of your body’s most important fuel –glucose.
You see, once glucose is converted into fat,
there's no going back; this process is essentially irreversible. Irreversible
by the human body, anyway. Plants, in contrast, are capable of performing this
metabolic feat.
For essentially the same reason
you can get fat on any diet.
At the end of the day, what
matters most is total calories consumed. I can't emphasize this enough. If you
aren't happy with the way you look in the mirror, you need to manage your
Glucose Economy more strictly, which ultimately means strictly monitoring the total amount of protein, carbohydrate, and fat calories that you eat
As you increase your intake of protein,
carbohydrate, and/or fat calories, your fat-burning rate will tend to fall.
Again, this is because carbohydrate, and to a lesser extent, protein, stimulate
their own oxidation, whereas they suppress the oxidation of fat. Fat, on
the other hand, only very weakly stimulates its own oxidation. Thus, as more
and more calories are consumed, you eventually reach a point where the rate at
which fat is being stored exceeds the rate at which it is being burned. You
have achieved positive fat balance –the sin qua non (essential
element) of gaining fat.
If you consume large quantities of carbohydrate day
after day, and fail to burn it up with exercise, you’ll eventually push your
glycogen storage capacity to its limit. Your fat-burning rate will
simultaneously fall, thereby increasing your risk of positive fat balance. That
is, a positive carbohydrate balance can eventually beget a positive fat balance.
Recall that compared to your virtually infinite
capacity to store fat, your glycogen storage capacity is very limited (Cahill,
1971; Flatt et al., 1985). Generally speaking, the more muscle you carry, and
the more you exercise, the greater your glycogen storage capacity will tend to
be. Yet another reason to pump iron!
Still, Mr. Olympia or Ironman triathlete
notwithstanding, if you continue to consume more and more carbohydrate, you
will eventually incur a positive fat balance and net fat gain. That is, you’ll
become fatter. However, even under these circumstances, the conversion of
dietary carbohydrate into fat per se is not the major contributory factor
(Hellerstein et al., 1996; Hellerstein, 2001).
The real ‘problem’ with dietary carbohydrate
(though it won’t be a problem for you!) relates to the ‘see saw’ of
fuel-burning metabolism.
You now know that carbohydrate tends to increase
insulin levels more than fat or protein. As sugars and starches in the food you
eat pass across your tongue and become digested in your gut, blood glucose and
insulin levels rise accordingly. In particular, insulin levels rise quite a bit
higher than do those of glucose, and take much longer to return to normal.
You also know that eating carbohydrate stimulates
the oxidation of glucose and its storage as glycogen (Acheson et al., 1982).
This is due to glucose per se, as well as its metabolic harbinger, insulin, the
level of which increases markedly as you eat more carbohydrate. Hence the
fuel-burning ‘see saw’: Glucose (or dietary carbohydrate) and insulin tilt your
body’s fuel-burning mixture in favor of glucose oxidation (Flatt et al., 1985).
At the same time, they suppress the oxidation of fat (Hussain et al., 1995).
Insulin’s metabolic ‘leverage’ is powerful in these
regards: Insulin levels well below
that found following most meals can reduce the oxidation of fat by some 50%
(Bonnadonna et al., 1990; Jensen et al., 1989; Swislocki et al., 1987).
Concerning carbohydrate calories, arguably the most
important factor determining your ability to lose body fat is the quantity
of carbohydrate you eat.
The more carbohydrate you eat, the faster you
oxidize glucose, and the slower you oxidize fat. This makes sense. When the top
fuel, glucose, is abundant, it is oxidized in ‘preference’ to less popular
fuels, namely, fat and protein. As the Glucose Economy shrinks, your body works
down the totem pole of oxidized fuels: It burns progressively more fat and
attempts to spare the small amount of glucose that is available.
This, research suggests to us, is why overeating
carbohydrate can make you fat. The problem is not that carbohydrate is
converted into fat. Rather, it is that eating carbohydrate stimulates metabolic
pathways involved in the burning of glucose at the same time that it slows down
those burning fat. But again, none of this really matters so long as you aren't
eating too many calories overall!
The combination of fat and
carbohydrate could be fattening...if you eat too many calories
overall.
Again, the more carbohydrate you consume, the
greater will be the suppression of fat oxidation. If your total intake of each
macronutrient is too high, this could lead to a net fat gain, even if you don’t
eat much in the way of fat. Most of this will result from the storage of fat
provided by the diet (all natural foods contain some fat). If you really go
overboard, however, there could certainly be a contribution from de novo fat
synthesis.
It’s at this point that many of you will begin to
understand (perhaps even visualize) why overeating carbohydrate and fat --a
combination common to nearly all of the world’s favorite dishes-- has the
potential to be so fattening. In the metabolic playground that is your body, dietary
fat, when compared to carbohydrate, is the short end of the fuel-burning see
saw (i.e., the end with the poorest leverage): Whereas dietary carbohydrate
powerfully ‘leverages’, or stimulates, its own oxidation, fat does so only very
weakly. That is, eating more fat does not substantially increase fat burning
metabolism, causing more of it to be stored (Flatt et al., 1985; Forslund et
al., 1999).
Needless to say, eating less carbohydrate is a
powerful way to threaten your Glucose Economy. Deficient in a more direct
source of glucose (i.e., sugars and starches), your body strives to synthesize
it indirectly from so-called ‘non-carbohydrate’ sources. The glucose so
produced is spared for those tissues that really need it by an increase in the
burning of fat.
This process of making ‘new’ glucose from
non-carbohydrate compounds is termed gluconeogenesis. Contrary to
popular belief, gluconeogenesis occurs all the time, even when you are well
fed. However, it occurs to a greater extent as your Glucose Economy begins
to dwindle in size (Jungas et al., 1992). Importantly, gluconeogenesis is an
energy-consuming process, and this energy is supplied by the burning of fat.
You can exploit this fact every time you sit down to eat a meal!
What are these indirect sources of glucose? One
important source is protein. In particular, the building blocks of protein,
called amino acids (see DETAILS, below).
As a bodybuilder or serious fitness enthusiast, you
are likely already aware of the importance of amino acids. Briefly, amino acids
function like letters of the alphabet. They can be strung together in myriad
combinations to yield ‘sentences’, or proteins, with unique form and function:
hemoglobin, insulin, growth hormone, and antibodies are just a few examples of
proteins essential to human life.
Your body makes, or synthesizes, its own proteins
from amino acids made available to it. The protein you eat provides amino
acids, of course, as does the breakdown, or catabolism, of your own tissue
protein (e.g., skeletal muscle protein). Certain amino acids can also be made
‘from scratch’ (so-called 'de novo' synthesis), provided your body has enough
nitrogen (provided by other amino acids) and carbon (as from carbohydrate).
Certain amino acids in the protein you eat, and in
the protein that makes up your tissues, can be converted into glucose. We call
these amino acids ‘glucogenic’. Two key glucogenic amino acids are glutamine
and alanine.
The amino acids lysine and leucine can be converted
into ketones (Jungas et al., 1992), another alternative fuel source. Ketones
can also be produced from fat. In fact, for our purposes, you can think of a
ketone as a water-soluble fat.
The increased use of fat and ketones by tissues
that can use them effectively spares the glucose yielded by gluconeogenesis for
those tissues that really need it. In fact, the oxidation of fat and ketones
provides the energy required to drive gluconeogenesis (Jungas et al., 1992;
Morand et al., 1993). Thus, the burning of fat and gluconeogenesis go
hand-in-hand; you can’t have one without the other. You may be able to harness
this fact to burn more fat for a given amount of calories.
Amino acids and glycerol are arguably the 2 most
important gluconeogenic substrates (Owen et al., 1998). The value of glycerol
as a component of body fat becomes especially apparent when you ponder the
dietary challenges faced during the bulk of our evolutionary history as a
species. As we shall ponder now…
Perhaps the single most important metabolic
function of your body fat (as unsightly as it may seem to you) is to serve and
protect your Glucose Economy. Most readers, including many medical researchers,
find this to be a revolutionary, eye-opening concept. Its implications are very
far reaching, providing explanations for everything from diabetes to obesity
and reproductive dysfunction.
Body fat both provides substrate (glycerol) for
gluconeogenesis and a source of energy (fatty acids) with which to fuel it.
Here’s how it works. Fat is stored inside the cells of your body (especially
fat cells, or adipocytes) as ‘oil droplets’ composed of triacylglycerols (a.k.a.
‘triglycerides’). Each triacylglycerol molecule consists of 3 fatty acid
molecules attached to 1 molecule of glycerol.
When body fat is broken down [termed lipolysis, meaning ‘splitting’ of lipid
(fat)], fatty acids and glycerol are released into your bloodstream. The fatty
acids can be oxidized to provide energy, whereas the glycerol can be converted
into glucose (Chen et al., 1993). In fact, and as noted above, the energy
provided by the former supplies the energy required to drive the latter.
Try to imagine yourself 100,000 or so years ago. There you are, wandering about
under the midday sun, searching for something to eat. You’re physically active
and short on food –the two most powerful ways to increase your fat-burning
rate. Though you carry only a small amount of body fat on your lean frame, it
can supply ample energy to keep you going for many days: More specifically, its
fatty acids can be oxidized, and the glycerol, via conversion to glucose, can
be used to preserve your suffering Glucose Economy. Nifty, huh? In fact, with
prolonged starvation, glycerol’s contribution to gluconeogenesis is roughly the
same as for that made by all amino acids combined (Owen et al., 1998).
Now back to the present. Same metabolic equipment, but a different –completely
opposite—set of dietary challenges. As a consequence of our modern day
conveniences, we eat not too little, but too much. We suffer not from too much
exercise, but too little. Yes, compared to prehistoric times, you spend each
day well fed and, despite your daily workouts, mostly inactive. This renders
your fat-burning rate fairly unspectacular for the greater portion of the day.
Armed with your current knowledge, you can
appreciate the fact that there is no truly 'carbohydrate-free' diet!
Every single gram of protein you eat contains amino
acids with carbon capable of being converted into glucose. Every single gram of
fat (triacylglycerol) you eat contains glycerol capable of being converted into
glucose. Thus, if you are eating food, you are, when viewed from this
perspective, eating carbohydrate. That's why we can survive on a
'carbohydrate-free' diet!
END OF DETAILS
Weight-training persons like bodybuilders and
serious workout enthusiasts can benefit from 1.6-1.7 grams of protein per kg
body weight per day (Lemon et al., 1997). (1 kg = 2.2 lb.). However, eating a
diet providing even more protein than this (2.5 g/kg bodyweight/day) yet lower
in carbohydrate may allow you to burn more fat both during exercise and at rest
(Forslund et al., 1999). And such a diet is superior to one lower (though still
adequate in) protein and higher in carbohydrate for establishing a positive
protein balance (Forslund et al., 1999) –an essential requirement for adding
pounds and inches of lean muscle to your body!
So will eating more protein than the aforementioned
2.5 g/kg/body weight/day figure dictates lead to faster fat loss? Possibly.
Keeping total calories constant, it makes sense to suggest that a diet providing
an 'excess' of protein and a relative shortage of sugars and starches
(conventional 'carbohydrate') may promote greater gluconeogenesis, thereby
increasing your body's overall fat-burning rate. Basically what you are doing
is encouraging your body to make glucose 'from scratch' --a less efficient
process than that involved in breaking down and absorbing sugars and starches.
So long as you don't eat too many calories overall,
will eating an excess of protein relative to carbohydrate (starches and sugars)
really get you leaner that much faster. Will it allow you to eat more calories
than would a more efficient diet consisting of more carbohydrate and less
protein?
Based on what we've discussed to this point, it
seems possible. However, based on my own personal experience, I'd have to say
that it may not make that big of a difference at all. Indeed, so long as I
don't consume too many calories overall, I have been able to get very
'shredded' on both a higher-carbohydrate/lower-protein diet, and a lower-carbohydrate/higher-protein
diet. That being said, I tend to prefer a somewhat more 'carbohydrate
restricted (in the conventional sense of the word) than do some.
Indeed, so long as you take in enough protein to
satisfy your body's tissue-building needs, plus a bit extra for 'accessory
functions', and provided you don't eat too many calories overall, an endless
variety of macronutrient profiles (ratio of fat:protein:carbs) can work well.
Only you can determine your protein needs. If you enjoy eating 40% of your
calories as protein, and 40% of your calories as carbohydrate, then go head. If
this brings you the results you want to see in the mirror, then stick with it.
If not, experiment until you see a body in the mirror that you do like.
Protein, whether from your own tissues (e.g.,
muscle), or from food, consists of amino acids linked together in
chains. Amino acids are the principle means by which we humans get nitrogen
–an essential element to your survival.
Building muscle is about balance –protein balance. If you make more muscle
protein than you break down (positive muscle protein balance) your muscles will
tend to increase in size and strength with time. Conversely, if you make less
muscle protein than you break down (negative protein balance), your muscles
will tend to get weaker and smaller.
Scientists refer to ‘building up’ processes as ‘anabolism’ or ‘anabolic’;
‘catabolism’, in contrast, describes processes of breakdown or degradation.
Thus, a positive protein balance indicates an anabolic state.
Since protein contains nitrogen, we can estimate your protein balance by
measuring your nitrogen balance. Technically speaking, however, the two should
not be considered equal. In any case, a positive nitrogen balance is generally
taken as a sign of an anabolic state with an overall gain (retention) of
nitrogen for the day, whereas a negative nitrogen balance indicates a catabolic
state.
Another, possibly more accurate, way to estimate your protein balance is by
measuring your body’s balance of a particular amino acid, such as leucine. A
positive leucine balance indicates protein anabolism (‘building’). Or, at
least, a positive leucine balance reflects a state (i.e., increased
availability of leucine inside your muscle cells) that promotes protein
anabolism. Conversely, a negative leucine balance indicates protein catabolism
(‘breaking down’). Simply said, a positive leucine balance is ‘good’; a
negative leucine balance, ‘bad’, if your interest lies in building bigger
muscles.
You don’t eat all the time; there are fluctuations in your protein intake, such
as in between meals and while you sleep.
So how does your body preserve its protein balance? How does it keep the total
amount of protein in your body from shrinking (and your muscles alongside) in
the face of fluctuating intakes of dietary protein? The answer is that it
increases or decrease tissue protein breakdown according to how much protein
you feed it (for review see Garlicky et al., 1999).
Generally speaking, in between meals you lose tissue (e.g., muscle) protein,
but after a protein-containing meal, you recoup what was lost through a
decrease in protein breakdown. The production, or synthesis, of tissue protein
typically doesn’t change too much after a protein-containing meal (Melville et
al., 1989; Price et al., 1994; Garlick et al., 1999), yet because protein
breakdown is reduced, the result is a net increase (gain) in protein such that
balance is achieved. You don’t get bigger, granted, but you don’t shrink,
either.
Of course, bodybuilders aren’t interested in maintaining the status quo. We
want to get bigger. The bottom line is that in order to actually gain enough
muscle protein to make your muscles bigger and stronger, you’ve got to address
both sides of the protein balance equation. Again, stimulating muscle protein
synthesis is by far the most important half of the muscle-building equation.
This cannot be emphasized enough. Stimulation of muscle protein synthesis is
the means by which resistance training (lifting weights) makes muscles grow
(Barr and Esser, 1999), and it’s also how some of the most powerful
muscle-building hormones used by athletes operate (e.g., testosterone, growth
hormone, insulin-like growth factor-1).
The amount of fat the ‘typical’ human burns each
day is not that great.
Ezell et al. (1999) demonstrated this in a series
of experiments that examined fuel oxidation in obese, post-obese, and
never-obese females (all were pre-menopausal, sedentary, non-smokers and
between 20 and 45 y of age). They found that resting fat oxidation was not
different between groups, averaging 1.63, 2.38, and 1.99 g/60 min for
never-obese, obese, and post-obese, respectively. Even during exercise, the amount
of fat oxidized isn’t that great.
In the same study, the women performed 60 minutes
of stationary cycling at 60-65% VO2 peak. Fat oxidation was greater in the
post-exercise period, but again, was not different between groups: NO = 2.85
g/60 min; O = 4.19 g/60 min; PO = 3.72 g/60 min.
For resting conditions, using an average of 2.0 g of fat oxidized per hour,
this amounts to 48 grams of fat burned in a 24-hour period. If your goal is to
achieve fat balance for the day (i.e., no gain of body fat), this leaves little
room for ‘cheating’.
Note that the women in the Ezell et al. study were
consuming maintenance diets broken down as 55% carbohydrate, 30% fat, 15%
protein. Coupled with your daily workouts at the gym, reducing your
carbohydrate intake to, e.g., 40% may allow you to burn somewhat more fat each
day than these relatively sedentary people.
NOTE: If you really want to take your dieting expertise to the next level, please read "MACRONUTRIENT BALANCE" in Edition #1 of The ROB Report.
"MACRONUTRIENT BALANCE" is a 23-page journey into calorie balance, and what it truly means --or can mean-- to be 'eating more calories than you are burning up'.
This is a MUST-READ article if you truly want to master the art of eating for the purpose of building a lean, muscular body.
REFERENCES CITED
Acheson KJ, Flatt PJ, Jequier E
(1982). Glycogen synthesis versus lipogenesis after a 500 gram carbohydrate
meal in man. Metabolism, 31: 1234-1240.
Baron AD, Brechtel G, Wallace P, Edelman SV (1988). Rates and tissue sites of
non-insulin- and insulin-mediated glucose uptake in human. Am J Physiol, 255:
E769-E774.
Boirie Y, Dangin M, Gachon P,
Vasson M-P, Maoubois J-L, Beaufrere B (1997). Slow and fast dietary proteins
differently modulate postprandial protein accretion. Proc Natl Acad Sci USA,
94: 14930-14935.
Bonnadonna RC, Groop LC, Zych
K, Shank M, DeFronzo RA (1990). Dose-dependent effects of insulin on plasma
free fatty acid turnover and oxidation in humans. Am J Physiol, 259: E736-E750.
Brosnan JT (1999). Comments on
metabolic needs for glucose and the role of gluconeogenesis. Eur J Clin Nutr,
53: S107
Cahill GF Jr (1971). Physiology
of insulin in man. Diabetes, 20: 785-799.
Chiasson JL, Liljenquist JE,
Finger FE et al. (1976). Differential sensitivity of glycogenolysis and
gluconeogenesis to insulin infusions in dogs. Diabetes, 25: 283.
Ezell DM, Geiselman PJ,
Anderson AM, Dowdy ML, Womble LG, Greenway FL, Zachwieja JJ (1999). Substrate
oxidation and availability during acute exercise in non-obese, obese, and
post-obese females. Int J Obes, 23: 1047-1056.
Felig P, Bergman M (1995). Fuel
Metabolism. The endocrine pancreas: diabetes mellitus. In: Felig P, Baxter JD
and Frohman LA, ed. Endocrinology and metabolism, 3rd edition. McGraw-Hill,
Inc., New York, NY.
Flatt JP, Ravussin E, Acheson
KJ, Jequier E (1985). Effects of dietary fat on post-prandial substrate
oxidation and on carbohydrate and fat balances. J Clin Invest, 76: 1019-1024.
Fereday A, Gibson NR, Cox M,
Pacy PJ, Millward DJ (1998). Variation in the apparent sensitivity of the
insulin mediated inhibition of proteolysis to amino acid supply determines the
efficiency of protein utilization. Clin Sci, 95: 725.
Flatt JP (1987). The difference
in the storage capacities for carbohydrate and for fat, and its implications in
the regulation of body weight. Ann NY Acad Sci, 499: 104-123.
Forslund AH, El-Khoury AE,
Olsson RM, Sjodin AM, Hambraeus L, Young VR (1999). Effect of protein intake
and physical activity on 24-h pattern and rate of macronutrient utilization. Am
J Physiol, 276: E964.
Garlick PJ, McNurlan MA, Patlak
CS (1999). Adaptation of protein metabolism in relation to limits to high
dietary protein intake. Eur J Clin Nutr, 53: S34.
Jenkins DJA, Wolever TMS,
Taylor RH, Barker H, Fielden H, Baldwin JM, Bowling AC, Newman HC, Jenkins AL,
Goff DV (1981). Glycemic index of foods: A physiological basis for carbohydrate
exchange. Am J Clin Nutr, 34: 362-366.
Jensen MD, Caruso M, Heiling V,
Miles JM (1989). Insulin regulation of lipolysis in non-diabetic and IDDM
subjects. Diabetes, 1595-1601.
Jungas RL, Halperin ML, Brosnan
JT (1992). Quantitative analysis of amino acid oxidation and related
gluconeogenesis in humans. Physiol Rev, 72: 419-470.
Hellerstein MK, Schwarz JM,
Neese RA (1996). Regulation of hepatic de novo lipogenesis in humans. Annu Rev
Nutr, 16:523-557.
Hellerstein MK (2001). No
common energy currency: De novo lipogenesis as the road less traveled. Am J
Clin Nutr, 74: 737.
Hussain MA, Schmitz O, Froesch
ER (1995). Growth hormone, insulin, and insulin-like growth factor I:
Revisiting the Food and Famine Theory. News Physiol Sci, 10: 81-86.
Lemon PW (1998). Effects of
exercise on dietary protein requirements. Int J Sport Nutr, 8: 426.
Melville S, McNurlan MA,
McHardy KC, Broom J, Milne E, Calder AG, Garlick PJ (1989). The role of
degradation in the acute control of protein balance in adult man: Failure of
feeding to stimulate protein synthesis as assessed by L-[1-13C]leucine
infusion. Metabolism, 38: 248-255.
Morand C, Remesy C, Demigne C
(1993). Fatty acids are potent modulators of lactate utilization in isolated
hepatocytes from fed rats. Am J Physiol, 264: E816-E823.
Owen OE, Smalley KJ, D’Alessio
DA, Mozzoli MA, Dawson EK (1998). Protein, fat and carbohydrate requirements
during starvation: anaplerosis and cataplerosis. Am J Clin Nutr, 68: 12-34.
Price GM, Halliday D, Pacy PJ,
Quevedo RM, Millward DJ (1994). Nitrogen homeostasis in man: 1. Influence of
protein intake on the amplitude of diurnal cycling of body nitrogen. Clin Sci,
86: 91-102.
Reeds PJ, Fiorotto ML, Davis TA
(1992). Nutrition partitioning. An overview. In: Bray GA, Ryan DH, eds. The
Science of Food Regulation. Volume 2. Baton Rouge: Louisiana State University.
p. 103-120.
Shigemitsu K, Tsjuishita Y,
Miyake H, Hidayat S, Tanaka N, Hara K, Yonezawa K (1999). Structural
requirement of leucine for activation of p70 S6 kinase. FEBS Lett, 447: 303.
Strack AM, Sebastian RJ,
Schwartz MW, Dallman MF (1995). Glucocorticoids and insulin: reciprocal signals
for energy balance. Am J Physiol, 268: R142-R149.
Swislocki ALM, Chen Y-DI, Golay
A, Chang M-O, Reaven GM (1987). Insulin suppression of plasma free fatty acid
concentration in normal individuals and patients with type II
(non-insulin-dependent) diabetes. Diabetologia, 30: 622-626.
Taylor R, Price TB, Katz LD,
Shulman RG, Shulman GI (1993). Direct measurement of change in muscle glycogen
concentration after a mixed meal in normal subjects. Am J Physiol, 265: E224-E229.
Vahouny GV, Hodges VA,
Treadwell CR (1979). Essential fatty acid deficiency and adrenal cortical
function in vitro. J Lipid Res, 20: 154.
Wang H, Walker SW, Mason JI et
al. (2000). Role of arachidonic acid metabolism in ACTH-stimulated cortisol
secretion by bovine adrenocortical cells. Endocr Res, 26: 705.
Wang X, Stocco DM (1999).
Cyclic AMP and arachidonic acid: a tale of two pathways. Mol Cell Endocrinol,
158: 7.
Wolfe RR (1998). Metabolic
interactions between glucose and fatty acids in humans. Am J Clin Nutr, 67:
519S-526S.