1 counts show the anti-inflammatory effects of
salsalate.
2 Salsalate (
3.5 g/d) or placebo orally over 30 months.
3 ly 2011) to 48 weeks of placebo (n = 140) or
salsalate,
3.5 g/d (n = 146), in addition to current the
4 Salsalate,
a nonacetylated prodrug of salicylate, has be
5 In conclusion,
salsalate activates BAT, presumably by directly activati
6 sgenic mouse model of FTD, administration of
salsalate after disease onset inhibited p300 activity, l
7 ion could explain some beneficial effects of
salsalate and aspirin in humans.
8 ents and no difference in change between the
salsalate and placebo groups (mean difference, -1 mm3; 9
9 p300-induced tau acetylation is inhibited by
salsalate and salicylate, which enhance tau turnover and
10 We found that
salsalate attenuated and reversed high-fat diet-induced
11 by synthetic derivatives such as aspirin and
salsalate,
both of which are rapidly broken down to sali
12 acid, and triglyceride levels decreased with
salsalate,
but weight and low-density lipoprotein choles
13 ved in these beneficial metabolic effects of
salsalate by treating mice with salsalate during and aft
14 of a second transcription factor inhibitor,
salsalate,
did not change this result.
15 Mild hypoglycemia was more common with
salsalate;
documented events occurred only in patients t
16 kout (AMPK-beta1KO) mice were treated with a
salsalate dose resulting in clinically relevant serum sa
17 c effects of salsalate by treating mice with
salsalate during and after development of high-fat diet-
18 ufficient to warrant recommending the use of
salsalate for type 2 diabetes at this time.
19 One hundred ninety participants (89 in the
salsalate group and 101 in the placebo group) completed
20 , and bilirubin levels were decreased in the
salsalate group compared with the placebo group, while h
21 s and atrial arrhythmias more common, in the
salsalate group compared with the placebo group.
22 c level over 48 weeks was 0.37% lower in the
salsalate group than in the placebo group (95% CI, -0.53
23 rine albumin concentrations increased in all
salsalate groups compared with placebo.
24 s of glycemic control also improved in the 3
salsalate groups, as did circulating triglyceride and ad
25 The salicylate prodrug
salsalate has been shown to improve metabolic parameters
26 indicate that the primary mechanism by which
salsalate improves glucose homeostasis and NAFLD is via
27 Salsalate improves glucose intolerance and dyslipidemia
28 Salsalate improves glycemia in patients with T2DM and de
29 Short-duration studies show that
salsalate improves glycemia in type 2 diabetes mellitus
30 In the Targeting Inflammation Using
Salsalate in Cardiovascular Disease (TINSAL-CVD) trial p
31 were randomly assigned to receive placebo or
salsalate in dosages of 3.0, 3.5, or 4.0 g/d for 14 week
32 cient to determine long-term risk-benefit of
salsalate in T2DM.
33 Salsalate increased brachial artery flow-mediated dilati
34 Salsalate increased expression of the inhibitor of NF-ka
35 of differentiated T37i brown adipocytes with
salsalate increased uncoupled respiration.
36 Salsalate is a dimeric form of salicylic acid that has b
37 Salsalate is a prodrug of salicylate that lowers blood g
38 Salsalate lowers HbA1c levels and improves other markers
39 These results suggest that
salsalate may be useful in reducing vascular injury and
40 fifty-seven participants were randomized to
salsalate (
n = 129) or placebo (n = 128).
41 articipants were analyzed (placebo, n = 137;
salsalate,
n = 146).
42 Salsalate (
nonacetylated salicylate, 4500 mg/d), a compo
43 f this study is to investigate the effect of
salsalate on vascular injury and repair in a rat model o
44 However, the effect of
salsalate on vascular injury has not been determined.
45 The beneficial effect of
salsalate on vascular injury was associated with upregul
46 ns reached in plasma after administration of
salsalate or of aspirin at high doses, salicylate activa
47 23, 2008, and July 5, 2012, to 30 months of
salsalate or placebo in addition to standard, guideline-
48 ation during placebo (P<0.001) but not after
salsalate (
P=0.23).
49 tions in concomitant diabetes medications in
salsalate recipients than in placebo recipients.
50 In men,
salsalate reduced 11beta-HSD1 expression in subcutaneous
51 Salsalate reduced nitrotyrosine (P=0.06) and expression
52 ates AMPK via the beta1 subunit, but whether
salsalate requires AMPK-beta1 to improve T2D and NAFLD h
53 Mechanistically,
salsalate selectively promoted the uptake of fatty acids
54 Treatment with
salsalate significantly decreased the intima-to-media ra
55 Salsalate treatment decreased total white blood cell, ly
56 The present study shows that
salsalate treatment decreases vascular damage caused by
57 Higher proportions of patients in the 3
salsalate treatment groups experienced decreases in HbA1
58 Salsalate treatment increased VO2, lowered fasting gluco
59 Salsalate treatment was started in female Zucker fatty r
60 L, P< or =0.0001 versus placebo) by day 4 of
salsalate treatment.
61 Moreover,
salsalate upregulated Ucp1 expression and enhanced glyce
62 Two weeks' administration of
salsalate was also investigated in a randomized double-b
63 brachial artery flow-mediated dilation with
salsalate was inversely related to baseline flow-mediate
64 The tau-lowering and protective effects of
salsalate were diminished in neurons expressing K174Q ta
65 Salsalate when added to current therapies that include a