Re: Carbohydrate restriction regulates the adaptive response to fasting

[Guest guest]

drsusanforshey wrote:

> Hmmm....

>

> " These results demonstrate that restriction of dietary carbohydrate,

> not the general absence of energy intake itself, is responsible for

> initiating the metabolic response to short-term fasting. "

>

> I don't know what to make of this but sounds interesting

>

> Can we get full text?

>

>

>

>

> Am J Physiol. 1992 May;262(5 Pt 1):E631-6.

>

> Carbohydrate restriction regulates the adaptive response to fasting.

>

> Klein S, Wolfe RR.

>

> Department of Internal Medicine, University of Texas Medical

> Branch, Galveston.

>

>

>

I don't know that this is very surprising. Carbohydrate restriction

forces our body into a ketogenic energy cycle (fat conversion to a sugar

equivalent to keep brain et al happy). Adkins and others have exploited

this energy pathway for quick water loss (from glycogen reduction) and

other apparent short term benefits. To begin fasting while the body is

already burning primarily fat would be a fairly modest shift to where it

gets that fat from than a major " source of energy " transition. Just

because we stop eating, doesn't mean the body doesn't still need and get

it's fuel.

I suspect this shift to fat only energy metabolism is the source of much

discomfort for first time fasters, especially if their body hasn't

experienced a low carbohydrate state previously. There have been

suggestions that our brains run better on ketones than sugar and some

research has suggested that as beneficial for epilepsy sufferers. IMO

pretty interesting stuff...

JR

[Guest guest]

drsusanforshey wrote:

> Hmmm....

>

> " These results demonstrate that restriction of dietary carbohydrate,

> not the general absence of energy intake itself, is responsible for

> initiating the metabolic response to short-term fasting. "

>

> I don't know what to make of this but sounds interesting

>

> Can we get full text?

>

>

>

>

> Am J Physiol. 1992 May;262(5 Pt 1):E631-6.

>

> Carbohydrate restriction regulates the adaptive response to fasting.

>

> Klein S, Wolfe RR.

>

> Department of Internal Medicine, University of Texas Medical

> Branch, Galveston.

>

>

>

I don't know that this is very surprising. Carbohydrate restriction

forces our body into a ketogenic energy cycle (fat conversion to a sugar

equivalent to keep brain et al happy). Adkins and others have exploited

this energy pathway for quick water loss (from glycogen reduction) and

other apparent short term benefits. To begin fasting while the body is

already burning primarily fat would be a fairly modest shift to where it

gets that fat from than a major " source of energy " transition. Just

because we stop eating, doesn't mean the body doesn't still need and get

it's fuel.

I suspect this shift to fat only energy metabolism is the source of much

discomfort for first time fasters, especially if their body hasn't

experienced a low carbohydrate state previously. There have been

suggestions that our brains run better on ketones than sugar and some

research has suggested that as beneficial for epilepsy sufferers. IMO

pretty interesting stuff...

JR

[Guest guest]

It's a surprise to me. I eat a very high carb (leafy greens, crucifers

etc), and very very low FAT diet. Fasting has documented physiologic

benefits and if restricting carbs mimics the effects of a fasting

state perhaps this outweighs any purported " antioxidant " benefits from

huge consumption of plants. Seems to me that this suggests perhaps

Caloric restriction with ADEQUATE nutrition (and low carbs) trumps

Caloric Restriction with SUPRA nutrition. (or am i reading too much

into this?)

Is it best to CRAN with restricted carbs, OR CRSN consuming mainly

leafy greens, crucifers etc??? IOW, what % of various macro's is CRON,

as it may be known at this time?

> > Hmmm....

> >

> > " These results demonstrate that restriction of dietary carbohydrate,

> > not the general absence of energy intake itself, is responsible for

> > initiating the metabolic response to short-term fasting. "

> >

> > I don't know what to make of this but sounds interesting

> >

> > Can we get full text?

> >

> >

> >

> >

> > Am J Physiol. 1992 May;262(5 Pt 1):E631-6.

> >

> > Carbohydrate restriction regulates the adaptive response to

fasting.

> >

> > Klein S, Wolfe RR.

> >

> > Department of Internal Medicine, University of Texas Medical

> > Branch, Galveston.

> >

> >

> >

>

> I don't know that this is very surprising. Carbohydrate restriction

> forces our body into a ketogenic energy cycle (fat conversion to a

sugar

> equivalent to keep brain et al happy). Adkins and others have exploited

> this energy pathway for quick water loss (from glycogen reduction) and

> other apparent short term benefits. To begin fasting while the body is

> already burning primarily fat would be a fairly modest shift to

where it

> gets that fat from than a major " source of energy " transition. Just

> because we stop eating, doesn't mean the body doesn't still need and

get

> it's fuel.

>

> I suspect this shift to fat only energy metabolism is the source of

much

> discomfort for first time fasters, especially if their body hasn't

> experienced a low carbohydrate state previously. There have been

> suggestions that our brains run better on ketones than sugar and some

> research has suggested that as beneficial for epilepsy sufferers. IMO

> pretty interesting stuff...

>

> JR

>

[Guest guest]

It's a surprise to me. I eat a very high carb (leafy greens, crucifers

etc), and very very low FAT diet. Fasting has documented physiologic

benefits and if restricting carbs mimics the effects of a fasting

state perhaps this outweighs any purported " antioxidant " benefits from

huge consumption of plants. Seems to me that this suggests perhaps

Caloric restriction with ADEQUATE nutrition (and low carbs) trumps

Caloric Restriction with SUPRA nutrition. (or am i reading too much

into this?)

Is it best to CRAN with restricted carbs, OR CRSN consuming mainly

leafy greens, crucifers etc??? IOW, what % of various macro's is CRON,

as it may be known at this time?

> > Hmmm....

> >

> > " These results demonstrate that restriction of dietary carbohydrate,

> > not the general absence of energy intake itself, is responsible for

> > initiating the metabolic response to short-term fasting. "

> >

> > I don't know what to make of this but sounds interesting

> >

> > Can we get full text?

> >

> >

> >

> >

> > Am J Physiol. 1992 May;262(5 Pt 1):E631-6.

> >

> > Carbohydrate restriction regulates the adaptive response to

fasting.

> >

> > Klein S, Wolfe RR.

> >

> > Department of Internal Medicine, University of Texas Medical

> > Branch, Galveston.

> >

> >

> >

>

> I don't know that this is very surprising. Carbohydrate restriction

> forces our body into a ketogenic energy cycle (fat conversion to a

sugar

> equivalent to keep brain et al happy). Adkins and others have exploited

> this energy pathway for quick water loss (from glycogen reduction) and

> other apparent short term benefits. To begin fasting while the body is

> already burning primarily fat would be a fairly modest shift to

where it

> gets that fat from than a major " source of energy " transition. Just

> because we stop eating, doesn't mean the body doesn't still need and

get

> it's fuel.

>

> I suspect this shift to fat only energy metabolism is the source of

much

> discomfort for first time fasters, especially if their body hasn't

> experienced a low carbohydrate state previously. There have been

> suggestions that our brains run better on ketones than sugar and some

> research has suggested that as beneficial for epilepsy sufferers. IMO

> pretty interesting stuff...

>

> JR

>

[Guest guest]

Hi Al:

One wonders whether the results might have been different if the

lipids had been ingested rather than injected?

Rodney.

--- In , Al Pater <old542000@y...>

wrote:

>

> Hi All,

>

> See the pdf-available paper below that suggests that it is the

carbohydrate levels,

> not calories in general, that matter in fasting effects.

>

> Klein S, Wolfe RR.

> Carbohydrate restriction regulates the adaptive response to fasting.

> Am J Physiol. 1992 May;262(5 Pt 1):E631-6.

> PMID: 1590373

>

> The importance of either carbohydrate or energy restriction in

initiating the

> metabolic response to fasting was studied in five normal

volunteers. The subjects

> participated in two study protocols in a randomized crossover

fashion. In one study

> the subjects fasted for 84 h (control study), and in the other a

lipid emulsion was

> infused daily to meet resting energy requirements during the 84-h

oral fast (lipid

> study). Glycerol and palmitic acid rates of appearance in plasma

were determined by

> infusing [2H5]glycerol and [1-13C]palmitic acid, respectively,

after 12 and 84 h of

> oral fasting. Changes in plasma glucose, free fatty acids, ketone

bodies, insulin,

> and epinephrine concentrations during fasting were the same in both

the control and

> lipid studies. Glycerol and palmitic acid rates of appearance

increased by 1.63 +/-

> 0.42 and 1.41 +/- 0.46 mumol.kg-1.min-1, respectively, during

fasting in the control

> study and by 1.35 +/- 0.41 and 1.43 +/- 0.44 mumol.kg-1.min-1,

respectively, in the

> lipid study. These results demonstrate that restriction of dietary

carbohydrate, not

> the general absence of energy intake itself, is responsible for

initiating the

> metabolic response to short-term fasting.

>

> ... Each subject served as his own control and com-

> pleted two study protocols separated by a 3-wk interval in a

> randomized crossover fashion. In one study the subjects fasted

> for 84 h, whereas, in the other, lipid calories were given intra-

> venously during " fasting " to meet resting energy requirements.

> All subjects were admitted to the CRC at The University of

> Texas Medical Branch and were given a standard meal in the

> afternoon and evening. After an overnight (12-h) fast

>

> ... After the infusion study was completed, the subjects random-

> ized to complete fasting continued to fast for another 72 h (84 h

> total), being given only water, vitamins, potassium chloride (40

> meq/day), and sodium chloride (8 g/day) orally. At 84 h of

> fasting, the infusion protocol and indirect calorimetry measure-

> ments performed after 12 h of fasting were repeated. The sub-

> jects randomized to receive lipid calories during fasting were

> given a commercial lipid emulsion (Intralipid 20%, Clintec

> Nutrition, Deerfield, IL) intravenously during the fasting period

> and also received water, vitamins, and electrolytes orally. The

> lipid emulsion contained lipid calories in the form of soybean oil

> at a concentration of 20 g/dl, phospholipids (1.2 g/dl), and small

> amounts of glycerol (2.25 g/dl). Intralipid was infused for 15 h

> each day to simulate normal cycles of daytime feeding and

> nighttime fasting. On the first day of fasting, Intralipid was

> infused after the first isotope infusion study was completed

> from 1100 to 0200 h. Plasma triglyceride concentration was

> measured 5 h after starting the lipid infusion to ensure adequate

> clearance. Intralipid was infused from 0600 to 2100 h during

> each subsequent day of fasting. The rate at which the lipid

> emulsion was infused was calculated to meet the measured

> RMR. After 84 h of fasting with daily lipid infusions (12 h after

> completing the final day's lipid infusion), the isotope infusion

> protocol and indirect calorimetry measurements performed

> after 12 h of fasting were repeated.

> ... After completion of the first fasting study, all subjects con-

> sumed a weight-maintaining free-choice diet for 3 wk as

> outpatients. The subjects were then readmitted to the CRC

> where they completed the second fasting (either with or without

> concomitant lipid infusion) study.

>

> ... RESULTS

>

> Data on energy, protein, and fluid balance during fast-

> ing are shown in Table 1. Infusion of the lipid emulsion

> during fasting provided 5% more calories daily than the

> measured resting energy requirements but provided only

> 19±2 g of carbohydrate calories as glycerol per day.

> Weight loss, measured between 12 and 84 h of fasting, was

> 0.78±0.16 kg greater (P = 0.008) during the control

> study than during the lipid study. Nitrogen excretion

> during fasting was the same in both studies. Fluid balance

> was more negative during the control study than during

> the lipid study because of the administration of intrave-

> nous fluids during the lipid study, but the differences in

> fluid balance were not statistically significant.

>

> Table 1. Metabolic factors during 12 and 84 h of fasting

> ============

> Control study Lipid study

> ============

> Weight loss, kg 2.64±0.13 1.86±0.22*

> Measured resting metabolic rate, kcal/kg/day-l 22±l 22±l

> Lipid emulsion infused, kcal/kg/day-l 0 23±l

> Glycerol infused, g/day 0 19±2

> Urinary nitrogen excretion, g/72 h 23.9±3 26.1±3

> Fluid balance, ml/72 h -2,761±470 -2,194±133

> ================

> Values are means ± SE.

> Fluid balance was fluid intake minus fluid output in urine and

estimated insensible

> loss of 800 ml/day.

> Significantly different from control value, * P = 0.008.

>

> The plasma substrate and hormone concentrations

> after 12 and 84 h of fasting are shown in Table 2.

> As expected, plasma glucose and insulin decreased, whereas

> total free fatty acids, ketone bodies, and epinephrine

> increased after fasting in the control study. Changes in

> substrates and hormones were the same in the lipid study

> as those during the control study despite the daily infu-

> sion of lipid calories. There was no significant change in

> plasma norepinephrine after fasting in either the control

> or lipid studies. Lipid infusion on the first day of fasting

> caused a fourfold increase in plasma triglyceride

> concentration. Plasma triglycerides increased from 68±26

> mg/dl in the basal state to 278±58 mg/dl at 5 h of

> lipid infusion. Basal triglycerides did not change after 84

> h of fasting in the control study but increased by -60%

> after 84 h of fasting (12 h after stopping the infusion of

> Intralipid) in the lipid study. The difference in triglycer-

> ide levels in the lipid study, however, were not statisti-

> cally significant because of the small sample size and the

> variability in the data.

>

> Table 2. Plasma substrate and hormone concentration

> =================

> Control study Lipid study

> 12-h fast 84-h fast 12-h fast 84-h fast

> =================

> Glucose, mg/dl 92±2 68±2* 86±2 66±3*

> Free fatty acid, µM 376±92 917±61* 487±66 1,023±80*

> Triglyceride, mg/d1 57±lO 61±8 68±26 109±33

> Acetoacetate, µM 72±8 1,060±213* 74±ll 980±80*

> ß-Hydroxybutyrate, µM 84±20 2,560±370* 108±50 2,540±440*

> Insulin, µU/ml 7.5±O.7 2.720.2±6.7k0.7 68+12t 3.2±O.l*

> Epinephrine, pg/ml 39±8 68±26† 42±9 70±15†

> Norepinephrine, ng/ml 142±21 194±45 179±15 163±25

> =================

> Values are means ± SE.

> For lipid study, 84-h fast was 12 h after stopping lipid emulsion

infusion.

> Significantly different from corresponding 12-h value, *P < 0.001,

†P < 0.01.

>

> Lipolytic rates and the absolute increase in the Ra of

> glycerol and palmitic acid during fasting were similar in

> both the control and lipid studies (Fig. 1). Glycerol Ra

> increased by 1.63±0.42 µmol/kg/min (from 1.94±

> 0.30 to 3.57±0.21 µmol/kg/min after 12 and 84 h of

> total fasting, respectively) in the control study (P <

> 0.001) and by 1.35±0.41 µmol/kg/min (from 2.28±

> 0.12 to 3.63±0.41 µmol/kg/min after 12 and 84 h of

> fasting plus daily lipid infusions, respectively) in the lipid

> study (P <0.001). Palmitic acid Ra increased by 1.41±0.46

> µmol/kg/min (from 1.50±0.35 to 2.91±0.23 µmol/kg/min

> after 12 and 84 h of total fasting,

> respectively) in the control study (P < 0.001) and by 1.43

> ±0.44 µmol/kg/min (from 1.57±0.23 to 3.01±0.32 -

> µmol/kg/min after 12 and 84 h of fasting plus daily

> lipid infusions, respectively) in the lipid study (P <

> 0.001).

> Triglyceride oxidation increased during fasting in both

> the control and lipid studies (P < 0.001; Fig. 1). Daily

> lipid infusion did not affect the rate of triglyceride oxi-

> dation, and the values at 12 and 84 h of fasting were

> similar in both studies. The rates of triglyceride oxidation

> in the control and lipid studies were 1.07±0.09 and 1.13

> ±0.17 µmol/kg/min, respectively, after 12 h of fast-

> ing and 1.77±0.10 and 1.67±0.08 µmol/kg/min,

> respectively, after 84 h of fasting. The percentage of

> released fatty acids that were oxidized for fuel was also

> the same in both studies and remained constant during

> fasting. Approximately 50% of mobilized triglycerides

> were oxidized after both 12 and 84 h of fasting.

> The rate of total triglyceride recycling was similar in

> both the control and lipid studies (Fig. 1). Total triglyc-

> eride recycling increased from 0.87±0.31 to 1.80±0.23

> µmol/kg/min after 12 and 84 h of fasting, respec-

> tively, in the control study (P < 0.01) and from 1.15±0.15

> to 1.96±0.37 µmol/kg/min, respectively, in the

> lipid study (P < 0.01). The rate of intracellular adipocyte

> triglyceride recycling was similar in both studies because

> the relationship between palmitic acid Ra and glycerol Ra,

> an index of intracellular recycling, was similar. The esti-

> mated energy cost of total triglyceride recycling was min-

> imal and accounted for - 1 and -2% of the daily RMR

> after 12 and 84 h of fasting, respectively. ...

>

> Al Pater, PhD; email: old542000@y...

>

>

>

>

> __________________________________

> - PC Magazine Editors' Choice 2005

> http://mail.

>

[Guest guest]

Hi Al:

One wonders whether the results might have been different if the

lipids had been ingested rather than injected?

Rodney.

--- In , Al Pater <old542000@y...>

wrote:

>

> Hi All,

>

> See the pdf-available paper below that suggests that it is the

carbohydrate levels,

> not calories in general, that matter in fasting effects.

>

> Klein S, Wolfe RR.

> Carbohydrate restriction regulates the adaptive response to fasting.

> Am J Physiol. 1992 May;262(5 Pt 1):E631-6.

> PMID: 1590373

>

> The importance of either carbohydrate or energy restriction in

initiating the

> metabolic response to fasting was studied in five normal

volunteers. The subjects

> participated in two study protocols in a randomized crossover

fashion. In one study

> the subjects fasted for 84 h (control study), and in the other a

lipid emulsion was

> infused daily to meet resting energy requirements during the 84-h

oral fast (lipid

> study). Glycerol and palmitic acid rates of appearance in plasma

were determined by

> infusing [2H5]glycerol and [1-13C]palmitic acid, respectively,

after 12 and 84 h of

> oral fasting. Changes in plasma glucose, free fatty acids, ketone

bodies, insulin,

> and epinephrine concentrations during fasting were the same in both

the control and

> lipid studies. Glycerol and palmitic acid rates of appearance

increased by 1.63 +/-

> 0.42 and 1.41 +/- 0.46 mumol.kg-1.min-1, respectively, during

fasting in the control

> study and by 1.35 +/- 0.41 and 1.43 +/- 0.44 mumol.kg-1.min-1,

respectively, in the

> lipid study. These results demonstrate that restriction of dietary

carbohydrate, not

> the general absence of energy intake itself, is responsible for

initiating the

> metabolic response to short-term fasting.

>

> ... Each subject served as his own control and com-

> pleted two study protocols separated by a 3-wk interval in a

> randomized crossover fashion. In one study the subjects fasted

> for 84 h, whereas, in the other, lipid calories were given intra-

> venously during " fasting " to meet resting energy requirements.

> All subjects were admitted to the CRC at The University of

> Texas Medical Branch and were given a standard meal in the

> afternoon and evening. After an overnight (12-h) fast

>

> ... After the infusion study was completed, the subjects random-

> ized to complete fasting continued to fast for another 72 h (84 h

> total), being given only water, vitamins, potassium chloride (40

> meq/day), and sodium chloride (8 g/day) orally. At 84 h of

> fasting, the infusion protocol and indirect calorimetry measure-

> ments performed after 12 h of fasting were repeated. The sub-

> jects randomized to receive lipid calories during fasting were

> given a commercial lipid emulsion (Intralipid 20%, Clintec

> Nutrition, Deerfield, IL) intravenously during the fasting period

> and also received water, vitamins, and electrolytes orally. The

> lipid emulsion contained lipid calories in the form of soybean oil

> at a concentration of 20 g/dl, phospholipids (1.2 g/dl), and small

> amounts of glycerol (2.25 g/dl). Intralipid was infused for 15 h

> each day to simulate normal cycles of daytime feeding and

> nighttime fasting. On the first day of fasting, Intralipid was

> infused after the first isotope infusion study was completed

> from 1100 to 0200 h. Plasma triglyceride concentration was

> measured 5 h after starting the lipid infusion to ensure adequate

> clearance. Intralipid was infused from 0600 to 2100 h during

> each subsequent day of fasting. The rate at which the lipid

> emulsion was infused was calculated to meet the measured

> RMR. After 84 h of fasting with daily lipid infusions (12 h after

> completing the final day's lipid infusion), the isotope infusion

> protocol and indirect calorimetry measurements performed

> after 12 h of fasting were repeated.

> ... After completion of the first fasting study, all subjects con-

> sumed a weight-maintaining free-choice diet for 3 wk as

> outpatients. The subjects were then readmitted to the CRC

> where they completed the second fasting (either with or without

> concomitant lipid infusion) study.

>

> ... RESULTS

>

> Data on energy, protein, and fluid balance during fast-

> ing are shown in Table 1. Infusion of the lipid emulsion

> during fasting provided 5% more calories daily than the

> measured resting energy requirements but provided only

> 19±2 g of carbohydrate calories as glycerol per day.

> Weight loss, measured between 12 and 84 h of fasting, was

> 0.78±0.16 kg greater (P = 0.008) during the control

> study than during the lipid study. Nitrogen excretion

> during fasting was the same in both studies. Fluid balance

> was more negative during the control study than during

> the lipid study because of the administration of intrave-

> nous fluids during the lipid study, but the differences in

> fluid balance were not statistically significant.

>

> Table 1. Metabolic factors during 12 and 84 h of fasting

> ============

> Control study Lipid study

> ============

> Weight loss, kg 2.64±0.13 1.86±0.22*

> Measured resting metabolic rate, kcal/kg/day-l 22±l 22±l

> Lipid emulsion infused, kcal/kg/day-l 0 23±l

> Glycerol infused, g/day 0 19±2

> Urinary nitrogen excretion, g/72 h 23.9±3 26.1±3

> Fluid balance, ml/72 h -2,761±470 -2,194±133

> ================

> Values are means ± SE.

> Fluid balance was fluid intake minus fluid output in urine and

estimated insensible

> loss of 800 ml/day.

> Significantly different from control value, * P = 0.008.

>

> The plasma substrate and hormone concentrations

> after 12 and 84 h of fasting are shown in Table 2.

> As expected, plasma glucose and insulin decreased, whereas

> total free fatty acids, ketone bodies, and epinephrine

> increased after fasting in the control study. Changes in

> substrates and hormones were the same in the lipid study

> as those during the control study despite the daily infu-

> sion of lipid calories. There was no significant change in

> plasma norepinephrine after fasting in either the control

> or lipid studies. Lipid infusion on the first day of fasting

> caused a fourfold increase in plasma triglyceride

> concentration. Plasma triglycerides increased from 68±26

> mg/dl in the basal state to 278±58 mg/dl at 5 h of

> lipid infusion. Basal triglycerides did not change after 84

> h of fasting in the control study but increased by -60%

> after 84 h of fasting (12 h after stopping the infusion of

> Intralipid) in the lipid study. The difference in triglycer-

> ide levels in the lipid study, however, were not statisti-

> cally significant because of the small sample size and the

> variability in the data.

>

> Table 2. Plasma substrate and hormone concentration

> =================

> Control study Lipid study

> 12-h fast 84-h fast 12-h fast 84-h fast

> =================

> Glucose, mg/dl 92±2 68±2* 86±2 66±3*

> Free fatty acid, µM 376±92 917±61* 487±66 1,023±80*

> Triglyceride, mg/d1 57±lO 61±8 68±26 109±33

> Acetoacetate, µM 72±8 1,060±213* 74±ll 980±80*

> ß-Hydroxybutyrate, µM 84±20 2,560±370* 108±50 2,540±440*

> Insulin, µU/ml 7.5±O.7 2.720.2±6.7k0.7 68+12t 3.2±O.l*

> Epinephrine, pg/ml 39±8 68±26† 42±9 70±15†

> Norepinephrine, ng/ml 142±21 194±45 179±15 163±25

> =================

> Values are means ± SE.

> For lipid study, 84-h fast was 12 h after stopping lipid emulsion

infusion.

> Significantly different from corresponding 12-h value, *P < 0.001,

†P < 0.01.

>

> Lipolytic rates and the absolute increase in the Ra of

> glycerol and palmitic acid during fasting were similar in

> both the control and lipid studies (Fig. 1). Glycerol Ra

> increased by 1.63±0.42 µmol/kg/min (from 1.94±

> 0.30 to 3.57±0.21 µmol/kg/min after 12 and 84 h of

> total fasting, respectively) in the control study (P <

> 0.001) and by 1.35±0.41 µmol/kg/min (from 2.28±

> 0.12 to 3.63±0.41 µmol/kg/min after 12 and 84 h of

> fasting plus daily lipid infusions, respectively) in the lipid

> study (P <0.001). Palmitic acid Ra increased by 1.41±0.46

> µmol/kg/min (from 1.50±0.35 to 2.91±0.23 µmol/kg/min

> after 12 and 84 h of total fasting,

> respectively) in the control study (P < 0.001) and by 1.43

> ±0.44 µmol/kg/min (from 1.57±0.23 to 3.01±0.32 -

> µmol/kg/min after 12 and 84 h of fasting plus daily

> lipid infusions, respectively) in the lipid study (P <

> 0.001).

> Triglyceride oxidation increased during fasting in both

> the control and lipid studies (P < 0.001; Fig. 1). Daily

> lipid infusion did not affect the rate of triglyceride oxi-

> dation, and the values at 12 and 84 h of fasting were

> similar in both studies. The rates of triglyceride oxidation

> in the control and lipid studies were 1.07±0.09 and 1.13

> ±0.17 µmol/kg/min, respectively, after 12 h of fast-

> ing and 1.77±0.10 and 1.67±0.08 µmol/kg/min,

> respectively, after 84 h of fasting. The percentage of

> released fatty acids that were oxidized for fuel was also

> the same in both studies and remained constant during

> fasting. Approximately 50% of mobilized triglycerides

> were oxidized after both 12 and 84 h of fasting.

> The rate of total triglyceride recycling was similar in

> both the control and lipid studies (Fig. 1). Total triglyc-

> eride recycling increased from 0.87±0.31 to 1.80±0.23

> µmol/kg/min after 12 and 84 h of fasting, respec-

> tively, in the control study (P < 0.01) and from 1.15±0.15

> to 1.96±0.37 µmol/kg/min, respectively, in the

> lipid study (P < 0.01). The rate of intracellular adipocyte

> triglyceride recycling was similar in both studies because

> the relationship between palmitic acid Ra and glycerol Ra,

> an index of intracellular recycling, was similar. The esti-

> mated energy cost of total triglyceride recycling was min-

> imal and accounted for - 1 and -2% of the daily RMR

> after 12 and 84 h of fasting, respectively. ...

>

> Al Pater, PhD; email: old542000@y...

>

>

>

>

> __________________________________

> - PC Magazine Editors' Choice 2005

> http://mail.

>