Sentences with phrase «tg levels»

Women also showed improvements in testosterone, cholesterol and TG levels.

Lowering of plasma TG levels after injection of [3H] triolein - labeled Liposyn particles was associated with a greater uptake of [3H] triolein in the liver, but not in organs such as the heart or skeletal muscle (Figure 8F), as would be expected if LPL activity were enhanced.

(E) Plasma TG levels of fasted mice before and after injection of 100 μl 20 % Liposyn II particles at the indicated time points.

ApoC - III ASO treatment reduced TG levels in chylomicrons, VLDL, and remnant particles in all of the mutants as measured by size - exclusion fast protein liquid chromatography (FPLC)(Figure 2, A — E), but had no effect in Ldlr — / — Lrp1fl / fl Alb - Cre + mice (Figure 2F).

Together, these findings suggest that the major mechanism by which ApoC - III affects plasma TG levels functions independently of LPL.

As reported by Noh et al. (43), tamoxifen transiently increases plasma TG levels, which return to normal 2 weeks after the last administration.

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).

Again, ApoC - III ASO treatment had no effect on plasma TG levels in mice lacking both Lrp1 and Ldlr (Figure 5, A and C), as observed with animals fed a standard chow diet (Figure 1) and under postprandial conditions (Figure 3).

These findings suggest that an ASO - mediated reduction of plasma TG levels depends on LDLR and LRP1.

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.

However, an increase in plasma TG levels also occurs in ApoC - III — transgenic mice that are deficient in ApoE (20, 35).

However, a recent clinical study showed that lowering plasma ApoC - III levels with volanesorsen, a generation 2.0 + ApoC - III — specific antisense oligonucleotide (ASO), dramatically lowered elevated plasma TG levels in patients who have genetic defects in LPL (familial chylomicronemia syndrome [FCS]-RRB-(16).

In chow - fed animals, ApoC - III ASO reduced fasting plasma TG levels by 30 % to 45 % in animals defective in hepatic Ndst1 and Ldlr and in animals with combined deletions of Ndst1 and Lrp1 or Ldlr (Figure 1, D and E).

However, the ASO had no effect on plasma TG levels in mice lacking both Lrp1 and Ldlr (Ldlr — / — Lrp1fl / fl Alb - Cre +)(Figure 1, D and E).

Elevated plasma TG levels represent a risk factor for CVD in humans, and an adjusted analysis of patients in the Framingham Heart Study suggests that each decrease of 1 mg / dl in plasma ApoC - III levels is associated with a 4 % decrease in CVD risk (11), further supporting the potential therapeutic benefit of suppressing plasma ApoC - III levels in humans to reduce CVD.

Plasma TG levels were determined 2 weeks after the last tamoxifen injection.

Total cholesterol and TG levels in plasma were determined using kits from Genzyme or Thermo Fisher Scientific.

(E) Liver TG levels in mutant mice on a high - fat diet treated for 5 weeks with control or ApoC - III ASO (n = 3 — 5 / group).

(D) Fasting plasma TG levels in mutant mice treated for 4 weeks with control or ApoC - III ASO (n = 5 — 10 / group).

We determined that a murine - specific ApoC - III — targeting ASO reduces fasting TG levels through a mechanism that is dependent on low - density lipoprotein receptors (LDLRs) and LDLR - related protein 1 (LRP1).

The high - fat diet raised plasma TG levels in Ldlr — / — , Ldlr — / — Ndst1fl / fl Alb - Cre +, and Ldlr — / — Lrp1fl / fl Alb - Cre + mice, reaching values of 515 to 1,045 mg / dl (Figure 5A).

However, the ApoC - III ASO did not lower TG levels in mice lacking both LDLR and LRP1.

Similarly, inactivating mutations affecting the expression of APOC3 in humans led to reduced plasma TG levels (8) and protection against CVD (9 — 11).

While LPL - deficient patients had higher TG levels than were detected in the LPL - deficient mice, the TG levels in the mice were not dissimilar from those seen in patients who strictly adhered to a low - fat diet that might be viewed as the equivalent of mouse chow.

A comparable reduction in plasma TG levels occurred after heparin injection of mice treated with ApoC - III ASO (Figure 7A).

Total cholesterol and TG levels were determined enzymatically as described above.

Large - scale genetic and clinical investigations are needed to clarify the effects of pharmacologic lowering of LDL - C and TG levels to gauge dysglycemic associations.»

Michael V. Holmes, M.D., Ph.D., of the University of Oxford, England, and colleagues examined the associations of LDL - C, HDL - C, and TG levels with CAD and diabetes through mendelian randomization (MR) using conventional MR and making use of newer approaches using genetics.

An analysis using genetics finds that increased low - density lipoprotein cholesterol (LDL - C), high - density lipoprotein cholesterol (HDL - C), and possibly triglyceride (TG) levels are associated with a lower risk of diabetes, and increased LDL - C and TG levels are associated with an increased risk of coronary artery disease, according to a study published online by JAMA Cardiology.

Increased LDL - C, HDL - C, and possibly TG levels were associated with a lower risk of diabetes.

«Although further studies are needed to examine whether specific pathways or lipid subtypes are implicated, our findings inform potential expected downstream consequences of interventions affecting lipid traits and provide cautionary evidence that therapeutics that lower LDL - C and TG levels may have dysglycemic [abnormal blood sugar levels] effects,» the authors write.

Lipoprotein lipid profile disturbances associated with an elevated TG level include low High Density Lipoprotein (HDL) cholesterol and HDL particle (HDL - P), and a predominance of small dense Low Density Lipoprotein (LDL) and LDL particle (LDL - P).

Not exact matches

As a model of IAPP aggregation, we used Tg mice overexpressing hIAPP at four - to fivefold levels of endogenous mouse IAPP (Janson et al., 1996).

Fasting blood glucose level became significantly higher in animals injected with Tg - hIAPP pancreas homogenate containing IAPP aggregates, as early as 8 wk compared with mice treated with WT pancreas extracts (Fig. 4 A).

Glucose levels continued increasing in the Tg / Tg groups throughout the course of the experiment.

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).

Since sucrose is one - half fructose, it appears that the level of dietary fructose is quite important in the rapid development of IR and hyper - TG in hamsters.

At these levels, the residual activity could be due to other lipases that cross-react in the TG hydrolysis assay (e.g., hepatic lipase, hormone - sensitive lipase, or adipose TG lipase).

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).

Treatment of iLpldf mice with ApoC - III ASO decreased Apoc3 mRNA levels (Figure 8A) and protein expression (Supplemental Figure 6A) and reduced plasma TGs (Figure 8B) and TGs in CR / VLDL particles (Figure 8C).

A usual consequence of enhanced lipolysis via LPL and TG reduction is an increase in HDL cholesterol levels.

This residual risk has shifted attention to elevated plasma triglyceride (TG) levels, which constitute an independent risk factor for coronary artery disease.

Hypertriglyceridemia is an independent risk factor for cardiovascular disease, and plasma triglycerides (TGs) correlate strongly with plasma apolipoprotein C - III (ApoC - III) levels.

Good day Please give me advice I had TG Antibodies = 28680 in 2016 year TG Antibodies = 17000 in 2017 year TG Antibodies = 6600 in 2018 year (TSH ~ norm) All last year I used Gluten free diet, every day took Selenium (200mcg), Omega 3, Milk Thistle, and Glutamine, I have good level of D3, B12, Ferritin, Мg I use enzymes and probiotics..

At a mechanistic level, thyroid autoimmunity induced by iodine is associated with synthesis of TG antibodies and the unmasking of a cryptic epitope of thyroglobulin, which is normally sequestered and unavailable to the immune system (19).

In individuals with anti-thyroid peroxidase (TPO) or anti-thyroglobulin (TG) antibodies, the incidence of elevated TSH increased with greater levels of iodine intake (18).

In fact, groups with the aforementioned thyroid diseases, as well as individuals with positive TG or TPO antibodies, have been demonstrated to exhibit significantly higher levels of urinary iodine, the main indicator of iodine nutritional status, compared to healthy controls (3).

Birth control pills do provide some benefits but also have been shown to increase LDL cholesterol, TG, CRP and Insulin levels in teens and adult women with PCOS and should be used with caution.

Chris, is is possible that ldl - p can rise substantially with rapid and significant weight loss in order to clear the higher level of TG being released from fat stores?

Transgenic (Tg) mice overexpressing FGF21 are markedly smaller than wild - type mice and have a corresponding decrease in circulating IGF - 1 concentrations despite having elevated growth hormone (GH) levels....