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cool. so, oj with meals, or at least with big ones!
cool. so, oj with meals, or at least with big ones!
Well it clearly wasnt the sugar, as glucose water did the opposite. So what was it?
We previously showed that the intake of 75 g (300 kcal) glucose induced an acute increase in reactive oxygen species (ROS) generation and inflammation as reflected in an increase in nuclear transcription factor κB (NF-κB) binding, a decrease in the expression of inhibitory κB-α, and an increase in inhibitory κB kinases in peripheral blood mononuclear cells (MNCs) (1, 2). An increase in NF-κB binding is associated with an increase in tumor necrosis factor-α (TNF-α) expression, activator protein-1 binding, early growth response factor-1 expression and binding, plasma matrix metalloproteinase (MMP)-2 and -9, and tissue factor after glucose intake (3). In terms of oxidative and inflammatory stress, a similar response follows the intake of a high-fat, high-carbohydrate (HFHC) meal (4). In contrast, the intake of orange juice containing sucrose, glucose, and fructose (total sugar content: 75 g = 300 kcal) does not cause an increase in ROS generation or NF-κB binding (5). In addition, hesperetin and naringenin, 2 major flavonoids that are contained in orange juice, but not ascorbic acid, are able to suppress ROS generation by MNCs in vitro by >50% (5). Toll-like receptor (TLR) 2 is the specific receptor for lipopeptides and peptidoglycans from gram-positive bacteria, and TLR4 is the specific receptor for lipopolysaccharide (LPS) or endotoxin from gram-negative bacteria (6, 7). TLR4 was also shown to play an important role in the pathogenesis of atherosclerosis (8–11), diet-induced obesity, and the related insulin resistance (12, 13), whereas TLR2 was shown to be involved in ischemia-reperfusion–induced myocardial injury (14). In a recent study (15) we showed that there was a significant increase in plasma concentrations of endotoxin and an increase in TLR4 and TLR2 expression in MNCs after the intake of an HFHC meal. This increase of endotoxemia induced by a fatty meal was also confirmed in previous reports in human and rodents (16–18). This increase could contribute to and prolong the inflammatory response that follows the intake of such a meal. Whether this increase of endotoxemia is due to the lipid solubility of endotoxin and its absorption into the circulation with the fat contained in the meal or is secondary to other factors such as the inflammation of the intestinal epithelium is not clear. If it is secondary to other factors, the potential antiinflammatory effect of orange juice intake could lower postprandial endotoxin increase.
In our recent study (15) we also showed that an HFHC meal induced an increase in the expression of the suppressor of cytokine signaling (SOCS)-3, a key protein responsible for interference with insulin signal transduction by causing the degradation of insulin receptor substrate-1. SOCS-3 is induced by proinflammatory cytokines TNF-α and interleukin (IL)-1β and IL-6. Proinflammatory meals may contribute to the pathogenesis of insulin resistance.
Because orange juice does not cause oxidative and inflammatory stress, and flavonoids in orange juice suppress ROS generation (5), we hypothesized that 1) orange juice is able to lower the increase in ROS generation and the inflammatory response in MNCs and plasma after a HFHC meal, and 2) the concentration of plasma endotoxin and TLR4 and SOCS-3 expression in MNCs, which increase after an HFHC meal, are reduced by the simultaneous intake of orange juice. Such a study is important because chronic oxidative stress and inflammation are the 2 basic mechanisms underlying atherosclerosis (19, 20). Obesity and diabetes are states of chronic oxidative and inflammatory stress and are major risk factors for atherosclerosis (21, 22). MNCs constitute the major cellular group (monocytes and T and B lymphocytes) that participate in intramural atherosclerotic inflammation and are known to be in a proinflammatory state in obese individuals who carry a high risk of atherogenesis and have a chronically elevated food intake (23). Furthermore, inflammatory factors contribute to interference with insulin signal transduction and insulin resistance.
The data presented in this article emphasize that the intake of glucose and a HFHC meal are profoundly and rapidly proinflammatory, that this process occurs at the cellular and molecular level, that specific proinflammatory genes are activated after the intake of glucose and a HFHC meal, and that these changes are observed in MNCs that participate in vascular inflammation.
@Westside PUFAs @haidut @ecstatichamster @ShirtTieFitness @schultz @Giraffe @taraWe were surprised to find no increase in glucose concentrations at 1 h after the orange juice intake. Indeed, even when orange juice was taken with the fast-food meal, there was no change in glucose concentrations. Although we do not have any data on blood glucose concentrations between 0 and 60 min, and it is possible that there may have been a peak of glucose during this period, it is also quite clear that there was no evidence of a significant change in blood glucose concentrations after orange juice intake at 60 min. In contrast, blood glucose concentrations were still elevated in the groups drinking either glucose or water with the meal. We tested the possibility that orange juice might interfere with our glucose assay. Our data show that adding orange juice to water, a glucose standard, or plasma did not interfere with glucose measurement (data not shown). We previously reported a higher insulin-to-glucose ratio after orange juice intake compared with that after glucose intake (5). However, in that report, there was a greater increase in glucose concentrations after orange juice intake. This difference is probably the result of the use of recently pasteurized, well-refrigerated orange juice in the current study in contrast to orange juice from a large can of reconstituted juice from a supermarket that was used repeatedly. Clearly, more experiments need to be done to address glucose-insulin relations after orange juice intake and the possible mechanisms underlying this preliminary observation. It is possible that incretin mechanisms are involved in the genesis of this phenomenon.
Was it the high fructose corn syrup? I stopped drinking it 6 months ago and don't miss it at all.Oranje juice with everything. It's the only thing I can drink while eating apart from red bull. I switched to coca cola the last few days and I feel like ***t right now. Coca cola not even once. Something bad is in that drink.
No, I'm in Spain and it has real sugar. There is something wrong in it, I don't know what.Was it the high fructose corn syrup? I stopped drinking it 6 months ago and don't miss it at all.
The polyphenols, at least in part.Well it clearly wasnt the sugar, as glucose water did the opposite. So what was it?
In Europe pepsi has no citric acid. I have noticed many times I tolerate it better than coke, but I checked again and coke has no citric acid on the label here either, not sure what is the difference between the two then.pepsi (some) has citric acid, ive never seen coke with citric acid only phosphoric. i noticed something off last time i bought a pack of mexicoke and haven't bought any since. Maybe something was wrong with the syrup but @Lucenzo01 is in spain and mine is from mexico it was like a weird metallic chlorine taste
Vitamin C enhances bioavailability of iron from plants not heme iron from meat. Heme iron is already bioavailable and doesn't needed Vitamin C.@Sucrates
Good stuff there, thanks for the links.
Lately however, I've read about the toxic effects of combining a high iron meal - say meat, with a high source of Vitamin C - say OJ.
So the question is, what is the takeaway here?
OJ will reduce inflammation of a high fat meal - MEAT, but it may do more harm than good at the same time via reaction of VitC. Or will it?
Vitamin C enhances bioavailability of iron from plants not heme iron from meat. Heme iron is already bioavailable and doesn't needed Vitamin C.