Sentences with phrase «tg reductions»

ApoC - III ASO — mediated plasma TG reductions in mice on a high - fat diet depends on hepatic LDLR and LRP1.
A usual consequence of enhanced lipolysis via LPL and TG reduction is an increase in HDL cholesterol levels.
ApoC - III ASO — mediated plasma TG reduction in mice on a chow diet depends on hepatic LDLR and LRP1.

Not exact matches

Examination of brain homogenates from immunized TG mice revealed no effect on monomeric human AS as compared with vehicle - treated animals, but a 45 % reduction in oligomeric AS and a trend toward reduction of human AS dimers.
In addition to the reduction in total numbers of activated microglia in AFF 1 - treated TG mice, it is of note that costaining studies indicated that those activated microglia that did emerge in treated mice were highly colocalized with recalcitrant (proteinase K - resistant) AS aggregate as compared to untreated PDGF - AS mice.
A comparable reduction in plasma TG levels occurred after heparin injection of mice treated with ApoC - III ASO (Figure 7A).
The iLpldf mice presented with elevated plasma TG and cholesterol levels (Supplemental Figure 5, C and D, respectively), along with a dramatic increase in VLDL TGs and a reduction in HDL cholesterol levels (Supplemental Figure 5, E and F), as observed in patients with LPL deficiency (16).
To examine whether hepatic clearance via these receptors contributed to an ApoC - III ASO — mediated reduction of plasma TGs, we administered the ApoC - III ASO for 4 weeks to mice lacking LDLR (Ldlr — / ---RRB-, HSPGs (Ndst1fl / fl Alb - Cre +), or hepatic LRP1 (Lrp1fl / fl Alb - Cre +), and to mice lacking various pairs of these receptors (depicted in Figure 1B).
We used a previously described tamoxifen - inducible, Lpl - deficient mouse model (Lplfl / fl Actb - MerCreMer +, referred to herein as iLpldf mice) to further assess the in vivo contribution of LPL to the reduction of plasma TGs by ApoC - III ASO (22).
Nevertheless, the reduction in plasma TG and cholesterol levels induced by ApoC - III ASO did not enhance hepatic steatosis (Figure 5, E and F) or induce weight gain or loss in the mice (Supplemental Figure 4).
We also present evidence that TRLs with reduced ApoC - III content do not affect lipolysis and that a reduction in LPL expression and activity does not suppress the impact of ASO inhibition on lowering plasma TG levels.
These findings suggest that an ASO - mediated reduction of plasma TG levels depends on LDLR and LRP1.
ApoC - III reduction enhances TG clearance via LDLR and LRP1 in animals fed a high - fat diet.
Hepatic ApoC - III reduction enhances postprandial TG clearance via LDLR and LRP1.
We show that an ApoC - III ASO — mediated reduction of plasma TGs is mediated predominantly through inhibition of hepatic TRL clearance via the LDL / LRP1 axis.
A reduction in TG levels also did not cause hepatic steatosis (Figure 3, A and B) or increase the production of ketone bodies (Figure 3C), and at most had only a modest effect on circulating nonesterified free fatty acid (NEFA) levels (Figure 3D).
Reduction in TPO antibodies ranged from 50 % -99 %, while reduction of TG antibodies ranged from 31 - 95 % over the course of 17 - 2Reduction in TPO antibodies ranged from 50 % -99 %, while reduction of TG antibodies ranged from 31 - 95 % over the course of 17 - 2reduction of TG antibodies ranged from 31 - 95 % over the course of 17 - 22 months.
The person was tested a total of 6 times, at the start, 3, months in, then 9, 14, 16 and 21 months after eradication.A pattern of reduction was seen within 3 months, and between month 16 and 21, TPO dropped from 100 kU / L to 45 kU / L, while TG dropped from 283 kU / L to 94 kU / L.
A pattern of reduction was seen within 3 months, and between month 16 and 21, TPO dropped from 100 kU / L to 45 kU / L, while TG dropped from 283 kU / L to 94 kU / L.
The other patients in the treatment group also showed patterns of reduction in TPO and TG antibodies.
One patient who started with TPO = 4745 kU / L, TG = 1783 kU / L was able to see a reduction in thyroid antibodies, from 4745 to 45 over the course of 21 months, and TG from 1783 kU / L to 94 kU / L.
CONCLUSIONS: Dietary supplementation with physiological doses of Se seems to be effective in preventing a reduction in thyroid echogenicity after 6 months of treatment and in reducing TPO - Ab and Tg - Ab after 12 months, but does not modify TSH or FT4.
The largest reduction occurred in hepatic TG content (− 85 %), whereas IMCLs accumulation in the skeletal muscle decreased by 38 %.
The EPRO / UFA condition resulted in a greater reduction in TGs and very low density lipoprotein (VLDL) cholesterol (18.5 % and 18.6 % respectively) than during the refined - carbohydrate condition (2.5 % and 3.6 % respectively).
With respect to TG antibodies, 8 people saw a reduction, 5 people did not see a change, and 2 saw an increase.
Though this was not explicit in the fact sheet, FAA's claim of a 10 million ton reduction in carbon dioxide over a five year period refers exclusively to commercial domestic flights, as evidenced by the data cited: 196 Tg in 2000 down approximately 10 million metric tons to 186 Tg in 2005.
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