5 replies to this topic

[Crepulance]

Moderators, please don't move this. It is pertinent here because many res users supplement with quercetin.

Here is the question. If you are currently taking quercetin, please post whether or not you are overweight (or just your weight), how much Q you take, and how long you've been taking it. Also post if you believe you've lost, or curbed your weight since you've started taking it.

I was looking through the clinical trials right now and there is a clinical trial about to get underway where they are trying to figure out if quercetin inhibits glucose absorption into the bloodstream, lowering weight, helping with diabetes.

Was weird to see a quercetin trial when we have so many quercetin users here.

So anyway, feel free to post any observations you Q users may have noticed in terms of weight loss or weight gain deterrance.


Cheers

Crep

[drmz]

searching pubmed again.

Resveratrol amplifies profibrogenic effects of free fatty acids on human hepatic stellate cells.Bechmann LP, Zahn D, Gieseler RK, Fingas CD, Marquitan G, Jochum C, Gerken G, Friedman SL, Canbay A.
Division of Gastroenterology and Hepatology, University Hospital Essen, Essen, Germany.

Aim: To ascertain whether resveratrol affects the expression of free fatty acids (FFA)-induced profibrogenic genes, death receptors, and/or apoptosis-related molecules in human hepatic stellate cells, using the LX-2 cell line. Methods: Cells were cultured in the presence of FFAs (2:1 oleate : palmitate) and subsequently treated with resveratrol. Gene expression rates were determined by quantitative real-time PCR. The 50% lethal dose (LD(50)) of resveratrol in the presence of FFAs was assessed with the MTT viability test. Results: Compared to vehicle controls, incubation of LX-2 cells with 0.5 mM FFAs induced profibrogenic genes (alpha-SMA x 2.9; TGF-beta1 x 1.6; TIMP-1 x 1.4), death receptors (CD95/Fas x 3.8; TNFR-1 x 1.4), and anti-apoptotic molecules (Bcl-2 x 2.3; Mcl-1 x 1.3). Subsequent addition of 15 microM resveratrol (LD(50) = 23.2 microM) significantly (P < 0.05) upregulated further these genes (alpha-SMA x 6.5; TGF-beta1 x 1.9; TIMP-1 x 2.2; CD95/Fas x 13.1, TNFR-1 x 2.1; Bcl-2 x 3.6; Mcl-1 x 1.9). Importantly, this effect was only observed in the presence of FFAs. Conclusion: Resveratrol amplifies the profibrogenic activation of human hepatic LX-2 stellate cells. This finding raises the possibility that in obese patients with elevated FFAs reserveratrol could provoke hepatic fibrogenesis. In-vivo studies are necessary to further validate this conclusion.

[maxwatt]

searching pubmed again.

Resveratrol amplifies profibrogenic effects of free fatty acids on human hepatic stellate cells.Bechmann LP, Zahn D, Gieseler RK, Fingas CD, Marquitan G, Jochum C, Gerken G, Friedman SL, Canbay A.
Division of Gastroenterology and Hepatology, University Hospital Essen, Essen, Germany.

Aim: To ascertain whether resveratrol affects the expression of free fatty acids (FFA)-induced profibrogenic genes, death receptors, and/or apoptosis-related molecules in human hepatic stellate cells, using the LX-2 cell line. Methods: Cells were cultured in the presence of FFAs (2:1 oleate : palmitate) and subsequently treated with resveratrol. Gene expression rates were determined by quantitative real-time PCR. The 50% lethal dose (LD(50)) of resveratrol in the presence of FFAs was assessed with the MTT viability test. Results: Compared to vehicle controls, incubation of LX-2 cells with 0.5 mM FFAs induced profibrogenic genes (alpha-SMA x 2.9; TGF-beta1 x 1.6; TIMP-1 x 1.4), death receptors (CD95/Fas x 3.8; TNFR-1 x 1.4), and anti-apoptotic molecules (Bcl-2 x 2.3; Mcl-1 x 1.3). Subsequent addition of 15 microM resveratrol (LD(50) = 23.2 microM) significantly (P < 0.05) upregulated further these genes (alpha-SMA x 6.5; TGF-beta1 x 1.9; TIMP-1 x 2.2; CD95/Fas x 13.1, TNFR-1 x 2.1; Bcl-2 x 3.6; Mcl-1 x 1.9). Importantly, this effect was only observed in the presence of FFAs. Conclusion: Resveratrol amplifies the profibrogenic activation of human hepatic LX-2 stellate cells. This finding raises the possibility that in obese patients with elevated FFAs reserveratrol could provoke hepatic fibrogenesis. In-vivo studies are necessary to further validate this conclusion.

I've gone blind trying to count the leading zeros, but aren't the in vitro concentrations they used to get these results several orders of magnitude greater than serum levels that can be achieved from oral feeding of resveratrol?

[Crepulance]

Umm guys, I was asking about quercetin, not resveratrol. Did I miss something in the write up that mentioned quercetin?

[maxwatt]

Umm guys, I was asking about quercetin, not resveratrol. Did I miss something in the write up that mentioned quercetin?

Well, this is the resveratrol forum. If you want evaluation of quercetin, you will get a better response in the supplements forum, which is a parent forum to this one. Many knowledgeable people post there who do not even read the resveratrol forum. I am not going to more the topic for you. You can repost under supplements and put a link to that post here.

[Crepulance]

I understand that, but a lot of people who take res, supplement it with Quercetin, so this is also a good place to post.


Crep

Umm guys, I was asking about quercetin, not resveratrol. Did I miss something in the write up that mentioned quercetin?

Well, this is the resveratrol forum. If you want evaluation of quercetin, you will get a better response in the supplements forum, which is a parent forum to this one. Many knowledgeable people post there who do not even read the resveratrol forum. I am not going to more the topic for you. You can repost under supplements and put a link to that post here.