Search citation statements

Order By: Relevance

Paper Sections

Select...
3
2

Citation Types

0
6
0

Year Published

1993
1993
2022
2022

Publication Types

Select...
7
1

Relationship

0
8

Authors

Journals

citations
Cited by 8 publications
(6 citation statements)
references
References 36 publications
0
6
0
Order By: Relevance
“…APOA4 modulates the activation of LPL by APOC2 (Goldberg et al, 1990) and participates in reverse cholesterol transport (Stein et al, 1986). The transcription of APOA4 is regulated synchronously with that of APOA1, supporting the relationship between these apolipoproteins (Malmendier, Alaupovic & Brewer, 1991) and APOA4 is associated with TG and HDL levels. APOA5 is a component of HDL and regulates TG levels via hydrolysis of TG-rich lipoproteins and endocytosis of lipoprotein remnants (Forte, Shu & Ryan, 2009).…”
Section: Introductionmentioning
confidence: 56%
“…APOA4 modulates the activation of LPL by APOC2 (Goldberg et al, 1990) and participates in reverse cholesterol transport (Stein et al, 1986). The transcription of APOA4 is regulated synchronously with that of APOA1, supporting the relationship between these apolipoproteins (Malmendier, Alaupovic & Brewer, 1991) and APOA4 is associated with TG and HDL levels. APOA5 is a component of HDL and regulates TG levels via hydrolysis of TG-rich lipoproteins and endocytosis of lipoprotein remnants (Forte, Shu & Ryan, 2009).…”
Section: Introductionmentioning
confidence: 56%
“…Hypertriglyceridemia was significantly higher in severe VL cases than mild/moderate group. Lipid disorders along with hypertriglyceridemia in VL cases have been reported earlier but none of them has ever studied the correlation between magnitude of serum triglyceride and the disease severity [16][17][18][19][20][21][22][23][26][27][28]. Recently, a study conducted on in vitro development of Leishmania donovani promastigotes exhibited that triglycerides are very much essential for Leishmania parasite growth [31].…”
Section: Discussionmentioning
confidence: 97%
“…The first case was reported in 1982 that described lipid disorders in an adult patient with kala-azar [16]. Thereafter, several studies revealed lipid disorders in children with active VL [17][18][19][20][21]. Severe hypocholesterolemia with reduced serum lipoprotein-alpha was reported in an adult patient with VL [22].…”
Section: Introductionmentioning
confidence: 97%
“…Therefore, in patients with VL, the reduction in HDL and LDL lipoproteins may be because of sequestration and degradation of these lipoproteins in the spleen and liver, which are organs that have high concentrations of Leishmania. 6,12 Other hypotheses to explain the reduction of HDL in serum include cytokine release during the acute phase response of the disease, which would have an inhibitory effect on lecithin cholesterol acyltransferase. 13 Furthermore, hypergammaglobulinemia and elevated serum b2-microglobulin levels described in VL patients 6,14 can affect cholesterol metabolism via the formation of immune complexes between HDL and antibodies, which would accelerate lipoprotein degradation, or the impairment of lipoprotein lipase activity, which is responsible for breaking down lipoproteins in the plasma so that the tissue can absorb its components, mainly cholesterol.…”
Section: Discussionmentioning
confidence: 99%