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Commentary :
This
article introduces the characteristics of postprandial Very Low Density Lipoprotein (VLDL)
remnants (remnant lipoproteins; RLP) in plasma which significantly increased
after fat load as a major component of increased Triglycerides (TG) and
involved in obesity and insulin resistance. It has been long believed that
postprandial RLP, mainly Chylomicron
(CM) remnants, increases as the result of disturbed lipoprotein lipase (LPL)
activity caused by insulin resistance, etc. However, based on this report, we recently
proposed that elevated postprandial VLDL remnants produced by food intake, such
as excessive fat and fructose, cause obesity and insulin resistance when
exposed continuously [1]. VLDL remnants, but not CM remnants, is the key word
of this article and VLDL remnants play a definitive role as a bridge between
food intake and its metabolism. Here, we have explained the bridging role of
VLDL remnants between the habit of food intake and its metabolism in body.
Following 6 aspects between fat-rich meal intake and the increase of plasma
postprandial TG and RLP are explained. (1) Why TG and RLP increase after food
intake? (2) Which lipoproteins increase most after food intake? (3) What
percentage of increased TG after food is comprised of RLP-TG? (4) How the
increased TG is metabolized by LPL? (5) The increase of postprandial RLP is the
result of obesity and insulin resistance or cause of obesity and insulin
resistance? (6)Why postprandial TG is a risk of cardiovascular diseases?
Dietary fat provides
as much as 30% to 40% of total daily caloric intake in the western diet and TG
constitutes the majority of that fat. Dietary
Long-Chain Triglycerides (LCTs), the most common dietary lipid structures, are
mainly digested into two fatty acids and an SN-2 monoglyceride molecule [2].
Re-esterification of fatty acids occurs in the enterocytes of the small
intestine. Subsequently, the resulting LCTs are incorporated into CM particles
and released into the blood through the lymphatic system after
food intake. Therefore, plasma TG concentration increases significantly after
food intake, especially after fat-rich meal with LCTs [3]. But certain fatty
acids such as Medium Chain Triglycerides (MCT) and Diacylglycerol (DG) do not
increase plasma TG, because MCT and DG are absorbed directly into the portal
circulation to liver rather than being incorporated into chylomicron particles
at intestine [4,5]. Therefore, fat intake (LCTs) affects the increase of CM
formation and secrete into blood circulation with increased amount of TG mostly
as VLDL remnants in 3-6 hours after fat intake. Zilversmit
first proposed the postprandial increase of TG to be the most common form of hyperlipidemia which
associated with increased RLP as a risk for Cardiovascular Disease (CVD).
Therefore, the postprandial TG increase has been long believed as the increase
of TG in CM, CM remnants in plasma [3]. Because,
increase of RLP and its ratio in the postprandial TG has not been clearly shown
by ultracentrifugation separation (IDL) or other separation methods [6]. Using
RLP immuno-separation method, the differences between increased TG and RLP in
the fasting and postprandial plasma have been clarified [7-11]. Although the
cholesterol content in RLP (RLP-C) is commonly found to be less than 10% even
in the postprandial plasma TC, TG content in RLP (RLP-TG) is found to be more
than 20% in the fasting plasma TG and as much as 50% in the postprandial plasma
TG under various physiological conditions [12]. The postprandial RLP contained
both apoB-48 and apoB-100 carrying particles. The increase of RLP apoB-100
particles (VLDL remnants) in fact was much greater (more than 80%) than that of
apoB-48 containing lipoproteins (CM remnants) in the postprandial state [13-15].
Because the particle sizes of postprandial RLP-apoB48 and RLP-apoB100 are very
similar (postprandial apoB48 particles in plasma are not large as being
believed) [10], we found that major component of postprandial TG increased is
VLDL remnants, but not CM remnants. Possibly, most of CM and CM remnants
increased in plasma after food intake are incorporated into liver within a very
short time [16,17] and re-constituted to VLDL and secreted as VLDL remnants in
plasma. Significantly
higher RLP-TG is contained in the postprandial plasma than in the fasting
plasma when the TG level is adjusted as the RLP-TG/TG ratio [18]. These results
show that the amount and ratio of RLP in the postprandial TG increased
significantly compared with the fasting plasma TG. In particular, the increase
in the postprandial delta RLP-TG (postprandial RLP-TG minus fasting RLP-TG)
levels contributed to approximately 50-60% of the increase in the postprandial
delta TG (postprandial TG minus fasting TG) after regular meal intake. However,
more than 80% of the increased delta TG was comprised of delta RLP-TG after a
fat load or fat rich meal [18]. These results clearly show that the kind of
food as contained in a fat rich meal greatly enhance the formation of RLP in
the postprandial plasma compared with a regular meal. Marcoux et al. [19], Ooi
et al. [20] and Nakajima et al. [21] previously reported similar results in
small number of Caucasian and Japanese volunteers, in whom approximately 60-80%
of the delta RLP-TG in delta TGs were found in 3-6 h after a fat rich meal. The
rest of the increased TG consisted of increased non-RLP-VLDL-TG, LDL-TG and
HDL-TG in the postprandial plasma, but do not comprise of TG a much as RLP-TG. We
have found that majority of LPL in plasma is bound to RLP and released into
circulation as RLP-LPL complex both in pre-heparin and post-heparin plasma [22].
LPL bound to RLP showed no activity in non-heparin plasma and didnt increase
after fat load in spite of the increase of RLP [23]. However, LPL levels in
non-heparin plasma reflect the LPL activity for hydrolysis of CM and VLDL at
endothelium. RLP-TG concentration and particle size increased in plasma after
food intake is mainly regulated by LPL activity at endothelium together with
other factors such as GPIHBP1 [24] and apoA5 [25]. A significant increase in the
RLP-TG/RLP-C ratio was always higher in the postprandial plasma and ratio of
LPL/RLP-TG was significantly lower. When LPL activity is not sufficient to
hydrolyze overloaded CM or VLDL on the endothelial cells, less efficient
hydrolysis occur and enhance the formation of less metabolized, large RLP
particles along with the higher RLP-TG/RLP-C ratio. Those RLP particles carry a
significantly lower LPL compared to small RLP particles, as shown by the low
LPL/RLP-TG ratio [23, 26, 27]. Therefore, when the LPL activity and
concentration is low, overloaded CM and VLDL are not hydrolyzed enough. Also
when CM and VLDL are over loaded, LPL cant hydrolyze the excessive amount of
TG-rich lipoproteins, resulting large size RLP particles are secreted into the
postprandial plasma. As large RLP particles carry small amount of LPL, the
function as ligand for the receptor incorporation of remnants [28], may become
less effective for the clearance of remnants and accumulate more in plasma [22].
These results suggest that the large RLP with reduced ratio of bound LPL
(LPL/RLP-TG) found in the postprandial plasma is a higher risk factor for obesity, insulin resistance and
cardiovascular disease, as shown previous reported [29-31]. We
have long thought that postprandial remnant lipoproteins (RLP) in plasma are
significantly increased as the results of disturbed lipoprotein metabolism
followed by the obesity and insulin resistance. Thereby, we believed that the
insulin resistance as the result of obesity caused the enhancement of
postprandial RLP formation. However on the contrary, we have proposed that RLP
cause to induce the insulin resistance as the results of obesity which is
induced by the excessive supply of RLP to visceral fat. Since the increase of
VLDL remnants in plasma is the first step of lipid metabolism right after
fat-rich meal intake as blood sugar after carbohydrate intake, we proposed that
postprandial VLDL remnants are the other factor which enables to play the role
for the storage of TG in adipose
tissue from the circulation. The consumption of fat-rich meal and fructose
are known to increase postprandial TG, fasting and postprandial RLP-C and
RLP-TG, whereas consumption of glucose did not in healthy volunteers without obesity
and insulin resistance [32,34]. Therefore, the kind of food intake
significantly affects the formation of VLDL remnants and enhances the visceral
fat obesity in normal volunteers. Therefore, we have recognized that the role
for the formation of VLDL remnants after food intake is to provide TG as energy
supply to organs and tissues, in particular to adipose tissue to prepare
against starvation [34]. Further excessive and continuous supply of RLP from
the blood stream enhances the accumulation of TG in visceral fat. The enlarged
adipocytes by accumulated TG increase the secretion of TNF-α and other
adipocytokines [35] and induce insulin resistance. Takahashi
et al. [36] reported that VLDL receptor, which is actually the most important
VLDL remnant receptor, played the key role to induce the obesity and insulin
resistance when fed with high-fat refined-sugar (HFS) in mice. Although there
are many experimental animal studies that HFS can induce obesity and insulin resistance [37-42],
those literatures reported simultaneous
increase of TG or postprandial hyperlipidemia with insulin resistance
and obesity or TG increase after insulin resistance and obesity. Goudriaan et
al [43] reported that mice increased TG (VLDL remnants) in plasma by HFS, but
mice could not proceed to store TG in adipose tissue without VLDL receptor and
could not induce insulin resistance. Therefore, the formation of VLDL remnants
as the first step after food intake should be positioned before the obesity and
insulin resistance at the metabolic domino as the same position with blood
sugar (Figure 1). RLP
is known to be cleared by LRP-1 and VLDL receptors in the liver, muscle, endothelium
and adipose tissue in humans [36,41,42]. We recently found that LPL and apo (a)
(a part of Lp(a)) were bound to RLP and formed RLP-LPL and RLP-apo(a) complex
in plasma [1, 22]. Therefore, LPL and apo (a) as well as apoE could be the
ligands for RLP to bind remnant receptors, especially VLDL receptor in adipose
tissue. Elevated plasma RLP-C and RLP-TG concentration have been reported with
the presence of insulin resistance [44-46]. Also, Yatsuzuka et al. [47]
reported that RLP-C and RLP-TG were strongly associated with visceral fat
volume. This suggests the VLDL receptor in adipose tissue reacts with ligands
of RLP [37,41,42] and RLP supply FFA or incorporate into adipocytes. However,
the mechanism of incorporation of RLP into adipocytes is not yet clarified
enough. Thus, enlarged adipocytes by the increase of TG storage leads to the
induction of insulin resistance. Therefore, we suggest that after the intake of
high fat and refined sugar diet and/or with the lack of exercise, excessively
increased RLP in plasma cause to initiate obesity and insulin resistance
through VLDL receptor. Nordestgaard
et al. [48] and Bansal et al. [49] as well as Iso et al. [50] reported that the
TG measured in non-fasting samples were more sensitive than the conventional
measurements of the fasting TG concentrations in predicting the risk of cardiovascular events
(the Copenhagen Heart Study, Womens Health Study and in a Japanese population
study). Also, the Framingham Offspring Study previously cardiovascular risk
factor, while RLP-C was an independent risk factor in the fasting plasma in
women[51]. Postprandial
TG and RLP are known to attain their highest levels 3-6 h after food intake
[7-9]. Therefore, we analyzed the RLP-TG/TG ratio (concentration) and
RLP-TG/RLP-C ratio (particle size) [10] associated with the lipoprotein lipase
(LPL) in both the fasting and postprandial plasma. We have shown that
significantly higher RLP-TG is contained in the postprandial plasma than
fasting plasma when the TG level is adjusted as the RLP-TG/TG ratio [18]. These
results show that the amount and ratio of RLP in the postprandial TG increased
significantly compared with the fasting plasma TG. Karpe et al. [29,30]
reported that endogenous TG-rich lipoproteins (TRL) accumulate in the human
plasma after fat intake and the mechanism behind this phenomenon is the delayed
lipolysis of the apoB-100 TRL particles due to a competition with CM for the
LPL active sites. The large apoB100 TRL is more atherogenic than small TRL.
Postprandial RLP with large particle size and low LPL are atherogenic
lipoproteins and cause higher risk of cardiovascular diseases. We
have shown that postprandial VLDL remnants are increased significantly after
fat rich meal or consuming fructose. Elevated VLDL remnants are significantly
large sized RLP particles along with a smaller ratio of LPL in RLP in the
postprandial plasma. Therefore, we have proposed that the increase of
postprandial VLDL remnants comes first associated with unhealthy life style
habit and cause to induce the insulin resistance as the results of obesity when
the excessive RLP is supplied continuously to visceral adipocytes. Therefore,
metabolic domino starts from the increased postprandial VLDL remnants in plasma
as shown in Figure 1 and cause various cardiovascular diseases followed by the
obesity and insulin resistance. The Japanese cuisine is an ideal food which
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Atherosclerosis 154: 229- 236.Triglyceride is Significantly Increased in Remnant Lipoproteins After Food Intake and its Association with Lipoprotein Lipase in the Plasma
Full-Text
Why TG increase
after food intake?
Which TG in
lipoproteins increase after food intake?
What percentage
of TG is comprised of postprandial RLP-TG?
How the increased
TG is metabolized by LPL?
The increase of
postprandial RLP is the result of obesity and insulin resistance or cause of
them?
Why postprandial
TG is a risk of cardiovascular diseases?
Conclusion
References
Keywords