Synthesis

Ann Biol Clin 2023 ; 81(5) : 475-482.

Low-density lipoprotein triglycerides: A marker for

metabolic diseases
Triglycérides des lipoprotéines de basse densité : un marqueur des
maladies métaboliques
Xiangniang Li Abstract. Dyslipidemia plays an essential role in the occurrence and
Hao Shen development of cardiovascular diseases, and the regulation of cholesterol
Clinical Laboratory, Suzhou Ninth and triglyceride metabolism has been applied in the diagnosis, treatment
and prognosis of clinical cardiovascular diseases. Following advances
Copyright © 2024 JLE. Téléchargé par MONSIEUR MONGI AYARI le 17/01/2024.

People’s Hospital, Soochow

University, Ludang Road, Suzhou,
China
Article received on September 14, 2023,
accepted on October 18, 2023
in methodology in recent years, low-density lipoprotein triglycerides
(LDL-TG) has been identified as a potential risk factor for the development
of cardiovascular disease and has some clinical significance in its diagnosis
and treatment. Meanwhile, LDL-TG metabolism regulation may also be
involved in the development of type 2 diabetes, chronic kidney disease,
hypothyroidism and other diseases, which may improve our understanding
of the prevention, control and risk assessment of clinically relevant diseases.
Key words: low-density lipoprotein triglycerides, cardiovascular disease,
type 2 diabetes, metabolic disease, biochemistry

Résumé. La dyslipidémie joue un rôle essentiel dans l’apparition et

le ­développement des maladies cardiovasculaires, et la régulation du
métabolisme du cholestérol et des triglycérides a été appliquée au diagnostic,
au traitement et au pronostic des maladies cardiovasculaires cliniques. À la
suite des progrès méthodologiques réalisés ces dernières années, la triglycéride
des lipoprotéines de basse densité (LDL-TG) a été identifiée comme un facteur
de risque potentiel pour le développement des maladies cardiovasculaires et
revêt une certaine importance clinique pour le diagnostic et le traitement de
ces maladies. Par ailleurs, la régulation du métabolisme des LDL-TG peut
également être impliquée dans le développement du diabète de type 2, des
maladies rénales chroniques, de l’hypothyroïdie et d’autres maladies, ce qui
peut améliorer notre compréhension de la prévention, du contrôle et de
l’évaluation des risques de maladies cliniquement pertinentes.
Mots-clés : triglycérides des lipoprotéines de basse densité, maladies
­cardiovasculaires, diabète de type 2, maladies métaboliques, biochimie

Introduction coronary artery disease (CAD) [3].

Low-density lipoprotein (LDL) is
the primary transporter of serum
cholesterol [1], while low-density
lipoprotein-cholesterol (LDL-C) is
doi:10.1684/abc.2023.1840
Additionally, a large meta-analysis
of randomized intervention trials
investigating different lipid-lowe-
ring agents, such as statins and
ezetimibe, revealed that each

a major risk factor for cardiovas- 1mmol/L decrease in LDL-C was

cular disease (CVD) [2]. A Mende- associated with a 20-25% reduc-
lian randomization study identified tion in CVD incidence [2]. Never-
Correspondence : H. Shen
<20144232033@stu.suda.edu.cn>
LDL-C as an independent cause of theless, there are still many CVD
To cite this article: Li X, Shen H. Low-density lipoprotein triglycerides: A marker for metabolic diseases. Ann Biol Clin 2023 ; 81(5) : 475-482.
doi:10.1684/abc.2023.1840
475
 Synthesis
cases that occur in patients with normal serum LDL-C
levels. Therefore, recent research on LDL focused
not only on its quantity but also on its q ­ uality, size,
particle quantity, composition, and surface proteins.
Studies have found that LDL-TG correlated more
strongly with CAD and mild systemic inflammation
than LDL-C [1]. Meanwhile, the studies also revealed
that smaller particles promoted enrichment in LDL as
opposed to total cholesterol (TC).
LDL-TG was first described in studies researching
familial dysbetalipoproteinemia [4], a condition
­characterized by remnant accumulation resulting from
impaired remnant clearance, leading to premature car-
diovascular disease. Reduction of LDL-TG levels has
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been linked to improvements in this disease. Initially,
the reduction of intermediate density lipoprotein (IDL)
was considered the first-line therapy for this condi-
tion. TG-rich LDL testing is also increasingly used in
the diagnosis and management of metabolic diseases
such as abdominal obesity [5], metabolic disturbance
[6], diabetes mellitus [7], and non-alcoholic fatty liver
disease [8].
Composition and metabolic
mechanism of LDL-TG
LDL (density (d) = (1.019-1.063) kg/L) is composed of
a complex mixture of particles. In addition to choles-
terol, its lipid moiety is mainly made up of phospho-
lipids and triglycerides. The LDL lipoprotein has four
binding parts: cholesterol, triglycerides, phospholipids,
and apolipoprotein B. Under physiological conditions,
LDL-TG levels were found to be only about 5% of
LDL-C levels on a molar basis [9].
Under physiological conditions (fasting TG levels
< 1.129 mmol/L), hydrolysis of TG efficiently converts
very low-density lipoprotein (VLDL) to LDL. This
process is catalyzed by lipoprotein lipase (LPL)
­ a standard peroxidase system. The principle of this
and hepatic lipase (HL) when LDL particles are
­predominantly large, buoyant and have low TG concen-
trations [10]. In contrast, the cholesterol ester transfer
protein (CETP) is activated in hypertriglyceridemia
to mediate the exchange of TG and c­ holesterol ester
(CE) between VLDL and LDL, leading to increased
LDL-TG concentrations. Meanwhile, LPL hydrolyzes
VLDL-TG into ILDL-TG, and ILDL is converted to
LDL under the action of HL and LPL. Subsequently,
LDL-TG is remodeled to small dense low-density
­lipoprotein (sdLDL) by the action of LPL and the
dominant HL. Reduced HL activity may also contri-
bute to increased LDL-TG, so the other causes of
reduced HL activity, such as hypothyroidism [11] and
476
chronic kidney disease [12], may induce an increase in
LDL-TG and IDL particles. Furthermore, LPL activity
has been shown to be associated with insulin resistance
in type 2 diabetes, although impaired LPL activity may
also result in increased LDL-TG content. This concept
is illustrated in figure 1 (by Figdraw).
Methodological of LDL-TG detection
Traditional methods for separating and measuring
LDL-TG include electrophoresis, density gradient
ultracentrifugation, and high-performance liquid chro-
matography (HPLC). Ultracentrifugation separates
LDL subfractions from LDL based on the particle
radius and molar ratio [13] but the required equipment
is expensive, and its operation is poorly reproducible.
Electrophoresis is often limited by its low specificity
and resolution. In contrast, HPLC separates compo-
nents according to the size of the particle [14], but it
requires more instruments and complex operating
steps. These techniques are not easily implemented for
routine clinical testing since they are neither simple nor
comprehensive.
The emergence of the homogenization method (Denka
Seiken, Tokyo, Japan) allowed LDL-TG detec-
tion by an automatic biochemical analyzer (Hitachi
7180 or Beckman AU400), using the hydrophilic-
lipophilic equilibrium as the basic principle [9]. Step
1: LPL breaks down TG-rich lipoproteins (TRLs)
and high-density lipoprotein (HDL) in the presence
of surfactant 1 and cholesterol esterase. The released
TG generates hydrogen peroxide under the action of
lipoprotein lipase, glycerol kinase and glycerol-3-phos-
phate oxidase. Hydrogen peroxide is enzymatically
cleaved to water and oxygen to produce a non-chro-
mogenic product. Step 2: Surfactant 2 reacts with LDL,
and LDL-TG generates a color-developing product in
homogeneous assay for LDL-TG is depicted in figure 2
(by Figdraw). The LDL-TG homogeneous assay was
evaluated for precision, linearity, and comparison with
ultracentrifugation according to Clinical and Labora-
tory Standards Institute guidelines EP05-A3, EP06-A,
and EP09-A3, respectively. Total CVs of precision were
within 4.0%. The intra- and inter-assay CVs on quality
control samples with low and high LDL-TG levels were
1.57% and 1.06%, respectively, and 2.38% and 1.60%,
respectively. The assay exhibited linearity up to 0.88
mmol/L and a lower detection limit of 0.022 mmol/L.
Furthermore, the method established reference intervals
for normal individuals based on age and gender [9]. The
automated homogeneous analysis of LDL-TG showed
Ann Biol Clin, vol. 81, n° 5, septembre-octobre 2023
 Low-density lipoprotein triglycerides: A marker for metabolic diseases

VLDL-TG
apo B100 apo C apo E
fibrates

LPL insulin
inflammatory cytokines
resistance
CETP
ILDL-TG

HL LPL
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LDL-TG sdLDL

CE LPL
TP inhibition

GFR Ca2+
ApoAV
activation

statins thyroid hormone Estrogen

MACESs

Figure 1. LDL-TG metabolism.

Inflammatory cytokines, insulin resistance, thyroid hormone, MACEs, Estrogen, statins, fibrates and other factors regulate LDL-TG by
influencing various aspects of LDL-TG metabolism.

a strong correlation with the gold standard ultracentri-
fugation method compared to other methods, and the
bias between the two methods (the homogeneous assay
and ultracentrifugation method) met the bias accep-
tance criteria. The homogenization method features
extremely high consistency between serum and plasma
results, and serum samples remain stable under refrige-
rated conditions (2-8 °C) for three months, unaffected
by two continuous freeze-thaw cycles. Moreover, the
homogeneous phase assay system is simple to operate
and has high specificity.
Cardiovascular disease and
chronic inflammation
The onset and progression of cardiovascular illnesses
and blood lipid metabolism are two major study
areas in recent years. The molecular mechanisms of
blood lipid subcomponents and related conditions are
also increasingly explored. The correlation between
TG and cardiovascular disease risk has been esta-
blished. Remnant-like particle cholesterol (RLP-C)
[15], a by-product of TG metabolism, is bound by
­macrophages and enters the arterial wall to generate
foam cells, which promote atherosclerosis without
chemical modification compared to LDL. TRLs also
exert atherogenic effects and are related to the deve-
lopment of CVD [16].
Multiple studies have demonstrated the correlation
between LDL-TG and the development of CVD. In
a study of metabolic syndrome in school children,
Tonouchi R et al. reported a significant association
between LDL-TG and all stages of metabolic syn-
drome (non-abdominal obesity, abdominal obesity,
pre-metabolic syndrome, and metabolic syndrome)
[6]. Considering that metabolic syndrome is an inde-
pendent risk factor for CVD [17], LDL-TG metabolism
may also be associated with the development of CVD.
Ito Y et al. studied a large sample of 12,284 cases in
Kyushu, Japan, reporting significantly raised LDL-TG
levels in hyperlipidemia patients, which were positively
associated with the progression of hyperlipidemia [9].

Ann Biol Clin, vol. 81, n° 5, septembre-octobre 2023 477

 Synthesis

TRLs Step 1
HDL

surfactant 1
LPL cholesterol esterase

glycerol kinase
glycerol-3-phosphate
Non oxidase catalase
LDL-TG H2O2 H20+O2
LPL
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Step 2
LDL

surfactant 2

glycerol kinase
glycerol-3-phosphate
oxidase peroxidase
red
LDL-TG H2O2 product
LPL

Figure 2. LDL-TG assay.

Step 1: LPL breaks down TRLs and HDL in the presence of surfactant 1 and cholesterol esterase. The released TG generates hydrogen
peroxide under the action of lipoprotein lipase, glycerol kinase and glycerol-3-phosphate oxidase. Hydrogen peroxide is enzymatically
cleaved to water and oxygen to produce a non-chromogenic product.
Step 2: surfactant 2 reacts with LDL; LDL-TG is measured in a standard peroxidase-based system.
CM: chylomicron.

Oxidized LDL is phagocytosed by macrophages in the
subendothelial layer of blood vessels, resulting in the
formation of foam cells with cholesterol as the main
component. This process promotes the development of
atherosclerosis. Furthermore, Feingold KR reported
the simultaneous enrichment of macrophages with
cholesterol and TG [18]. These findings may corrobo-
rate the atherogenic effect of LDL-TG.
LDL-TG is related to the risk of CVD occurrence, which
is an independent risk factor for the occurrence of CVD,
and may be related to metabolic disorders of RLP-C
involved in LDL-TG [19]. A study by Marz W et al.
revealed that altered LDL metabolism, characterized
by high LDL-TG, was positively associated with CAD,
mild systemic inflammation and vascular injury [1]. In
addition, the predictive value of LDL-TG in CAD was
slightly greater than that of LDL-C, which is consistent
with the above findings. Marz W also found that in addi-
tion to the inflammatory markers C-reactive protein
(CRP), serum amyloid A, fibrinogen and interleukin 6,
LDL-TG was also elevated in CAD patients, indicating
the positive association between LDL-TG and systemic
inflammatory markers [1]. T ­ herefore, the TG content in
LDL may be a­ ssociated with inflammation and athe-
rosclerosis formation. LDL-TG is chiefly hydrolyzed
by hepatic lipase. Like lipoprotein lipase, hepatic lipase
is regulated by inflammatory cytokines. The downre-
gulation of lipase ­ provides a partial explanation for
the elevated TG levels during the acute-phase response
[20]. Thus, low-grade systemic inflammation may be the
cause rather than the consequence of elevated LDL-TG
levels. Further observations revealed that LDL-TG was
associated with both CAD and circulating adhesion
molecules (independently of CRP) [21], suggesting that
the TG-rich LDL may be a pro-inflammatory agent.
Moreover, LDL-TG was negatively correlated with
serum adiponectin levels, which are believed to exert
both anti-inflammatory and cardioprotective effects.
Existing evidence indicates that low-grade inflammation
is a risk factor for cardiovascular events, but evidence

478 Ann Biol Clin, vol. 81, n° 5, septembre-octobre 2023

 Low-density lipoprotein triglycerides: A marker for metabolic diseases
on harmful substances and increased inflammatory
­response of vessel walls remain insufficient. Due to the
lack of ­evidence on endogenous lipid metabolism and
inflammatory pathways, further studies are required to
explore the mechanisms between them and LDL-TG.
However, some findings do not support the associa-
tion between LDL-TG and CVD. A study showed
that LDL-TG could not predict the occurrence of
cardiovascular events, but the experiment also had
some limitations [22]. All the selected cases took ­statin
lipid-lowering drugs to normalize LDL metabolism
and reduce systemic inflammation, all selected cases
were men, and the lack of inter-laboratory standardi-
zation of assay methodology was a potential confoun-
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ding factor.
Insulin resistance and type 2 diabetes
Relevant evidence suggests that increased insulin
­resistance (assessed by HOMA-R score) plays a crucial
role in regulating LDL-TG levels [23]. Tonouchi R also
found that both total LDL-TG and LDL-TG subfrac-
tions were negatively correlated with insulin resistance
to some extent, regardless of gender [6]. Insulin resis-
tance has also been shown to be associated with risk
factors for cardiovascular disease [24]. These findings
indicate that insulin resistance may be one of the major
factors in LDL-TG metabolism and may influence the
distribution of TG in the LDL subcomponents. Fur-
ther studies revealed that the regulation of insulin
sensitivity is influenced by hepatocyte hepatic lipase
promoter region gene polymorphisms, which may pre-
dict the transition from impaired glucose tolerance to
type 2 diabetes, further affecting the LDL-TG content.
The conversion of TG from VLDL to LDL is triggered
by CETP, and HL then catalyzes TG in LDL to form
sdLDL [25]. Therefore, increasing CETP and decrea-
sing HL results in the production of TG-rich LDL and
can increase LDL-TG levels [7]. Insulin resistance is
reported to modulate HL activity, which is associated
with the progression of type 2 diabetes [26]. The small
dense low-density lipoprotein-cholesterol (sdLDL-C)
content decreases after insulin treatment [7]. In addi-
tion, high sdLDL-C content was correlated with the C
peptide content. High levels of fasting C peptide reflect
hyperinsulinemia caused by endogenous insulin resis-
tance, and insulin resistance may be an effective upregu-
lation factor of sdLDL levels. However, this experiment
showed no significant correlation between insulin or C
peptide and LDL-TG, and further studies are required
to confirm the results.
Ann Biol Clin, vol. 81, n° 5, septembre-octobre 2023
LDL-TG and non-alcoholic fatty
liver disease
Non-alcoholic fatty liver disease (NAFLD) is the
most common type of liver lesion [27]. From mild to
severe, liver lesions can be categorized into simple fatty
liver disease, non-alcoholic steatohepatitis (NASH),
and NASH-related cirrhosis. The staging of NAFLD
mostly relies on liver biopsy. In recent years, a greater
proportion of non-viral hepatitis liver cancer developed
from NASH has been observed [28]. NAFLD is closely
associated with central adiposity [29]. Its pathogenesis
­originates from insulin resistance, which leads to ­hepatic
steatosis. In some individuals, increased oxidative stress
from steatosis may cause steatohepatitis, fibrosis, and
cirrhosis. The majority of patients with NAFLD also
have hyperlipidemia, and growing evidence suggests
that the condition is associated to hepatic lipid meta-
bolism disorders.
Yuki F reported a significant elevation in serum
LDL-TG levels and the ratio of LDL-TG to LDL-C
(LDL-TG/LDL-C) in a small sample study of NASH
patients [27]. LDL-TG / LDL-C was not ­substantially
correlated with the degree of hepatocyte steatosis, but
its ratio was significantly elevated in lobular liver inflam-
mation, balloon-like changes, and fibrosis. ­ Possible
mechanisms for the above observation are discussed
below. HL binds to glycans on the surface of hepatic
sinusoidal endothelial cells to promote the lipolysis
of TG in LDL. However, imaging of NASH patients
revealed disordered hepatic sinus function, as evi-
denced by the decreased uptake of ultrasound contrast
microbubbles by Kupffer cells [30]. Thus, the changes
in HL activity in NASH patients may be responsible
for the disturbed LDL-TG metabolism. Furthermore,
CETP regulates the conversion of TG between various
lipoproteins, and CETP inhibition can lead to fatty
liver and insulin resistance [31]. Therefore, CETP acti-
vity is related to LDL-TG to some extent. Moreover,
increased TG-rich VLDL levels are associated with
insulin resistance in NASH patients [32], and TG-rich
VLDL may be a precursor of TG-rich LDL, which
may also be implicated in the metabolism of LDL-TG
in NASH patients.
LDL-TG and other diseases
Estrogen and LDL-TG metabolism: Applebaum DM
et al. found that estrogen induces inhibition of HL, which
further leads to elevated levels of TG in LDL, and may
partially explain the high TG levels in women during
pregnancy or lactation [33]. However, some ­ studies
479
 Synthesis
concluded the opposite, reporting about 10% higher
LDL-TG levels in men than in women [33]. The reason
for the discrepancy may be that other factors are invol-
ved in regulating the differential metabolism of LDL-TG
between men and women or differences in inclusion crite-
ria and treatment regimens between the two experiments.
Hypothyroidism and LDL-TG metabolism: HL a­ ctivity
is also reduced during hypothyroidism [34], resulting in
a further elevation in TG content in LDL. In addition,
other mechanisms may also participate in LDL-TG
metabolism. Thyroid hormone improves CETP acti-
vity, and thyroid hormone also stimulates LPL to
break down TG-rich lipoproteins. It can hydrolyze
HDL2 to HDL3, contributing to the conversion of
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IDL to LDL, which is further converted to sdLDL.
Thyroid hormone also upregulates apolipoprotein AV,
which is thought to play a major role in the regulation
of TG metabolism [35]. Since both estrogen and thy-
roxine participate in the metabolism of TG between
lipoproteins by regulating HL, so the metabolic
changes and lipid regulatory mechanisms in pregnant
women with hypothyroidism should also be explored
in depth. Nevertheless, some studies reported that the
degree of atherosclerosis and thyroxine levels are posi-
tively correlated [36]. In contrast to the above results,
the cause may be related to the potential existence of
various pathways and processes in lipid and hormone
metabolism.
Chronic kidney disease and LDL-TG metabolism:
reduced glomerular filtration rate is a risk factor for
the development of CVD. Furthermore, glomerular fil-
tration rate may be negatively correlated to LDL-TG
content in patients suffering from major adverse car-
diovascular events (MACEs) [37]. However, this cor-
relation needs further verification. Chronic renal
impairment can affect the concentration of calcium
ions in hepatocytes and high calcium is a potential
factor for abnormal cellular function in chronic renal
failure. This further impairs hepatic lipase activity and
leads to elevated LDL-TG levels, which may explain
the elevated LDL-TG in patients with MACEs and
renal impairment [38]. On the contrary, MACEs impair
hepatic lipase activity due to chronic inflammation and
other factors, causing abnormal lipid metabolism. The
accumulation of LDL-TG and other lipids can cause
damage to glomerular thylakoid cells and endothelial
cells. Meanwhile, oxidized LDL can promote the pro-
duction of extracellular matrix by thylakoid cells and
induce apoptosis of glomerular thylakoid cells. These
effects exacerbate glomerulosclerosis and the prolifera-
tion of renal interstitial thylakoid cells, which may lead
to renal impairment.
480
Lipid-lowering drugs and LDL-TG metabolism: studies
have found that statins cause a decrease in LDL-TG
[7]. Statins mainly reduce cholesterol in LDL and have
relatively little effect on TG. Meanwhile, statins exert
many non-lipid-lowering effects, including inhibiting
atherosclerosis, which may be one of the mechanisms
involved in LDL-TG decline. Fibrates drugs lead to
increased LDL-TG levels in type 2 diabetes, suppor-
ting our new finding that LDL-TG is not ultimately
regulated by plasma TG levels, as fibrates mainly
lower TG. The specific mechanism may be that fibrates
increase LDL size. Thus sdLDL levels decreases and
large buoyant LDL (lb-LDL) levels increase, resulting
in the TG content in lb-LDL being more than twice
that in sdLDL [39]. The result may eventually lead to
an increase in TG content.
Discussion
In summary, current research on LDL-TG has focused
on metabolic diseases, particularly cardiovascular-­
related dyslipidemia. These studies on LDL-TG have
yielded several additional findings compared to other
biomarkers. It has been indicated that total LDL-TG
was a valuable predictor for metabolic disturbance
in children, comparable to non-HDL cholesterol
(non-HDL-C) and TG/HDL-C [6]. Additionally,
LDL-TG subclass analysis was a more accurate
method for evaluating CVD risks in children with
metabolic disturbance than LDL-C. Furthermore,
additional studies have indicated that LDL-TG levels
can serve as a predictor of atherosclerotic cardiovascu-
lar disease (ASCVD) beyond LDL-C, even after adjus-
ting for age, sex, risk factors, TG, HDL-C, and LDL-C
[1, 5, 7]. These studies indicate that LDL-TG may better
reflect the atherogenic potential of LDL than LDL-C.
Moreover, abundant evidence indicates that low-grade
systemic inflammation is predictive of CVD. LDL-TG
levels were more closely associated with the inflamma-
tory marker CRP than LDL-C and non-HDL-C [7].
Further findings demonstrate that LDL-TG, although
positively related to systemic markers of inflamma-
tion, is an independent risk factor of CAD [1]. Besides,
­studies found that the predictive power of LDL-TG
was superior to that of RLP-C, which represents athe-
rosclerotic TRL remnants [19]. Furthermore, studies in
NASH have demonstrated that the diagnostic efficiency
of LDL-TG for NASH is higher than that of the stan-
dard marker serum glycans and cytokeratin-18 [8].
Recent studies suggest that non-HDL-C levels may be
a more accurate predictor of developing atherosclerotic
diseases than LDL-C levels. As an emerging biomar-
Ann Biol Clin, vol. 81, n° 5, septembre-octobre 2023
 Low-density lipoprotein triglycerides: A marker for metabolic diseases
ker, non-HDL-C has the advantage over LDL-C of
including remnant cholesterol and being independent
of triglyceride variability. Therefore, due to the dearth
of relevant research, it is necessary to conduct further
investigations into the association between LDL-TG
and non-HDL-C levels regarding lipid metabolism and
the progression of related diseases.
The metabolic mechanisms of LDL-TG and related
lipid subfractions under physiological or pathologi-
cal conditions need further investigation. Subsequent
experiments should focus on the following aspects:
(1) CETP, CE, HL, and LPL are involved in the
­synthesis and catabolism of LDL-TG. Its activators or
inhibitors can be used as supplementary therapeutic
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targets for lipid reduction. These metabolic enzymes
may also be involved in other pathophysiological meta-
bolic reactions, such as LPL gene mutations [40], and
have been shown to participate in the pathological
process of hyperlipidemic acute pancreatitis. The rela-
tionship between related diseases and LDL-TG is also
a direction that can be explored in the future.
(2) The diagnostic and predictive value of LDL-TG
for cardiovascular-related diseases has been inferred,
but experimental results on the correlation between
LDL-TG levels and the severity of cardiovascular-re-
lated diseases are relatively scarce, which could be the
focus of future research.
(3) The relationship between non-HDL-C, RLP-C,
sdLDL, TGs, etc. and LDL-TG and their metabolic
mechanisms in related diseases remains elusive and
requires further study.
(4) The practical applications of these results in large-
scale clinical studies also need to be determined. Using
these lipoprotein parameters as markers of cardiovas-
cular disease could provide new options for routine
­clinical treatment.
Disclosures: None of the authors have any conflicts of
interest to disclose.
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