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Lipid Faal Am J Clin Nutr-1995-Frayn-250S-61S
Lipid Faal Am J Clin Nutr-1995-Frayn-250S-61S
Keith N Frayn
sugars
and Susan large
other
in
,2
ABSTRACT
the diets of humans
When
and
of sugars
alterations
are included
in concentrations
in of
low-
context regarding We
of first
an
area
of
active studies
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
effects of sugars on blood lipid concentrations developments in this field in the main areas concentrating on literature published
These in the
effects Western
of
above,
is needed on postprandial triacylglycerol may be affected more readily than fasting elevation
increased secretion to
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
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
consumption; common concentraactivity associated the many tniacyland weight facas canbohy-
l995;62(suppl):250S-63S.
fructose, plasma
tions,
in the
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
not surprising that the of dietary sugars (suconcentrations so when and test
has been recognized in (1)]. Consumption increased but been carried plasma changes observed. out extensively of the 1970s was and
have Such
> 5%
of energy centrations
which (8-13)
tniacylglycerol
plasma
in plasma cholesterol concentrations Many studies in animals and humans to examine (2-7). relatively this effect, and these have
in some
Western
observational
in human lead
summarized
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
To some
considerable
containing
of energy
of dietary
From
the Oxford
Metabolism UK. to KN
Group, Frayn,
underlying
of fruc-
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
of fasting men. Similarly, amounts containing increases subjects. in female were is not the
plasma of
SUGARS Dietary
AND fructose
concentrations
Hallfnisch
( 1 1)
7.5%, glycerol study, second
of energy)
in a diet
In addition trations, dietary energy has been low-density-lipoprotein subjects in which each change in which (=28% however, of dietary
on
led to proportional was therefore, factors that (saturated carbohydrate diet may Subjects elderly coronary (18). be may not seen dose
at 7.5-20%
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
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
triacylglycerol
of fat consumed
the
dietary discrepancies
authors
of the
fat as a result
or fructose-induced to respond sedentary (13), subjects that the effect plasma have It is not more males subjects,
sucrose on the effects of dietary subjects sucrose have on plasma been more choles-
concentrations
in normal
equiv-
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
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
complementary
of the subjects
concentrations effects
studied very
by Mann et al (22), dietary plasma cholesterol in normal saturated that some of the
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
in more
plasma effects
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
to dietary several
consumed
hypenlipidemic However, aspect. and have has some than is the with so-called in rats
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-
information high
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
attributed amount
an equivalent
by normal
of equimolan
of fructose effect,
be deleterious
in relation
of cardiovascular
FRAYN amount
AND of
several of the
sugars, phosphorylation
including
fructose, of fructose
research.
which,
as an intermediate
(see
MECHANISMS TRIACYLGLYCEROL
FOR
THE
ELEVATION
OF BY
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
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
small intestine), phosphorylates forming because activities fructose-6-phosphate, further therefore route This and under aldolase with to and
within consequences
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
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.
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
tose-6-phosphate
of fructose-i-phosphate
of the only
phosphofructokinase. is an important
yields molecule
of which,
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
production
triose or the
glyceraldehyde-3-phosphate glucose, that represents metabolism phosphorylated the glycolytic using the isotopes subsequent
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
hexokinase throughout
or fructokinase.
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
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
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
___
ri
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
by
fatty net
synthesis, fat
be counterbalanced
The
glycerol
(fructose
reviewed by Hill and Prentice the absolute rate of fatty consumption one abstract
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).
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
by increases
tniacylglycerol
is dependent
(whereas
suggested cylglycerol
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
depots
by fructose,
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).
availability
thereby
increase
tniacylglycerol
Therefore, although enzyme fructose-induced increase in for the and differential fructose from both reseen rats of glucose animals. liver slices
fatty sponses
synthesis,
it cannot
account
recycling of fatty acids triacylglycerol secretion are not aware that this
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
in animals
Additionally, conversion
impairment
to enhanced
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
in peripheral
to antagonize either
in the liver
from
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
allow
lipogenesis
a defect
et al (47)
on triacyiglycerol
showed
that
and
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
supporting To elevate
from animal studies for a or fructose feeding. Posthe(52, rats tissue in suA tniacyl-
increased hepatic by increases in secretion and there facilitates these livers, infusion resulted metabolism in a shift in favor
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
fructose fatty
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
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.
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
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
to predict Although
is largely
of glucose glycemic
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
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
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
mmol/L findings
reassuring
An alternative
people
with
Insulin-dependent There diabetes showed subjects few have mellitus no beneficial with more were control in serum (63, been
mellitus few perhaps studies because of insulin-dependent early reports (76) in control However, good found of a 4 wk
immediate consumption
response to sugar with that in nondoes extent not raise the as does gluinsulin small
diabetic plasma
Although concentration
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
deleterious
effects
nondiabetic
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.
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
on VLDL-tniacylglycerol
of energy
count for the lack of elevation in people with high fasting However, elevation (ie, chronic there are problems concentrations of of insulin stimulation
hypothesis.
10 d and
no effects
(under
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
diabetes findings
tniacylglycerol and cholesterol reassuring in trials of long-term diets using large alternative patients treatments subjects to people with
BETWEEN
SUGARS
AND
DWTARY
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
SUGARS
AND
LIPID
METABOLISM
255S
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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
of In
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
sucrose
triacylglycerol
not raise
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
these agree
is necessarily
relatively
with
those (87,
in carbohydrate, lipids.
inconsistent
TABLE
Effects
Diet2 Fat 1% (total not controlled, weight Fat 4% energy controlled, weight fructose change) (total not no change); 1 1% of energy no
Main and
et al,
Normal
(n
=
(n = 5 M);
hypertriacylglycerolemic
4? M)
(n = 4 F, 12 M)
et a!, 1973
(24)
Normal
in total
cholesterol
plasma
removal
Ginsberg (91)
et at, 1976
Range (n
of TG 3 F, 24 M)
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
=
45% for
concentration);
Melish
et al, 1977
(92)
Type (n
IV 3) (n
=
75%
hyperlipoproteinemia
Coulston (93)
et at,
1983
Normal
6 F, 5 M)
60% 40%
sucrose total
diet
HDL cholesterol
Liu
et at, 1983
(94)
Hypertriacylglycerolemic (n 4 F, 4 M)
60% 40%
15 d
Fasting
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
sucrose text)
Utlmann
(96)
et at, 1991
Mildly (n
hyperlipidemic 2 F, 6 M)
10 d after
over (part 10 d
phasing
in
Fasting phased
30 d; or 2) started for
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
studies in fasting
in Table triacylglycerol
2. The
results
concentrations,
is the
HDL-cholesterol any
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
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
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
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
diets (93). However, fructose with involved (24)]. Stanford of the formula In most total
between
concentrations to a fat
be related of CHD
of postpnandial response
supplemented
is a better
marker
moderate
of the later
from a fixed
the sucrose
is given
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
sucrose (on
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
.
evidence
consumption changes
high-starch
accompanied
IMPAR
BLOOD CHD
TRIACYLGLYCEROL FAT
POSTPRANDIAL
METABOLISM,
triacylglycerol
concentrations
as a risk
factor
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 VLDL During
components
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
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
concentrations
concentrations
concomitantly the be
In separate
tniacylglycerol-nich
of fructose
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
is that in the
as is thought
of sensitivity metabolism
demonstrated impairments
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
resistance.
increased risk
in corpulent
VII coagulant activity habitual fat intake and meals containing large
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
(particularly
by the to in-
postpnandial secretion
a widespread role for insu(including CHD) in 1988. In lipoprotein could be metabolism seen to affect
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-
provided,
an elevation
tniacylglycerol
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
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
whereas
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-
carbohydrate
3. Synergistic
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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
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
by the observation 27% fat mmolfL (150 (54 Furthermore, metabolic conditioning unit to 1 . 13-1
.
carbohydrate
as possible sessions
consuming
had excellent 14 mg/dL) 5 mg/dL) conditioning equivalents I 9 mmol/L activity total high-
5 mg/dL)
well-trained protein,
21 mg/dL);
mg/dL),
physical
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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This
review
concludes
that
there
is compelling
the average American be eating in terms carbohydrates? Is there a study that benefits of complex lipid studies on lipid exists compared metabolic have been with of long-term long-term that effects little and evidence starches. changes? reported. high-fiber
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
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
development obesity
in the
of sucrose
distinguishes
not considered
former)
triacylglycerol
concentrations. in tniacylglycerol
Garrity serum TF, lipid Wood CL, et at. Prospective, of low-fat Am and low-fat Nutr J Clin randomized, plus high1992;56: comparison of the effects
of insulin resistance and changes are a result of controllable these variables in relation most of the fructose. In addition,
The effects
not consider
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of sucrose
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
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
exponential of age).
to be < 4-S
carbohydrates starch (complex carbohydrate). may affect versus glucose is by differences insulin what kind
Gerontological
replaced by sucrose two ways by which effects and Kingman. Sucrose stimit is not always studies. carbohybe seen as
that extrapolation rodents to older (1, 2). The several is illustrated cited
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exchange
One
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