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Originally Posted by bodybuilder45
the carbs and protein with minimal fat yielded pretty good results but i had to drop calorie intake lower than the fat + protein diet. im sure the reason deals with insulin output being so low leaving fat oxidation remotely higher. energy levels suffered with both but i feel the higher fat intake gave me a little bit of an edge over the higher carbs. even though i consumed less cals with the carb diet, i was able to retain more mass. in all fairness, i used dicana with the cut diet and this most likely increased catabolism but who knows?
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HSL is upregolate when insulin is low, leptin goes down and adiponectin goes up with epinephrine and norepinephrine, this bring to an optimal lypolisis and fats oxidation, ever in caloric deficit...
The proteins sparing effect on H-fat diet depend by the level of BHB (betaydrossybutirrate, ketone body) and norepinephrine, as we see during a fasting period..
Resting energy expenditure in short-term starvation is increased as
a result of an increase in serum norepinephrine1,2
Christian Zauner, Bruno Schneeweiss, Alexander Kranz, Christian Madl, Klaus Ratheiser, Ludwig Kramer, Erich Roth,
Barbara Schneider, and Kurt Lenz
ABSTRACT
Background: The effects of food restriction on energy metabolism
have been under investigation for more than a century. Data
obtained are conflicting and research has failed to provide conclusive
results.
Objective: The objective of this study was to test the hypothesis
that in lean subjects under normal living conditions, shortterm
starvation leads to an increase in serum concentrations of
catecholamines and thus to an increase in resting energy
expenditure.
Design: Resting energy expenditure, measured by indirect
calorimetry, and hormone and substrate concentrations were
measured in 11 healthy, lean subjects on days 1, 2, 3, and 4 of an
84-h starvation period.
Results: Resting energy expenditure increased significantly
from 3.97 ± 0.9 kJ/min on day 1 to 4.53 ± 0.9 kJ/min on day 3
(P < 0.05). The increase in resting energy expenditure was
associated with an increase in the norepinephrine concentration
from 1716. ± 574 pmol/L on day 1 to 3728 ± 1636 pmol/L
on day 4 (P < 0.05). Serum glucose decreased from 4.9 ± 0.5
to 3.5 ± 0.5 mmol/L (P < 0.05), whereas insulin did not change
significantly.
Conclusions: Resting energy expenditure increases in early starvation,
accompanied by an increase in plasma norepinephrine.
This increase in norepinephrine seems to be due to a decline in
serum glucose and may be the initial signal for metabolic changes
in early starvation. Am J Clin Nutr 2000;71:1511–5.
Elevation of Plasma Epinephrine Concentrations Inhibits Proteolysis
and Leucine Oxidation in Man via @i-Adrenergic Mechanisms
M. E. Kraenzlin, U. Keller, A. Keller, A. Thelin,* M. J. Arnaud, and W. Stauffacher
Department ofMedicine, University Hospital, CH-4031 Basel, Switzerland; and *Nestec SA, CH-1800 Vevey, Switzerland
Abstract
The role of elevated plasma epinephrine concentrations in the
regulation of plasma leucine kinetics and the contribution of
,8-receptors were assessed in man. Epinephrine (50 ng/kg per
min) was infused either alone or combined with propranolol
(f,-blockade) into groups of six subjects fasted overnight; leucine
flux, oxidation, and net plasma leucine forearm balance
were determined during 180 min. Constant plasma insulin and
glucagon concentrations were maintained in all studies by infusing
somatostatin combined with insulin and glucagon replacements.
Plasma leucine concentrations decreased from
baseline during epinephrine infusion by 27±5 gmol/liter (P
< 0.02) due to a 22±6% decrease in leucine flux (P < 0.05 vs.
controls receiving saline) and to an increase in the metabolic
clearance rate of leucine (P < 0.02). Leucine oxidation decreased
by 36±8% (P < 0.01 vs. controls). fl-Blockade abolished
the effect of epinephrine on leucine flux and oxidation.
Net forearm release of leucine increased during epinephrine (P
< 0.01), suggesting increased muscle proteolysis; the fall of
total body leucine flux was therefore due to diminished proteolysis
in nonmuscle tissues, such as splanchnic organs. Nonoxidative
leucine disappearance as a parameter of protein synthesis
was not significantly influenced by epinephrine. Plasma
glucose and FFA concentrations increased via f,-adrenergic
mechanisms (P < 0.001). The results suggest that elevation of
plasma epinephrine concentrations similar to those observed in
severe stress results in redistribution of body proteins and
exerts a whole body protein-sparing effect; this may counteract
catabolic effects of other hormones during severe stress.
Effect of ,0-Hydroxybutyrate on Whole-Body Leucine Kinetics and Fractional
Mixed Skeletal Muscle Protein Synthesis in Humans
K. Sreekumaran Nair, Stephen L. Welle, David Halliday,* and Robert G. Campbell
Department ofMedicine, University ofRochester School ofMedicine and Dentistry, Rochester NY 14603;
and the *Nutrition Group, Clinical Research Centre, Harrow HA] 3UJ, United Kingdom
Abstract
Because intravenous infusion of 0-hydroxybutyrate (8-OHB)
has been reported to decrease urinary nitrogen excretion, we
investigated in vivo metabolism of leucine, an essential amino
acid, using L-11-'3Cjleucine as a tracer during t9-OHB infusion.
Leucine flux during ,B-OHB infusion did not differ from leucine
flux during normal saline infusion in nine normal subjects,
whereas leucine oxidation decreased 1841% (mean = 30%)
from 18.1±1.1 pmol * kg-' * h-1 (P < 0.01), and incorporation
of leucine into skeletal muscle protein increased 5-17% (mean
= 10%) from 0.048 + 0.003%/h (P < 0.02). Since blood pH
during jt-OHB infusion was higher than the pH during saline
infusion, we performed separate experiments to study the effect
of increased blood pH on leucine kinetics by infusing sodium
bicarbonate intravenously. Blood pH during sodium bicarbonate
infusion was similar to that observed during the
,B-OHB infusion, but bicarbonate infusion had no effect on
leucine flux or leucine oxidation. We conclude that #-OHB
decreases leucine oxidation and promotes protein synthesis in
human beings.
Short-Term Alterations in Carbohydrate Energy Intake in Humans
Striking Effects on Hepatic Glucose Production, De Novo Lipogenesis, Lipolysis, and Whole-Body
Fuel Selection
Jean-Marc Schwarz,* Richard A. Neese,*" Scott Tumer,* Doris Dare,* and Marc K. Hellerstein**
*Department of Nutritional Sciences, University of California, Berkeley, California 94720-3104; and tDivision of Endocrinology and
Metabolism, Department of Medicine, San Francisco General Hospital, University of California, San Francisco, California 94110
Abstract
Short-term alterations in dietary carbohydrate (CHO) energy
are known to alter whole-body fuel selection in humans,
but the metabolic mechanisms remain unknown. We used
stable isotope-mass spectrometric methods with indirect calorimetry
in normal subjects to quantify the metabolic response
to six dietary phases (5 d each), ranging from 50%
surplus CHO (+50% CHO) to 50% deficient CHO (-50%
CHO), and 50% surplus fat (+50% fat). Fasting hepatic
glucose production (HGP) varied by > 40% from deficient
to surplus CHO diets (1.78+0.08 vs 2.43+0.09 mg/kg per
min, P < 0.01). Increased HGP on surplus CHO occurred
despite significantly higher serum insulin concentrations.
Lipolysis correlated inversely with CHO intake as did the
proportion of whole-body lipolytic flux oxidized. Fractional
de novo hepatic lipogenesis (DNL) increased more than 10-
fold on surplus CHO and was unmeasurable on deficient
CHO diets; thus, the preceding 5-d CHO intake could be
inferred from DNL. Nevertheless, absolute hepatic DNL accounted
for < 5 g fatty acids synthesized per day even on
+50% CHO. Whole-body CHO oxidation increased sixfold
and fat oxidation decreased > 90% on surplus CHO diets.
CHO oxidation was highly correlated with HGP (r2 = 0.60).
HGP could account for 85% of fasting CHO oxidation on
+25% CHO and 67% on +50% CHO diets. Some oxidation
of intracellular CHO stores was therefore also occurring.
+50% fat diet had no effects on HGP, DNL, or fuel selection.
We conclude that altered CHO intake alters HGP specifically
and in a dose-dependent manner, that HGP may
mediate the effects of CHO on whole-body fuel selection
both by providing substrate and by altering serum insulin
concentrations, that altered lipolysis and tissue oxidation
efficiency contribute to changes in fat oxidation, and that
surplus CHO is not substantially converted by the liver to
fat as it spares fat oxidation, but that fractional DNL may
nevertheless be a qualitative marker of recent CHO intake.
(J. Clin. Invest. 1995. 96:2735-2743.)
good find nonetheless
Linear Mode
