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Dietary

Keith N Frayn

sugars
and Susan large
other

and lipid metabolism


M Kingman amounts
animals,

in

,2

ABSTRACT
the diets of humans

When
and

of sugars
alterations

are included
in concentrations

in of
low-

context regarding We

of first

postprandial cardiovascular summarize

metabolism, risk. the results

an

area

of

active studies

interest conand desince

of plasma
tniacylglycerol density-lipoprotein lipoprotein sugars

lipid

constituents
concentrations cholesterol

may

be observed:
and and sometimes depression are not diet,

usually
elevation of seen although with

elevation
of high-densityamounts more infor-

of observational

cerning the then assess scnibed 1986.

effects of sugars on blood lipid concentrations developments in this field in the main areas concentrating on literature published

cholesterol. typical of those

These in the

effects Western

of

above,

mation which The


both erol

is needed on postprandial triacylglycerol may be affected more readily than fasting elevation
increased secretion to

concentrations, concentrations. appears


people

Downloaded from ajcn.nutrition.org by guest on November 22, 2012

of tniacylglycerol
hepatic and these in dependent impaired effects many or of

concentrations
clearance. dietary Some sugars people than with dependent,

to reflect
triacylglycare others. more Per-

SUGARS

AND

PLASMA

TRIACYLGLYCEROL

very-low-density-lipoprotein

CONCENTRATIONS The effects of sugars on fasting plasma centrations in humans must be considered the many other most important concentrations genetic tons. drate) triacylglycerol conwithin the context of

responsive haps either

are diabetes

surprisingly, insulin

studies

mellitus, seem to be

non-insulin

influences on triacylglycerol metabolism. The causes of raised fasting plasma tniacylglycenol are obesity and fasting short and renal diet ( plasma term. excessive failure
55%

protected about by

from large

alterations amounts

in plasma of dietary

lipid sugars.

concentrations
Am J

brought
Clin Nutr

alcohol are less of energy

consumption; common concentraactivity associated the many tniacyland weight facas canbohy-

abnormalities A high-carbohydrate may also raise particularly

l995;62(suppl):250S-63S.

tniacylglycenol Increased physical fats are Given and plasma in body

KEY WORDS metabolism, sucrose

Diabetes mellitus, plasma cholesterol,

fructose, plasma

glucose, lipid tniacylglycerol,

tions,

in the

and consumption with reductions factors glycerol that may

of n - 3 polyunsaturated in plasma tniacylglycerol. confound times, describing studies including of diet changes

concentrations,

INTRODUCTION The large crose, given with ular, also been reviewed Many 1960s position Sugars studies fructose findings content, mechanisms tose studies such 2505 or sucrose have diets and and elevation amounts of blood of dietary lipid sugars, for > of these concentrations particularly 30 y [early sugars has concentrations in response fructose and to su-

choice of sampling body of literature crose and fructose) contains conflicting diets diets. contrast, consumed plasma studies few have Food by the in this been and field carried Drug date from the the and out since Administration then several In particular, of sucrose or Some further especially fat sugars. effect although activity the enzyme within
Nuir

it is perhaps the effects

not surprising that the of dietary sugars (suconcentrations so when and test

on plasma tniacylglycerol findings. This is particularly


> 20%

has been recognized in (1)]. Consumption increased but been carried plasma changes observed. out extensively of the 1970s was and

references are been associated in partichave have been

have Such

contained from diets there in fructose,

of energy is more but of several

from than not that (7, high extent 15%,

sucrose is usual triacylglycerol

> 5%

of energy centrations

which (8-13)

in Western con15). fructose influence subIn (14, and

tniacylglycerol

appear cases is very amounts it is clear containing

to elevate little evidence

plasma

in plasma cholesterol concentrations Many studies in animals and humans to examine (2-7). relatively this effect, and these have

in some

in others sucrose diets 16-18). studies

typical concentrations from certain example, of sucrose abnormally

Western

tniacylglycenol that fructose diets

observational

Nevertheless, jects may,

in human lead

amounts the effect and

of sucrose to hypenseems energy) to that

summarized

under (8-13). For

circumstances, Reiser (2%, 44%

Task Force in 1986 (4). However, since in related areas have amplified these findings. emphasis has been placed on the role in the diet of people with diabetes mellitus. suggest that other components of the diet, play a part have addressed others in modulating not have been changes placed the effect clarified in hepatic the effect
Am

tniacylglycerolemia be dose increasing in a controlled dependent. proportions diet

To some

et al (9) showed 30% as carbohydrate

considerable

containing

of energy

of dietary

The some with

From

the Oxford

Lipid Oxford, requests

Metabolism UK. to KN

Group, Frayn,

Sheikh Oxford Infirmary,

Rashid Lipid Oxford

Laboratory, Metabolism OX2 6HE,

underlying

the triacylglycerol-raising in detail,

of fruc-

Radcliffe Infirmary, 2 Address reprint Group, UK. Printed Sheikh Rashid

Laboratory,

Radcliffe

general

J Clin

1995;62(suppl):250S-63S.

in USA.

1995

American

Society

for

Clinical

Nutrition

SUGARS

AND

LIPID

METABOLISM

25 1 S PLASMA CHOLESTEROL

resulted enol

in increasing demonstrated and 15% that

elevations in normal increasing

of fasting men. Similarly, amounts containing increases subjects. in female were is not the

plasma of

triacylglycet al (0%, tniacylfirst in the dietary of and fructose 43%

SUGARS Dietary

AND fructose

concentrations

Hallfnisch

( 1 1)
7.5%, glycerol study, second

of energy)

in a diet

of energy in the and

In addition trations, dietary energy has been low-density-lipoprotein subjects in which each change in which (=28% however, of dietary

to its effects fructose shown 29). was habitual cholesterol

on

plasma for to elevations cholesterol study

tniacylglycerol starch in plasma in healthy

concenof total and normal

as carbohydrate the effect

led to proportional was therefore, factors that (saturated carbohydrate diet may Subjects elderly coronary (18). be may not seen dose

in plasma subjects by sole

substituted to lead (LDL) Only one administered

at 7.5-20%

in hypeninsulinemic study normal subjects

However, unaffected

the

manipulation; response. Dietary fructose portion content between different glycenolemia. sugars established sulinemic also some in subjects trations various influences other Study tniacylglycerol ing the effects (45% glucose). on fasting the metabolic amounts (mainly diets different, integrated diets prandial later A studies on Most very Evidence supplement IV time this Both in the tenuation (10). important sucrose diet, of (23, the designs include

determinant of sucrose include (19-22),

(1 1, 26, fructose in plasma fructose of total the

in normal subjects (16), at 50-107 g/d (one-third of intake) indicated In another F1 - d decreased; in the intake (13). no study
1

subjects

carbohydrate concentrations.

influence

the effects

on plasma of total of the studies sensitivities

triacylglycerol

concentrations in the diet, some by the and use

the type the profiber with

of fat consumed

or polyunsaturated) In addition, explained

was administered energy), plasma attributed of the this high

at 2 g kg body total cholesterol to a reduction fructose consumption

the

dietary discrepancies

authors

of the

fat as a result

of subjects hypertriacylreadily (9), (9, and

to sucroseshown subjects, artery to suggest initially and elevated many disease

or fructose-induced to respond sedentary (13), subjects that the effect plasma have It is not more males subjects,

Dietary Studies terol is with

sucrose on the effects of dietary subjects sucrose have on plasma been more choles-

to dietary those hyperin-

Downloaded from ajcn.nutrition.org by guest on November 22, 2012

concentrations

in normal

equiv-

or carbohydrate-sensitive evidence with 24)

1 1). There pronounced concensubjects with obesity with only for these fasting descnib-

ocal. Several authors have reported lesterol in response to sucrose, even a very 25, 30). centrations sumption 22) and sumption (18) led study raised high proportion were observed of the diet in other to rise In contrast, studies,

no change in plasma chowhen sucrose was given as (11-65% plasma in response of energy) cholesterol to sucrose (15, 16, concon-

is more

triacylglycerol involved clear whether

studies

hyperlipoproteinemias. effect that of dietary of and plasma sucrose-rich triacylglycerol corn review. issue and that lipid those of study diet) subjects the hyperlipidemic there fructose, been shown been sugar, in has syrup. 65% They independently include sugars. formula metabolic abnormalities.

of its association measurements may be inadequate et al (25) containing of sucrose although significantly profiles The relevance is considered not been fully the concentrations effects diets that Hayford of

within a broad range (18-52% with some evidence of dose studies, reduction by substitution reductions of sucrose to significant

of energy) dependency

(8, 9, 12, (9). In two habitual conor starch In the

complementary

of the subjects

concentrations effects

with glucose (17) in plasma cholesterol. sucrose subjects

studied very

the high syrup

by Mann et al (22), dietary plasma cholesterol in normal saturated that some of the

at 34% of energy when the accomlargely may be diet.

of energy) found tniacylglycerol diets

or corn were with in more addressed

of these not 24-h these detail in of post-

panying dietary fat was unsaturated, suggesting explained This by the nature interaction

but not when it was of the discrepancies other components detail below.

of the

increased compared to health

is discussed proportion fractions but in containing

in more

plasma effects

containing in this relevant of sugars studies, large from fructose-induced

Changes in the various lipoprotein largely subjects unreported, given diets

of cholesterol carried by the in response to sucrose have been a study 5%, of 18%, carbohydrate-sensitive or 33% of energy as (VLDL)-, LDL-, and fractions all inwhereas When sucrose, is principally studies have total the ratio plasma it is reain the suga (9).

of dietary

sugars

metabolism in which have which was suggests effects is very given The that little

is whether is diets lasted fructose that of other there this have only (80 may

sucrosetransient. contained for g/d be days. as atwith on amounts effect of fructose; with which (27). been sugar, a

sucrose, very-low-density-lipoprotein high-density-lipoprotein (HDL)-cholesterol creased of HDL cholesterol sonable VLDL to or with increasing has LDL risen sucrose in response that fractions the because consumption declined increment to total assume cholesterol

hypertniacylglycerolemia especially

amounts one to a normal

to dietary several

consumed

for 28 d by type sugar

hypenlipidemic However, aspect. and have has some than is the with so-called in rats

gested that high-sucrose this cholesterol hydrate, later The conflicting


dietary sugars

HDL-cholesterol concentrations diet (18, 31, 32). However, effect of sucrose may in general. above fall This indicates concentrations

are reduced by it is uncertain whether per se, because more there are HDLfully many to high-carbo-

is an independent low-fat in this summary findings diets

information high

in response is discussed that

at abnormally plasma to its content the effect of invert and which tniacylglycerol-raising

review. presented in the literature concerning on plasma lipid concentrations deal of controversy. Nevertheless, conditions, atypically to changes to risk consumption large in the proportions lipoprotein the effects of and these have it also indicates subjects or may For that disease. of sucrose profile

to raise

tniacylglycerol

concentrations of sucrose however, sucrose consists This demonstrated

(9, 1 1, 13, 26). usually studies show proportions disaccharide (28).

attributed amount

is greater glucose has also

led to a great that, fructose under can of diets

an equivalent

certain containing lead

by normal

of equimolan

of fructose effect,

be deleterious

in relation

of cardiovascular

252S this reason, the subject has attracted an enormous

FRAYN amount

AND of

KINGMAN phorylate product olism routes okinase and


way.

several of the

sugars, phosphorylation

including

fructose, of fructose

at carbon by hexokinase in the

6. The is metabsame hexin this potenat fructhe a reis and

research.

fructose-6-phosphate, POSSIBLE BLOOD SUGARS Metabolism Although metabolized from The


sugars

which,

as an intermediate
(see

MECHANISMS TRIACYLGLYCEROL

FOR

THE

ELEVATION

OF BY

of glucose, as described has


Fructose

is subsequently for glucose affinity


mainly

metabolized by the Figure 1). However, compared with metabolized in the liver (and which the possesses molecule

CONCENTRATIONS

a low
is

for is only

fructose minimally

glucose

in practice

fructose

of glucose glucose differently and

and

fructose are similar of fructose of the two glucose 1. The In the and molecules, it is thought consumption sugars fructose they are stem are me-

metabolized

fructose

tially the tokinase. carbon action greater phate phate reaction fructose of fructose Cleavage enzyme one The and other it is

kidneys and This enzyme

small intestine), phosphorylates forming because activities fructose-6-phosphate, further therefore route This and under aldolase with to and

within consequences

the cell and

that many at this stage.

of the physiological differences metabolic are


begins

in the 1-position, that occurs rapidly than is not before of the combined Unlike cleavage glucose this metabolism fructose-i-phosphate dihydroxyacetone is the the

fructose-i-phosphate, liver fructokinase of hepatic

activity

in the metabolism pathways by which illustrated in Figure with phosphorylation. under which the influence phosphorylate and of further and

hexokinase fructose-1-phos-

glucokinase.

tabolized takes place glucokinase, resulting bisphosphate limiting

metabolism of both case of glucose, this

phosphonylated metabolism. metabolic compared

fructose-1,6-bisphosthe rate-limiting flux of the rapidity allows increases that the greater of glucose.

bypasses

of the enzymes hexokinase or the molecule at carbon 6. The is subsequently phosphorylated isomenized to This feature to frucis a rateof the by fructose-1,6-

through

glucose-6-phosphate by the enzyme step glycolysis

Downloaded from ajcn.nutrition.org by guest on November 22, 2012

tose-6-phosphate

of fructose-i-phosphate

influence two tnioses,

of the only

phosphofructokinase. is an important

yields molecule

of which,

phosphate, of this molecule,

is phosphorylated. glyceraldehyde, rather than the of the breakdown between

metabolism of glucose. Fructose-1,6-bisphosphate aldolase into two phosphorylated tniose molecules, etone phosphate and or can pathway. enzymes, in tissues glyceraldehyde-3-phosphate. in the glycolytic be used for begins pathway glycogen with the phosphates lipid synthesis gluconeogenic The by one nase metabolism of two is present can continue

is then split dihydroxyacThese to oxidation synthesis via

unphosphorylated produced the fundamental

production

triose or the

glyceraldehyde-3-phosphate glucose, that represents metabolism phosphorylated the glycolytic using the isotopes subsequent

from the difference

of the two sugars. In fact, glyceraldehyde to glyceraldehyde-3-phosphate and pathway have metabolism in this suggested form. that of the and Kinetic this molecule. phosphorylated further down and studies is the principal However, the

is readily can enter and studies route to 2-phospathway. in the for it can

of fructose

its phosphorylation Hexokican phosbody and

hexokinase throughout

or fructokinase.

also be converted phoglycerate to [ctJ

to glycerate enter glycolysis be converted

L#{176}#{176}

Alternatively synthesis

it can

to glycerol

be used

of tniacylglycenol.

1
F-i-P

C-i-P

]--PGIVcoQSn

*L]
rt
Li1frP1

Under anaerobic conditions, the metabolism of glyceraldehyde3-phosphate via glycolysis results in an accumulation of lactic acid; the under pyruvate aerobic conditions, however, (PDH) pynuvate is oxidized by acetyl dehydrogenase complex to produce

CoA, which can either be oxidized acid cycle or used in lipogenesis,


Because

for energy via the tricarboxylic for which it is the carbon source. to glycerol of acylglycerols or acetyl both thus and has the potential to produce

glyceraldehyde the metabolism acid and triacylglycerol of fructose

can of fructose

be converted moieties

CoA,

L!,m!J

the fatty

the glycerol

: Grcerate

I
1. Pathways
the potential to F-6-P) triacylglycerols

2-phohogPycerate

to facilitate Effects One glycerol synthesis

production. on hepatic fatty acid synthesis

___
ri

route by which concentrations in the liver.

fructose may is by altering The effects

increase blood tniacylthe rate of fatty acid on hepatic fatty

of fructose

acid synthesis were reviewed in detail by Zakim (33, 34). Note that there is a distinction between net de novo lipogenesis in the whole (in FIGURE
liver, moieties pathways showing of for the metabolism for from or synthesis fructose. pathways of glucose of both Dashed not and arrows relevant to fructose and the fatty show in the acid minor present

body a net
in

(as

evidenced hepatic that


consuming

by

a respiratory acid by lipogenesis


a Western

exchange which oxidation

ratio may in other

> 1 .0) and tissues.


process

increased sense) evidence


humans

fatty net

synthesis, fat

be counterbalanced

The

glycerol

is not an important diet is thoroughly measurements in humans of after

(fructose

reviewed by Hill and Prentice the absolute rate of fatty consumption one abstract

(35). Isotopic acid synthesis

discussion. F, fructose; etone phosphate; TCA

P. phosphate; G, glucose; DHAP, cycle, tricarboxylic acid cycle.

dihydroxyac-

of sugars have not yet been published, that shows marked stimulation after

except in frequent

SUGARS

AND

LIPID

METABOLISM

2535 was that also favored might CoA. on the liver Plasma evidence fructose enhancing tissue. increased by and availability present of fatty from may the Because rate studies facilitate release of glycerol it is of reesof in the fatty acids in by acids. is some diets that the by infusion be mediated of insulin (33).

fructose fructose converted Because

consumption load labeled to glucose, plasma they that would fructose

(36). with but have may (37). the

In normal subjects 13C, 50% of the remainder fallen have Further after studies was oral on concentrations contributed

given an oral fructose was for. by 45% it was to triakinetics of area. liver rose

acid It was in the


fatty

esterification suggested concentration acids, both

the effect of malonyl

by increases

unaccounted glucose), directly the

tniacylglycerol

Tniacylglycerol plasma acid from rats

synthesis synthesized fatty may tissue and high-fructose acids there

is dependent

(whereas
suggested cylglycerol

as nonestenified concentrations adipose receiving

nonesterified

synthesis

be increased

by release

fatty acid synthesis in humans The synthesis of fatty acids occurs when substrate production enzymes. of the pathway stimulate acid-synthesizing of either contribute dietary fatty is available of energy synthesizing regulated the ylase. glycolytic and basis,
by

are required to clarify this from carbohydrate in the in excess of the requirements

and requires the activation of fatty acid The rate of fatty acid synthesis may be of acetyl particularly glucose the acid sugar. to the amounts enzymes synthesis. in the of either increase fatty CoA and acetyl by activation CoA of acetyl On liver are carboxalong a long-term induced the CoA of pathway, will

hepatic triacylglycerol nonestenified fatty release thought from that adipose the

synthesis by from adipose is not is mediated

depots

by fructose,

by the availability Increasing the flux

effect

a reduced

enzymes

or fructose

tenification of fatty acids ular, fructose may inhibit fied fructose thesis and fatty acid may VLDL release further secretion release then

within adipose tissue the insulin suppression from adipose the into the rate tissue of circulation. (43).

(42). In particof nonesteniIn this If both way synnonesof fatty increased

availability

thereby

increase

tniacylglycerol

high induction acid

influxes may to high

Therefore, although enzyme fructose-induced increase in for the and differential fructose from both reseen rats of glucose animals. liver slices

tenified fatty acid acids are increased,

and hepatic the potential (in addition arising from

estenification exists for an

Downloaded from ajcn.nutrition.org by guest on November 22, 2012

fatty sponses

synthesis,

it cannot

account

recycling of fatty acids triacylglycerol secretion are not aware that this

to any increased VLDLde novo lipogenesis). We

both in humans Nevertheless,

and in experimental experiments using

has

been

investigated. catabolism on an VLDL have impairment This more VLDL was extensively catabolism, or in its rats, studies hydrolysis as impaired defect size and appears tniacylglycerol in the ratio either an in the isoVLDL secretion been found appear challenged in humans investigated either absence, both in has nonsuggest of VLDL hepatic to be

and humans have shown that substrate than glucose for fatty because acetyl olism, activity tose further may at a greater of its CoA fructose facilitate processes. rate rapid than metabolism, to the does molecules

fructose is generally a better acid synthesis (38, 39), largely which fatty (33). allows Unlike it to provide enzymes glucose by the CoA diet, however, by metablimiting fructwo of it was acid-synthesizing restrained to acetyl a high-fructose

Effects Although

of fructose the studies from an and latter: demonstrated (45-47) feeding of VLDL with an and
fructose

on VLDL effects

of fructose these

to be well
by

established, the

conclusions

some 44)

demonstrating circulation. but VLDL in fructosediabetic may (47). increase result This in was of

of tniacylglyc-

glucose is not

erol (24,

removal

metabolism its own First,

in animals

of phosphofructokinase. in rats fed

Additionally, conversion

in the addition been diabetic


that

impairment

to enhanced

synthesis (48, tissues the 49).

or sucrose-fed These in reduced as well catabolic

shown that the enzyme PDH (40). to acetyl inhibition de novo Interference would possible Effects VLDL

fructose activates PDH by inhibiting PDH kinase, which phosphorylates This CoA. of PDH further Second, by fatty encourages fructose acids released in this the present from feedback from this metabolism is thought

the action and inactivates of fructose

tniacylglycerol the clearance associated

in peripheral

to antagonize either

in the liver

from

lipogenesis or of fructose greater the from metabolism

adipose tissue (41). inhibition process sugar than would be

content of VLDL of apolipoproteins alteration removal lated lysis from in the mechanism.

particles (50) and E and C (51). nature of rats lipase rats The latter VLDL by LPL of the was (LPL) finding particles, occurs Mamo

with a reduction It might reflect or found that

allow

lipogenesis

particles relatively ex vivo impaired implies only

a defect

of glucose. esterification and

et al (47)

of fructose secretion widely of

on triacyiglycerol

from fructose-fed by lipoprotein fructose-fed uptake hydrolysis

resistant and also removal defective

to hydrothat livers of VLDL receptortissues.

showed

It has been the metabolism in the synthesis

accepted amounts triacylglycerol

that

in both of fructose and

animals leads its release

and

humans into the this blood

tniacylglycerol. mediated glycerol There change

of large

to increases

because

VLDL-tniacyl-

in extrahepatic

plasma in the form view was reviewed tniacylglycerol thesis must estenification suggest iments centrations nonestenified rather than tniacylglycerol. although lating sucrose that with be

of VLDL. The evidence by Vr#{225}na and F#{225}bry (2).

supporting To elevate

is conflicting direct evidence in LPL activity in sucrose

from animal studies for a or fructose feeding. Posthe(52, rats tissue in suA tniacyl-

concentrations, accompanied VLDL also rat acid

increased hepatic by increases in secretion and there facilitates these livers, infusion resulted metabolism in a shift in favor

fatty acid syntriacylglycerol is evidence to

parin plasma LPL 53) or unaffected or increased LPL activity crose-fed prior bout

activity (measured ex vivo) was reduced (47) in chronic sucroseor fructose-fed in monkeys (48, 55) or there exercise is only nullifies fructose (57). (54). Adipose increased (56) indirect the evidence. plasma

and fructose perfused of

processes. In experof physiologic conin the balance of of estenification

two- to threefold is unchanged rats. In humans of exhaustive

fructose fatty

oxidation This infusion

and caused effect was further

an increase in the secretion of not seen with glucose alone, of glucose enhanced and fructose the effect. (simuFatty

glycerol-raising effect of acute oral bly via stimulation of LPL activity tniacylglycerol, is impaired emia (24) administered during as it is (compared carbohydrate-induced with the

ingestion, probaThe clearance of lipid state) emulsion, 2 and 4 h hypertriacylglycerol-

as an intravenous starved

of a mixture metabolism)

2545 after findings a single probably meal containing reflect sucrose (1.5 of LPL g/kg) activity.

FRAYN (58); these

AND

KINGMAN drate than had higher did others. fasting Thus plasma triacylglycerol again, the expected on triacylglycenolemia concentrations adverse effect was

impairment

of not in that

high-carbohydrate observed. SUGARS There sucrose cemic amount people use AND has and response of with of fructose with control. been fructose glucose. diabetes LIPID METABOLISM interest with of is much use insulin in less fructose an attractive independent, IN DIABETES in the diabetes than as roles because that idea. the a sweetener Because replacement to improve in nondiadiets, with (59) concenwith insulin nonreof dietary the glyfor the to an equal

intake

considerable in people The to fructose

Despite the general favorableness Table 1, Hollenbeck et al (80) advise of high-sucrose long-term concentrations been thoroughly individuals in which effects, and diets for people with of HDL and that changes including depression adverse explored elevation

of the findings listed caution in the prescription NIDDM, of plasma cholesterol, might occur. suggesting tniacylglycenol have

not yet it

is therefore fructose However,

we are not yet able

to predict Although

is largely

of glucose glycemic

the diet may help the changes observed

may be true that details of each the near unanimity of finding triacylglycerol cholesterol enriched with the question One the adverse concentrations concentrations diets in subjects with findings in nondiabetic as to why possibility effects there is that that should people might

of the studies can a lack of elevation and mostly a lack to fructose-

be criticized, of plasma of effect or sucroseon

betic subjects as discussed diabetes. atherosclerosis and there trations may The

consuming high-sucrose or high-fructose above, are potentially undesirable for people incidence that a causal diabetes of macrovascular vessels, plasma (60). role disease, is high Many (NIDDM) triacylglycerol people are of the coronary in diabetes

in response

including

diabetes is in marked contrast subjects. This prompts the be such with be associated a distinction. already with sugar display diabetes

is evidence play

high

Downloaded from ajcn.nutrition.org by guest on November 22, 2012

insulin-dependent

mellitus

con-

sistant and have the features with increased risk of coronary tniacylglycerolemia tions. Because sucrose initial betes Many their or fasting fructose

of insulin resistance associated heart disease, including hyperconcentraof dietary related with to dia-

sumption (particularly hypertniacylglycerolemia) further capacity for response. This suggestion however, control normal mmol/L] al (70)]; that greater display fructose the by the studies listed in Table concentrations of Bantle plasma tniacylglycerol [eg, the IDDM subjects to high [eg, in any case, greater the response the 3.31 the initial to sugar suggestion

and have no is not borne out, studies, from mean the low0.72 range et al (73):

and depressed HDL-cholesterol the tniacylglycerol-raising effects may be (as mentioned earlier) people tniacylglycerol concentrations,

1. In these

might be particularly studies have addressed results have been

at risk when following these concerns, and (Table 1).

such a diet. on the whole

mmol/L findings

for subjects in normal

of Anderson et subjects suggest concentration, the diabetes

tniacylglycerol consumption. might be that insulin compared

reassuring

An alternative

people

with

Insulin-dependent There diabetes showed subjects few have mellitus no beneficial with more were control in serum (63, been

diabetes relatively (IDDM),

mellitus few perhaps studies because of insulin-dependent early reports (76) in control However, good found of a 4 wk

an exaggerated or sucrose) people. glucose

immediate consumption

response to sugar with that in nondoes extent not raise the as does gluinsulin small

diabetic plasma

Although concentration

fructose ingestion to the same

effects of fructose on glycemic severe diabetes (reviewed in 77). on plasma found 73, 77), triacylglycerol with Bantle although came 2.46 Perrotti consuming simple on fasting in subjects reasonably

cose, there is, in subjects with NIDDM, response to an oral fructose load even doses [eg, 15-50 g (81)]. This is not

an immediate with relatively seen in

deleterious

effects

or cholesterol et al (73) after

nondiabetic

concentrations glycemic a rise

subjects (82), perhaps because the insulinotropic tose is strongly dependent on the initial plasma centration concentrations suppressive (83); effect thus, may people display of insulin (at secretion with least (84, elevated in cultured 85) could a potentiating effect.

effect of frucglucose conplasma The perhaps glucose acute ac-

LDL-cholesterol energy were diet). were

concentrations

diet in which 20% of the cholesterol concentrations mmol/L patients diet the (60% control with with the IDDM diet, found but that, control who from with

from fructose (LDLcompared with 2.08 et al (78) compared sugar lipid studied with 41% six in for to a high-carbohydrate intakes) concentrations have led predisposed

hepatocytes) concentration concentrations. Chronic effects secretion), opposite

on VLDL-tniacylglycerol

of energy

carbohydrate identical of diet

count for the lack of elevation in people with high fasting However, elevation (ie, chronic there are problems concentrations of of insulin stimulation

of tniacylglycerol plasma glucose with this may have

hypothesis.

10 d and

no effects

(under

conditions hypertniacylglycenolemia to such an effect).

as reviewed below, might in nondiabetic subjects

VLDL-tniacylglycerol

and this hypothesis cannot induced hypertniacylglycerolemia who are unable to mount ingestion. of

explain an

the protection against sugarseen in people with IDDM acute insulin response to sugar

Non-insulin-dependent As plasma erally for IDDM, the

diabetes findings

mellitus concerning the elevation

tniacylglycerol and cholesterol reassuring in trials of long-term diets using large alternative patients treatments subjects to people with

concentrations are genfeeding of fructoseor NIDDM


(see

INTERACTIONS FAT It has long been

BETWEEN

SUGARS

AND

DWTARY

sucrose-enriched even in trials an interesting lowed

Table

i),

amounts of the sugar approach, Gallagher with NIDDM who for 4 y. Simple with lower intakes

(eg, 220 g/d). In et al (79) folwere assigned to sugar intake was of total carbohy-

known

that

the

nature

of dietary

fat

influ-

5 1 male

differing dietary not reported, but

ences the lipoprotein increase serum total unsaturated fatty acids;

profile. cholesterol n-3

Saturated fatty concentrations unsaturated fatty

acids tend to compared with acids also tend to

SUGARS

AND

LIPID

METABOLISM

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2565 reduce fat for were saturated (22). diet with may 2 wk, higher fatty In patients the with very normal the tniacylglycerol interact subjects serum if the acids with high starch) with the fed a diet tniacylglycerol fat component than if it was content did various concentration. sugar containing and (30% 34% Moreover, of of energy

FRAYN

AND

KINGMAN

the type the diet. as sucrose was fatty mainly

of In

EFFECTS Although dietary ing the

OF

HIGH-CARBOHYDRATE of and this fructose, of energy been diet [early recognized may references emphasis diet, (90). which itself lead both (CHD) The disease intake diet, may elevate are recently as a means and question to adverse review there in the concerns

DIETS the issue 1950s in (89)]. supplied the effects concernby carbothat There the fat risk as in blood to a of

composition cholesterol of energy) polyunsaturated

most proportion It has

concentrations acids even as sucrose and diet was a

sucrose

is a widen diet since plasma given

hydrate. concentrations has been content of coronary average whether

hyperlipoproteinemias, of 40% plasma of energy tniacylglycerol of the

high-carbohydrate considerable of the energy a low-fat Western heart

triacylglycerol

(compared cholesterol mainly saturated More Some others

not raise

on reducing of reducing then changes arises as a means

concentrations polyunsaturated fatty acids,

if the fat component fatty acids. If the these concentrations interactions have from 88). been human

fat component was increased (19-21). studied studies in animals. (54, 86) but

of reducing high

recently results are

these agree

is necessarily

relatively

with

those (87,

in carbohydrate, lipids.

inconsistent

TABLE
Effects

2 of high-carbohydrate Authors diets on plasma Subjects 1971 lipid concentrations

Downloaded from ajcn.nutrition.org by guest on November 22, 2012

Diet2 Fat 1% (total not controlled, weight Fat 4% energy controlled, weight fructose change) (total not no change); 1 1% of energy no

Duration 8 d (normal), (patients) 10-70 d 14 d Rise in total

Main and

findings VLDL but VLDL but TG decreased TG; rise in

Ruderman (89) Mancini

et al,

Normal
(n
=

(n = 5 M);

hypertriacylglycerolemic

VLDL cholesterol Rise

cholesterol unaffected3 and fell; test)

plasma TG; rise (fat in

4? M)
(n = 4 F, 12 M)

et a!, 1973

(24)

Normal

in total

VLDL cholesterol tolerance

cholesterol

plasma

removal

Ginsberg (91)

et at, 1976

Range (n

of TG 3 F, 24 M)

CHO (-50-60 55% CHO, 30%


40% sucrose total
diet

g/d)
fat vs fat; each Not stated of 7d Fasting related unaffected; unaffected Fasting VLDL TG TG concentration rate TG increased; increased4 10 d Fasting and synthetic TG increased TG cholesterol glucose tolerance (absolute rise to initial

concentrations
=

CHO, 24% CHO

45% for

concentration);

Melish

et al, 1977

(92)

Type (n

IV 3) (n
=

75%

hyperlipoproteinemia

CHO, 0% fat vs 45% CHO, 40% fat


CHO, CHO, CHO CHO, CHO, CHO CHO, CHO, 21% 41% for 21% 41% for 21% 41% varied 22-25% 22-25% fat vs fat; of each fat vs fat; of each fat vs fat; (see

Coulston (93)

et at,

1983

Normal

6 F, 5 M)

60% 40%

postprandial total but cholesterol

increased; unaffected fell

sucrose total
diet

HDL cholesterol

Liu

et at, 1983

(94)

Hypertriacylglycerolemic (n 4 F, 4 M)

60% 40%

15 d

Fasting

and

postprandial (particularly and

TG VLDL subfractions

increased unaffected

sucrose total
diet

TG); cholesterol

Liu

et at, 1984

(95)

Hypertriacylglycerolemic (n 6 F, 4 M)

60% 40%

15 d

Fasting intake

TG held

(total but

and less

VLDL) so if sucrose total HDL only if

increased, cholesterol cholesterol sucrose

sucrose text)

constant; unaffected; fell slightly increased and

intake TG (total when in; total, fell. in, TG

Utlmann
(96)

et at, 1991

Mildly (n

hyperlipidemic 2 F, 6 M)

65% CHO, 20% fat vs 45% CHO, 40% fat;


simple (test) (control) sugars or 28% of energy 25%

10 d after
over (part 10 d

phasing

in

Fasting phased

VLDL) and not total and HDL

30 d; or 2) started for

unchanged cholesterol phased VLDL

high-CHO LDL, When

immediately

fasting rose

TG, triacylglycerol.
Carbohydrate Gives Abstract references only. (CHO) and fat percentages work. are percent of energy intake.

-I 4

to earlier

SUGARS

AND

LIPID

METABOLISM

2575 other factor less variable between factor plasma across with which they are

Representative showed mainly tration, a rise reflecting

studies in fasting

are listed plasma

in Table triacylglycerol

2. The

results

of all concendiet to this after in (and,

presence associated. There and subjects, variation effect may of

of some This is an inverse

concentrations,

is the

HDL-cholesterol any

concentration. HDL-cholesterol population biological protective CHD HDL the that of

an increase

in VLDL-tniacylglycenol high-carbohydrate Some adaptation falling cholesterol even fall because in LDL cholesterol). the diets studies, The results

relation

(
diet 2-6 are

55%

after consumption of energy from been (24, noted, 97, 98). unaffected

of a low-fat, carbohydrate). with Total plasma plasma by a fall or may

triacylglycerol

concentrations

has wk

concentrations

with the former showing (within one individual). a high is HDL-cholesterol (at least for a marker be explained Despite

considerably less Thus, the apparent concentration in part) aspect of some by the fact of studies

concentrations increases cholesterol

against tniacylglycerol to identify

generally

in fact

VLDL

cholesterol

are offset

cholesterol metabolism.

some

in some studies, a small ings seem independent formula typical authors diets, foods, to advise as in most as in the caution

fall in HDL of whether of the earlier later studies.

These findwere unusual or were have based of low-fat of sucrose earlier soft [eg, =50-60 the group proportion with two a they other of total constantlow-fat in part by et al (93) if subentirely of However, is no hard diet by a studies, and g/d at drinks or on led some

the failure

fasting plasma tniacylglycerol risk marker, in other studies sometimes people The terol with links only low in specific HDL-cholesterol plasma and fat load risk metabolism;

concentration it does appear groups [eg, concentrations tniacylglycerol of CHD the may integrated

as an independent as such, although people (100-102)]. and HDL-cholesto aspects than A brief and is the overHDLin tniacylglycerol or in

in elderly

in the widespread issue concerns observed. of fructose originating content and was therefore

adoption the role The with

diets (93). However, fructose with involved (24)]. Stanford of the formula In most total

between

an unresolved in producing diets, at least University, carbohydrate were

concentrations to a fat

be related of CHD

the changes intakes studies, intake

of postpnandial response

supplemented

is a better

marker

moderate

of the later

from a fixed

fasting tniacylglycerol view of the current cholesterol Figure 2. metabolism

concentration understanding in the

(103, 104). of tniacylglycerol postprandial period

Downloaded from ajcn.nutrition.org by guest on November 22, 2012

the sucrose

is given

increased et al (95) maintained when diet, the 15% and in the

the high-carbohydrate different manipulations constant changed group energy). lestenol sucrose diet sucrose from raised The group. the their effects Thus, lipid intake low-

diets. In the study were used; one (13% to intake fasting were the effects concentrations of total (from high-carbohydrate

by Liu group energy) 9% to

sucrose (on

triacylglycenol minimized may of a high-carbohydrate,

HDL-cho-

concentrations)

on plasma

be mediated

increased sucrose or fructose noted that the deleterious jects consumed carbohydrate legumes, without substantial this would high-sucrose possibly that lead to exaggerates increased adverse intake.

intake. Indeed, Coulston effects would be eliminated diets composed amounts of the position almost sucrose. there

E
? 9JGARS
.

because of any unless

evidence

consumption changes

high-starch

accompanied

IMPAR

BLOOD CHD

TRIACYLGLYCEROL FAT

CONCENTRATIONS, AND RISK OF


FIGURE 2. Postprandial sugars. (TG). lipoprotein for clearance tissue. adipose the which tissue lipoprotein the TG-rich the greater species, ester is prolonged, to depression resistance. Dietary Endogenous (VLDL). by The lipid fat enters TG In the metabolism is secreted lipase rise fatty period. (unesterified) high-density (chylomicrons for neutral TG sugars directly will of the move may TG-rich concentrations. HDL; Dietary the residence leading by insulin suppression free such as and potential from (LPL) the liver points of action triacylparticles tissues, of VLDL Insulin from Insulin LPL action, (FC) are with the lipoproteins effects (HDL). in also adipose activates excess move to The the other of and

POSTPRANDIAL

METABOLISM,

Elevated for CHD The

triacylglycerol

concentrations

as a risk

factor

of dietary glycerol density

the circulation postprandial

as chylomicron period, in concentration these

as very-low-

evidence

reviewed

in the

previous

sections

leads

to the

compete especially suppresses tissue; adipose surface other longer circulation, lipoprotein for

lipoprotein consequent

in peripheral

conclusion that, in some persons, atypically high amounts of certain sugars, particularly fructose and sucrose, in the diet may lead to elevation of plasma tniacylglycerol concentrations. Whether hypertniacylglycerolemia controversial. tniacylglycerol or existence itself is a risk factor for CHD is somewhat ies, fasting plasma associated as independent with In several epidemiologic concentrations are of CHD but analysis studstrongly in

TG is minimized

by suppression release reinforces LPL in the including species lipoproteins the opportunity including (CE). Thus, of nonesterified the postprandial

of its secretion. acids (NEFAs) TG.

of VLDL During

components

cholesterol lipoprotein and lipid into exacerbate VLDL) exchange HDL

the risk predictors

do not emerge (reviewed

in multivaniate

99). However, this reflects at least because fasting plasma tniacylglycerol high degree of biological variability one individual, tions will not as well emerge

in part a statistical quirk: concentrations show a (from day to day within the concentrafactors in the

in exchange in the

cholesteryl

insulin circulation potentially

as between individuals), as independent risk

to hypertriacylglycerolemia

of HDL-cholesterol

2585 The question the that may period. hypothesis rophages LDL times particle the association these tions tion findings are factor also VII, membered particles as many (60 000 for between (103; fasting associated an important evidence epidemiologic of whether evidence elevated decreased associated atherogenic, first these arterial (particularly in this context molecules compared this view CHD and clearly particles wall, much oxidized that with comes remnant in 106). tniacylglycerol activation for CHD factor of cholesterol 2000, with does not directly

FRAYN address concentrations is a body and by Zilversmit their in the be internalized LDL). It should contains a typical the also of belief remnants (105). to occur be

AND the or

KINGMAN profiles erol meals chronic studies, showed contained effects acute consistent (25, the were addition thus 27, sugars daytime 1 12, 1 13). typical not clearly elevations In these diet, distinguished. to an oral fat load of the of tniacylglycstudies, and the acute increased effects Several or sucrose 115of a methus studies nesisto lipid such (53, in terms of lipid of test and

triacylglycerol HDL-cholesterol CHD. lipoproteins particularly stated may There

concentrations

concentrations

concomitantly the be

are causatively directly This was

In separate

tniacylglycerol-nich

of fructose

postprandial The with re-30 LDL by mac-

postprandial lipemia markedly (114). One general mechanism mediating sugars studies, consumption 119). reduced state Although sensitivity is usually also may albeit be leads this the in rats, has induction showed usually to a loss of glucose associated of that been with

the longer-term insulin high resistance. fructose to insulin to insulin,

is that in the

as is thought

of sensitivity metabolism

a chylomicron as does respectively). from have accumulation in part studies

demonstrated impairments

Although observed in type confirmed concentraof coagula(107). HowIII

tabolism (reviewed in 109, i 10). found in many studies of fructose be a consequence are tance obesity. concentrations More lipid metabolism of insulin lipid fatty of the needed induced In one specifically, in of insulin such rodents dietary rats that Among from dietary in a way resistance. section. acids suppression metabolism to clarify study issues by

The hypertniacylglycerolemia or sucrose feeding might However, the feeding increased not may were the most are potential adipose of nonestenified in lean alter the largely important increased tissue fatty the more insulin is related plasma controls kinetics summarized changes as whether fructose

hyperlipoproteinemia, Elevated and

mechanistic reviewed with postprandial

resistance.

increased risk

sucrose but sugars These

Downloaded from ajcn.nutrition.org by guest on November 22, 2012

in corpulent

(115). of charin terms release acids of of

even, factor mainly with


by

VII coagulant activity habitual fat intake and meals containing large

has so far is increased amounts

been associated experimentally in

accentuates

feeding

of fat (reviewed

actenistic

108). The The many concept role of insulin resistance changes at risk (109) first in common outline 2, insulin for resistance in postprandial CHD (or proposed diseases resistance may diminished metabolism be tied together sensitivity seen in

in the mechanisms of postprandial of nonestenified impairment release hepatic

(particularly

deleterious individuals of insulin

by the to in-

by insulin in the VLDL tniacylglycerol

postpnandial secretion

period), stimulation (particularly failure period), LPL by areas

sulin). Reaven lin resistance relation given to the in Figure

a widespread role for insu(including CHD) in 1988. In lipoprotein could be metabolism seen to affect

suppression by insulin ment of the activation suggest cally. that future

in the postprandial of adipose tissue studies address these

and impairinsulin. We more specifi-

of postprandial

several steps (reviewed in 110). Impaired activation of adipose tissue LPL in insulin resistance may be exacerbated by a failure of suppression of hepatic VLDL-triacylglycenol secretion in the postprandial zation process meal, (1 1 1). liver then. of but period. nonestenified suppression delivery to augment of a lower is normally Increased is likely Because Insulin fatty completely is less of resistance acids also from affects adipose by in fatty in the insulin the tissue; insulin acids secretion postprandial into the via lipid after resistance to the furmobilithis a

CONCLUSIONS In studies diet are centration stances, fructose Effects there extent drate to the the links ingestion might effects fasting in which amounts of sugars of plasma typical of the Western con-

suppressed complete nonestenified of LPL

provided,

an elevation

tniacylglycerol

is not usually diets containing can on increase other plasma

observed. atypically plasma lipid

Under particular cincumlarge amounts of sucrose or concentrations. are less clear and to what carbohyto relate into may research metabolism about the of the it is now

VLDL-tniacylglycerol activity

tniacylglycerol constituents

period, there will be less active transfer of cholesterol HDL pool and more active loss of HDL cholesterol exchange addition, effects smooth process. between concentration, Dietary Sugar sugars mediated chronic in insulin muscle Thus, by cholesteryl-ester hypeninsulinemia may resistance proliferation there and and are CHD such and intimate risk. lipid aggravate metabolism these processes as direct aggravation links depressed

are several areas of uncertainty. sugars have an effect independent content individuals between of specific be very of the in the diet diet. than sensitivity insulin informative. aspects Some subjects to insulin. and are others; sensitivity Some

It is not known of the total are more predisposition Further the lipid uncertainty measurement whereas responses

transfer protein. In have further adverse stimulation in insulin of arterial resistance of the atherogenic HDL-cholesterol

sensitive

the sugars

to sugar

of postprandial of the

hypertniacylglycerolemia,

of dietary sugars reflects uncritical plasma triacylglycerol concentration, tniacylglycerol consistently effects of

postprandial might

clear that the postprandial relevant measure and more at sev2). tion. The time course

response is a more altered by sugar ingesdietary sugars is not lipids is (75) has on blood group

consumption

of the

eral points, That dietary

both in the short and in the long term (see Figure sugars may have a specific effect on postprandial by studies in normal plasma triacylglycerol sucroseor fructose-rich subjects, concentrations diets, in

clear. It has been suggested that any effect transient (particularly in diabetes). Reavens consistently experimental evidence argued that such claims evidence. In reality, there either way. This question will

lipemia is shown overnight-fasting not altered by

which were 24-h

are not based on solid is no solid experimental only be addressed by

whereas

SUGARS longer-term case-control studies studies. (of at least 1 y) or possibly by

AND large

LIPID

METABOLISM
21. Antar kinds tients. lipids. 22. Mann MA, Part Little JA, Lucas C, et al. and effects 1970;1 GS, fats DA, Manning fat Interrelationship in hyperlipoproteinemic and animal between

259S
the pa-

of dietary Atherosclerosis JI, Watermeyer dietary

carbohydrate

3. Synergistic

of sucrose 1:191-201. EB, with AS,

fat on serum on serum diet. Clin lipids Sci

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COMMENTARY Sherman: produce blood as much carbohydrate less, and despite ample, containing hydrate, profile 15% exercise provide the an lipid Although atherogenic profile, stores training relative consumption i2.55 [tniacylglycerol, MJ/d a high-carbohydrate, response endurance in their between can protection runners (3000 and 14% 1.03 diet training favorably alter against who kcal/d) fat had 0.24 from athletes the are low-fat perspective advised (1). to restore lipid diet. consumed 71% serum diet may of the to consume body profile disease For exa diet carbolipid Neverthe-

glycerol,

0.05

0.01 4.11

mmol/L;

fatty

acid,

0.36

0.04

mmol/L; and (61 trained 62%

total cholesterol, high-density-lipoprotein 6 mg/dL)] These runners results (WM

0.47 mmol/L cholesterol, Sherman, supported 10.59 protein, 0.99 0J3 0.13 MJ/d and 0.i6

(i59 18 mg/dL); i.58 0.16 mmol/L observations,1980). that kcal/d) comprising also (88

unpublished (2530

are also 11% profiles: 388 and 1.40

by the observation 27% fat mmolfL (150 (54 Furthermore, metabolic conditioning unit to 1 . 13-1
.

carbohydrate

as possible sessions

consuming

the blood cardiovascular

carbohydrate, blood lipid tniacylglycerol, cholesterol, density-lipoprotein activity (METs)/wk (100-105 of

had excellent 14 mg/dL) 5 mg/dL) conditioning equivalents I 9 mmol/L activity total high-

mmol/L mmol/L (2). > 6 less tniacylglycenol

of a high-carbohydrate typically comprising an excellent (91 mmollL

5 mg/dL)

well-trained protein,

cholesterol an reduces intensity blood whereas

21 mg/dL);

mg/dL),

physical

2625 does 1 18-123 eastern References


1.

FRAYN not alter mg/dL), Finland (3). blood as tniacylglycerol found in 1675 (1.33-1.39 middle-aged mmol/L, men

AND or from

KINGMAN

References
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What should and complex assesses the

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of di-

evidence that increased consumption can, under certain conditions, increase concentrations. the authors feeding between glycerol many insulin that of were physical can of diets insulin factors, resistance activity affect That review One is the of these certain of insulin induction

of sucrose or fructose plasma tniacylglycerol conditions resistance suggested by long-term The interaction in plasma triacylreview. and and preventing There fructose degree the serum are of by

simple

carbohydrates Authors Some diet long between Reference


I . Anderson controlled fiber diets JW, on

in terms reply: Few suggests beneficial but sugars

high in fructose or sucrose. resistance and the increase is one that are (the insulin is, much concentrations does and theme of this for example, most and likely the however, accounting independent here. For latter resistance

concentrations

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a high-carbohydrate, concentrations that

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in the

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887-94. Wolever-reply versus complex abolic complex which (simple this changes? to Khan: carbohydrates The answer Is there a study comparing simple in terms of long-term lipid metto this depends There was at least on how are several simple studies and in

using animal tniacylglycerol sucrose developmentally and growth

models to evaluate possible interactions concentrations, insulin resistance, and fructose immature phase, referenced rodents generally research of results age groups importance by times the work been rats in this by the authors still have within quite impossiage same and (ie, rodents accepted has established

dietary used the mo clearly mature bly group If groups

exponential of age).

to be < 4-S

carbohydrates starch (complex carbohydrate). may affect versus glucose is by differences insulin what kind

are defined. carbohydrate) There are lipids.

Gerontological

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that extrapolation rodents to older (1, 2). The several is illustrated cited

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exchange

One

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invalid

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when (5). are the

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18 mo

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We have done a in which the comthe GI). subjects as an serum that the types of starchy

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starch

on

Blood containing

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