Do fruits/ vegetation contain compounds, which help the digestive
system to regulate the absorption of fructose? If so, what are they?
Yes, many polyphenols (e.g. resveratrol, curcumin, quercetin, anthocyanins, phloretin, etc.) do this and much more. Each fruit and vegetable has its polyphenol composition. There are other beneficial fruit and vegetable compounds as well, but I'll talk only about polyphenols in the current post.
Sucrose is split by digestive enzymes (sucrase, glycoside hydrolase) in the small intestine into fructose and glucose. These enzymes are inhibited by polyphenols.
Glucose is transported by SGLT1, while fructose is transported by GLUT5 into enterocytes in the intestines. After that the cells transport these sugars with GLUT2 into the blood. Polypheonls can inhibit these transporters and decrease their expression.
Fructose and glucose is transported to the liver from the blood, with GLUT2, and they do nasty things in there. Fructose is more dangerous than glucose, because it is transformed without any regulation. It uses the same pathways as glucose and mostly fatty acids are created from it, which increase the blood VLDL, LDL, FFA level and cause insulin resistance. The byproducts are urate and free radicals, which cause hyperuricaemia and oxidative stress. Hyperuricaemia cause decreased NO levels (by counteracting with eNOS and reacting with NO directly), which cause increased blood pressure due to vasoconstriction. Hyperuricaemia damages the liver and the kidney too. Too high urate levels enhance LDL oxidation as well, which cause atherosclerosis. The free radicals deplete the antioxidants of the body and cause cancer. Polyphenols prevent atherosclerosis, restore NO levels, restore urate levels, scavenge free radicals, counteract with insulin resistance and prevent liver and kidney damage. So they can fix most of the problems fructose cause.
The interactions of gallic acid and tannic acid with purified brush
border sucrase (EC 188.8.131.52) from mouse intestine have been studied.
These findings indicate that both gallic acid and tannic acid inhibit
sucrase activity, which is pH dependent.
The effects of tea polyphenols on the sucrase activity are shown in
Table .1. Among 10 compounds, esterified (gallated) polyphenols (ECg,
EGCg, TF2A, TF2B, and TF3) were potent inhibitors.
Quercetin reduced the effect of sucrase and maltase in the in vivo and
in vitro treatments.
In conclusion quercetin and its glycoside derivatives have alfa-glucosidase inhibitory activity and high peroxyl radical scavenging-linked antioxidant activity. The above benefits (anti-hyperglycemia and antioxidant activity) of quercetin and its glycoside derivatives taken together could support the evidence that diets rich in fruits and vegetables are associated with lower incidences of oxidation-linked diseases such as diabetes
Phloretin (Ph), which can be obtained from apples, apple juice, and cider, is a known inhibitor of the type II glucose transporter (GLUT2).
The ATPase inhibitor quercetin, which inhibits tumor glycolysis, was shown to be a glucose transport inhibitor like the chemically related compound phloretin.
Glucosides of some other flavonoid classes such as naringenin-7-O-glucoside, genistein-7-O-glucoside and cyanidin-3,5-O-diglucoside were ineffective as well. Thus, dietary quercetin monoglucosides, for example, Q3G and Q4G, have an impact on intestinal nutrient transporters such as SGLT1 and related systems.
Excessive post-prandial glucose excursions are a risk factor for developing diabetes, associated with impaired glucose tolerance. One way to limit the excursion is to inhibit the activity of digestive enzymes for glucose production and of the transporters responsible for glucose absorption. Flavonols, theaflavins, gallate esters, 5-caffeoylqunic acid and proanthocyanidins inhibit α-amylase activity. Anthocyanidins and catechin oxidation products, such as theaflavins and theasinsensins, inhibit maltase; sucrase is less strongly inhibited but anthocyanidins seem somewhat effective. Lactase is inhibited by green tea catechins. Once produced in the gut by digestion, glucose is absorbed by SGLT1 and GLUT2 transporters, inhibited by flavonols and flavonol glycosides, phlorizin and green tea catechins.
In addition, curcumin suppressed glut2 expression by stimulating the activity of peroxisome proliferator-activated receptor-gamma (PPARγ) and de novo synthesis of glutathione. In conclusion, hyperglycemia stimulated HSC activation in vitro by increasing intracellular glucose, which was eliminated by curcumin by blocking the membrane translocation of GLUT2 and suppressing glut2 expression.
This study investigated the effects of an anthocyanin-rich berry-extract on glucose uptake by human intestinal Caco-2 cells. Acute exposure (15 min) to berry extract (0.125%, w/v) significantly decreased both sodium-dependent (Total uptake) and sodium-independent (facilitated uptake) 3H-D-glucose uptake. In longer-term studies, SGLT1 mRNA and GLUT2 mRNA expression were reduced significantly. Polyphenols are known to interact directly with glucose transporters to regulate the rate of glucose absorption. Our in vitro data support this mechanism and also suggest that berry flavonoids may modulate post-prandial glycaemia by decreasing glucose transporter expression.
RES increased SIRT1 expression, but decreased the expression of GLUT5 and aldolase B in aortas from HFr-fed rats. These results suggest that RES contributes to the restoration of HFr-induced vascular dysfunction in rats, at least in part, by up-regulation of SIRT 1 and down-regulation of GLUT5 and aldolase B in the aorta. Moreover, RES may have a positive influence on vasculature by partly restoring the plasma arginine:ADMA ratio and leptin levels.
The present study demonstrates that resveratrol is more effective than metformin in improving insulin sensitivity, and attenuating metabolic syndrome and hepatic oxidative stress in fructose-fed rats.
Quercetin supplementation improved some risk factors of cardiovascular disease, yet exerted slightly pro-inflammatory effects.
In conclusion, dietary HFCS causes vascular insulin resistance and endothelial dysfunction through attenuating IRS-1 and eNOS expressions as well as increasing iNOS in rats. Resveratrol has capability to recover HFCS-induced disturbances.
The major flavonoid is Quercetin, which belongs to the class called flavonols and is mainly found in apples, tea, onions, nuts, berries, cauliflower, cabbage and many other foods. It exhibits a wide range of biological functions including anticarcenogenic, anti-inflammatory and antiviral; it also inhibits lipid peroxidation, platelet aggregation and capillary permeability. This review focuses on the main effects of Quercetin on obesity and diabetes.
These results indicate that resveratrol ameliorated FF A-induced insulin resistance by regulating mTOR and p70-S6K phosphorylation in skeletal muscle cells, through a mechanism involving sirtuins.
Resveratrol, trans-4-hydroxystilbene, pterostilbene, polydatin, and mulberroside A were found to have antihyperuricemic activities. The uricosuric and nephroprotective actions of resveratrol and its analogues were mediated by regulating renal organic ion transporters in hyperuricemic mice, supporting their beneficial effects for the prevention of hyperuricemia.
Adult male Wistar rats were treated with a normal or high-fat/sucrose diet (HFS) with or without Res for 13 weeks. HFS and in vitro treatment with high glucose increased hyperpermeability in rat aorta, heart, liver and kidney and cultured bovine aortic endothelial cells (BAECs), respectively, which was attenuated by Res treatment. Application of Res reversed the changes in eNOS and Cav-1 expressions in aorta and heart of rats fed HFS and in BAECs incubated with high glucose. Res stimulated the formation of NO inhibited by high glucose in BAECs.
In summary, all 3 tea polyphenol extracts induced weight loss and anti-inflammatory and angiogenic effects, although the tissue content of polyphenols differed significantly.
Blackcurrants and lingonberries, as either whole berries or nectars, optimize the postprandial metabolic responses to sucrose. The responses are consistent with delayed digestion of sucrose and consequent slower absorption of glucose.
Resveratrol prevented the HFS-induced arterial wall inflammation and the accompanying increase in PWV. Dietary resveratrol may hold promise as a therapy to ameliorate increases in PWV.
Taken together the data suggest that dietary flavonoids exhibit three distinct modes of action with regard to cancer prevention, based on their hydroxyl and methoxy decoration: (1) inhibitors of CYP1 enzymatic activity, (2) CYP1 substrates and (3) substrates and inhibitors of CYP1 enzymes.
These data demonstrate that resveratrol inhibits CYP1A1 expression in vitro, and that it does this by preventing the binding of the AHR to promoter sequences that regulate CYP1A1 transcription. This activity may be an important part of the chemopreventive activity of resveratrol.
As a chemoprevention agent, resveratrol has been shown to inhibit tumor initiation, promotion, and progression, as well as inhibit the growth of cancerous cells through increased apoptosis and/or cell cycle blockage. Inflammatory processes are associated in the pathogenesis of many chronic diseases including heart disease and cancer. Resveratrol has been shown to reduce inflammation via inhibition of prostaglandin production, cyclooxygenase-2 activity, and nuclear factor-кB activity. In addition, the estrogenic activity of resveratrol may help prevent post-menopausal bone loss.
These findings suggest that fructose-induced metabolic syndrome is attenuated by the polyphenol-rich fraction of amla.