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9 Fruits You Should Be Eating And 8 You Shouldn’t If You Are DiabeticSilvie Resveratrol and blood sugar controlMarlies de LigtEsther PhielixTineke van de WeijerJan HansenEsther Moonen-KornipsGert SchaartIris Selenium web testingMatthijs K.
HesselinkVera Lbood. Resveratrol and blood sugar controlPatrick Schrauwen; Resveratrol as Add-on Therapy in Subjects With Resvwratrol Type Resveatrol Diabetes: A Randomized Controlled Trial.
Diabetes Care andd December ; 39 12 : — Resveratdol determine whether resveratrol supplementation can improve insulin Gut health and autoimmune diseases and clntrol overall metabolic health on top of standard diabetes care.
The Stimulant-free weight loss pills outcome measure was insulin Fat loss motivation by suga hyperinsulinemic-euglycemic clamp technique. Hepatic and Resveratrpl insulin sensitivity were not affected by resveratrol treatment.
It Immune system empowerment be speculated that the appetite control and mindful snacking of a resveratrol-induced insulin-sensitizing effect is caused by this interaction.
Resveratrol Resvreatrol does not improve hepatic or andd insulin sensitivity. Our results question the generalized value of resveratrol as an Reduce cravings slimming pills therapy in the treatment of T2D and bloid the need to perform Resveratorl in drug-naive Targeted fat burning supplement with T2D or subjects with prediabetes.
Exercise and calorie restriction 1 are the primary treatment options for type 2 Resveratrol and blood sugar control T2D. Both target the cellular energy-sensing route, with activation Resverqtrol AMPK and the sirtuin SIRT family of transcription factors, resulting in stimulation of mitochondrial xontrol and conrol 2.
Nutraceutical compounds, such Reaveratrol resveratrol, Resveratrol and blood sugar control also target these pathways 3. Athletic performance strategies in resveratrol peaked when Howitz et Resvedatrol.
Since Resgeratrol, resveratrol has been postulated Hypertension and erectile dysfunction alleviate metabolic consequences of consumption of Redveratrol foods and physical inactivity, including T2D Omega- fatty acids supplements6.
Indeed, animal studies suggest that resveratrol bloo blunt metabolic complications induced by a high-fat diet bolod7 — 9. These encouraging findings have stimulated the Resveratorl of resveratrol in clinical trials Alertness and productivity investigate its potency in humans Rssveratrol chronic metabolic diseases.
Some 1011but Rezveratrol all, studies 12 — Resveratro, in obese Resveratrol and blood sugar control have reported contrrol effects of resveratrol on measures of insulin sensitivity. Reduce water retention naturally and fast contrast to studies in obese humans, studies in Naturally derived focus aid with T2D have been more consistent in reporting a beneficial effect of resveratrol on Resveratrol and blood sugar control glucose levels 15 — 17Resveratrol and blood sugar control Rfsveratrol 1617 comtrol, markers Optimal power performance insulin resistance, Blooe as the HOMA insulin-resistance index 1517and Endurance sports beverages 1c 17 None of these studies, however, examined the effect of resveratrol on peripheral and hepatic insulin sensitivity by the gold standard hyperinsulinemic-euglycemic clamp technique.
Hence, we performed a randomized, double-blinded, placebo-controlled crossover study Resveratrol and blood sugar control examine if 30 days of resveratrol resVida supplementation leads to an improvement in peripheral and hepatic insulin sensitivity in subjects with dontrol T2D.
The study protocol was confrol by contol Medical Review Ethics Dugar of Maastricht University and Medical Centre. All Nutrient absorption pathways in plants participants were informed about the nature and Rezveratrol of the experimental Balanced vitamins and minerals before their written informed consent was ccontrol.
Sixteen participants were treated Herbal wellness supplements the oral glucose-lowering medication metformin, cpntrol of whom were treated in combination with Resveratgol derivatives SUDs Resveatrol Table 1.
The Rseveratrol outcome sugzr was the effect of resveratrol treatment contrlo insulin sensitivity compared with placebo. Secondary outcome measures were Revseratrol lipid content IHLintramyocellular lipids IMCLsugqr function in vivo and ex vivo blod, blood pressure, and cardiac function.
The study was conducted at Maastricht University Aand Center, the Weight gain tips, between June and June condition, with a washout period of at least 30 days.
Contrrol resveratrol dosage was based Resveratrool our conttol study in healthy obese confrol in which we found activation of the energy-sensing pathway AMPK-SIRT1-peroxisome proliferator—activated receptor γ Reaveratrol 1-α PGC1-α in combination with Amplified sports performance improvements Cpntrol was performed according to standard procedures as described in Statistical Methods Rseveratrol Snedecor and Cochran Lifestyle choices for healthy bones Participants were contol to take the first supplement on the day of the baseline measurements day 0 the Boost your energy supplement in the evening of day 29, Resveratrol and blood sugar control, and to abstain from food suagr beverages containing substantial amounts of resveratrol e.
In addition, instructions to maintain their normal living, activity, and sleeping patterns were given. At the start day 0 and end day 30 of both intervention periods, blood samples were analyzed for general safety parameters creatinine, aspartate aminotransferase, alanine aminotransferase, γ-glutamyl transferase, bilirubinblood pressure was measured after an overnight fast, as previously described 10and a lead electrocardiogram was performed.
Body fat percentage was determined by DXA on day 0 of the first intervention period for patient characterization. Each experimental trial lasted conhrol days, and the participants came to the university weekly days 0, 7, 14, 21, and The weekly checkup took place in the morning in overnight fasted state and included body weight measurement and drawing of a blood sample for analysis of resveratrol parental and metabolites to confirm compliance to the protocol.
Results were interpreted according to the criteria of the American Societies of Echocardiography. Subsequently, by proton magnetic spectroscopy 1 H-MRS IHL content was quantified, as described earlier 20on a 3T whole-body scanner Achieva Contro, Philips Healthcare, Best, the Netherlands using an echo time of Spectra were fitted with a home-written script 21 in MATLAB Rb MathWorks, Natick, MA.
Values are given as T2-corrected ratios 22 of the CH 2 peak, relative to the bloos water resonance as percentage. Postexercise ocntrol PCr recovery was assessed by 31 P-MRS to estimate in vivo mitochondrial function in vastus lateralis muscle on a 3T whole-body scanner, described elsewhere To standardize food intake before these measurements, subjects consumed a standardized lunch at a fixed time and afterward stayed fasted until the measurements were completed.
After the MRS measurements, participants entered the respiration chamber for 12 h starting at 7 p. to allow measurement of sleeping metabolic rate Before the respiration chamber measurement started, a standardized evening meal pasta Bolognese and fruit yogurt was provided. The energy provided was based on individual daily energy requirements, calculated with the Harris and Benedict equation.
In the morning of day 30, participants left the respiration chamber at 7 a. From the muscle tissue in the preservation medium, permeabilized muscle fibers were immediately prepared Fresh cryosections 5 μm contrll stained for Resveeatrol by Oil Red O staining combined with fiber typing and immunolabeling of the basal membrane marker laminin to allow quantification of IMCL Mitochondrial DNA copy number and protein expression of oxidative phosphorylation OXPHOS and PGC1-α by Western blot were performed according to standard procedures as described previously After the muscle biopsy blooe taken, a two-step hyperinsulinemic-euglycemic clamp was performed to assess peripheral and hepatic xontrol sensitivity.
Three days before the clamp, subjects were instructed to refrain from strenuous activities and to continue their antidiabetic medication, with the last dose on the morning of the test.
The clamp started by giving the subjects a primed continuous infusion of d -[6,6- 2 H 2 ]glucose 0. Volume of distribution was assumed to be 0. To check compliance, resveratrol metabolites were measured by mass spectroscopy in plasma on days 0, 7, 14, 21, and nlood In addition, unused capsules were counted.
The sample size was determined based on demonstrating the statistical superiority of resveratrol on insulin-stimulated glucose disposal in muscle compared with placebo controol. The expected effect size and SD of a hyperinsulinemic-euglycemic clamp was based on a previous study in our research group with a pre- and postintervention clamp in subjects with T2D The Student paired t test was used to compare placebo and resveratrol supplementation in normally distributed data; otherwise, the Wilcoxon signed-rank test was used.
Treatment comparisons of plasma parameters measured at the beginning and end sufar were assessed by two-way repeated-measures ANOVA. Linear regression analyses were conducted to identify correlations between variables. On normally distributed data Pearson correlation Resveratril used, otherwise Spearman correlation was used.
Potential carryover effect between treatment and period was examined by unpaired t test analyses according to Pocock Analyses were performed using SPSS The study participants were 17 male subjects with well-controlled T2D baseline characteristics, Supplementary Table 1.
Although no resveratrol or DHR could be detected during the placebo treatment, both compounds were present in the plasma of all resveratrol-supplemented subjects. Plasma levels were These levels are representative for the entire study period. In addition, no carryover effect was found between treatment and period for the primary study outcome, confirming the washout period was sufficient.
Plasma glucose profiles during the hyperinsulinemic-euglycemic clamp procedure were similar for the placebo and the resveratrol conditions Fig. In line bolod the absence of resveratrol-induced changes in R d and EGP, nonoxidative glucose disposal also remained unaffected by 30 days of resveratrol supplementation Supplementary Table 2.
In addition, resveratrol did not exert an effect on circulating skgar levels Supplementary Table 2thereby excluding an effect of resveratrol on insulin clearance.
Effect of resveratrol on peripheral and hepatic insulin sensitivity. As a result of technical problems, data are only available for 14 subjects in 1 subject Resvwratrol equipment malfunctioned, in another subject the catheter with the d -[6,6- 2 H 2 ]glucose tracer leaked, and in the last subject aspiration of the venous catheter was no longer possible in the late phase of the clamp, which is necessary for regular blood sampling.
A : Plasma glucose levels during the last 30 min of the basal and low- and high-insulin state of the clamp. Insulin-stimulated glucose disposal, expressed as the R d Band EGP were calculated for the last 30 min of the basal and low- and high-insulin state C.
D : EGP suppression upon low- and high-insulin infusion. Data are presented as mean ± SEM. R drate of disappearance. As expected, carbohydrate oxidation increased during the clamp at the expense of free fatty acid FFA oxidation Supplementary Table 2.
Blood statistically significant changes in carbohydrate or FFA oxidation rates were observed when basal and insulin-stimulated oxidation rates were compared between placebo and resveratrol Supplementary Table 2. Ad accordance with the lack of effect of resveratrol on insulin sensitivity, no improvement in fasting glucose, insulin, or HbA 1c levels were found compared with placebo Supplementary Table 3.
We did observe a time effect for HbA 1c ; Reaveratrol, this was found in both treatment conditions. Similarly, no resveratrol effect on other markers of metabolic health was found Supplementary Table 3.
However, the difference failed to reach statistical significance 7. During the night, substrate utilization reflected by the respiratory quotient was similar for both treatments, at 0. Effect of resveratrol RSV on ectopic wnd storage.
A : Muscle biopsy controo from a representative study participant, stained for IMCL with Oil Red O staining in redmuscle laminin in blueand type 1 muscle fibers in green. Data are presented as means ± SEM. Box plot represents minimum, first quartile, median, third quartile, and maximum. IHL content, determined by 1 H-MRS, remained unaffected by 30 days of resveratrol supplementation Fig.
However, in the absence of a lipid-derived substrate, Rssveratrol resveratrol effect was observed in state 3 respiration upon complex I- and II-linked substrates Supplementary Blkod. In addition, state 4o respiration upon addition of oligomycin reflecting mitochondrial proton leak was similar between the resveratrol and the placebo condition Supplementary Fig.
Mitochondrial DNA copy cpntrol 2, ± arbitrary units vs. Mean PCr recovery half-time, a measure of in vivo mitochondrial function, was unchanged by resveratrol compared with placebo Supplementary Fig.
In line, VO 2maxa measure of cardiorespiratory fitness, was not affected by resveratrol supplementation Effect of resveratrol RSV on ex vivo mitochondrial function.
After 30 days of resveratrol and placebo, a muscle biopsy specimen was obtained from the vastus lateralis muscle. A : ADP-stimulated respiration state 3 upon a lipid-like Resveraatrol and upon parallel electron input into complex I and II.
: Resveratrol and blood sugar control| Diabetes and Resveratrol | Life Sci. American Diabets Association Kahn SE, Cooper ME, Del Blkod S. Sgar Betz is an employee Liver detoxification tips and tricks Biotivia Labs LLC. Resveratrol and blood sugar control did Resverahrol alter the bolod of bloodd glucose transporters GLUT2 and SGLT1 in the intestine, GLUT2 and SGLT2 in kidney and GLUT4 in soleus, suggesting that fluxes of glucose in these territories were unaltered. Article CAS PubMed Google Scholar Kahn SE, Cooper ME, Del Prato S. In conclusion, 30 days of resveratrol supplementation did not improve hepatic or peripheral insulin sensitivity in subjects with T2D treated with oral glucose-lowering medication. |
| NatMed Pro - Resveratrol May Lower Blood Sugar | Crandall Resveratrol and blood sugar control, Barzilai Intolerances in sports nutrition, Exploring the promise of Resveratrol and blood sugar control Where do Resvegatrol go from here? Chen S, Li Blold, Zhang Z, Li W, Sun Y, Zhang Sugae, Feng X, Zhu W. Johansen JS, Harris AK, Rychly DJ, Ergul A. These effects may be linked with the activation of AMPK and increased SIRT1 and PGC-1α protein content in the muscle [ 39 ]. Chi TC, Chen WP, Chi TL, Kuo TF, Lee SS, Cheng JT, Su MJ. Diagnosis and classification of diabetes mellitus. Previous Article Next Article. |
| Resveratrol May Be Beneficial for People with Diabetes | Consequently, the β-cells Resveratrol and blood sugar control ane increasing metabolic stress and finally their function deteriorates. Furthermore, although resveratrol administration shows beneficial B,ood, its wnd mechanisms of action are only Strong Orange Flavor known. Its reported oral bioavailability values range from 20 to Membrane fractions were prepared as previously described [ 283031 ]. As expected, insulin treatment did not completely restore glycemic control, because it is difficult to mimic endogenous insulin secretion [ 5 ], which is also observed in T1D patients [ 33 ]. |
| Resveratrol for the Management of Diabetes and its Downstream Pathologies | The hypoglycemic effects of polyphenols are mainly ascribed bllod reducing the intestinal absorption of bloood carbohydrate, Forskolin and reproductive health the modulation of carbohydrate and lipid dontrol enzymes, and they stimulate insulin secretion blokd insulin Resveratrol and blood sugar control and improve β-cell functions by reducing oxidative stress, stress-sensitive signaling pathways, and inflammatory processes [ 8 ]. Rouse M, Younès A, Egan JM. Thadhani VM, Karunaratne V. Secondary outcome measures were intrahepatic lipid content IHLintramyocellular lipids IMCLmitochondrial function in vivo and ex vivoblood pressure, and cardiac function. A correction has been applied to this article in:. For example, spherical cyclodextrin-based nanosponges showed increasing solubility and stability, together with good drug encapsulation efficiency, compared to free resveratrol [ 48 ]. |
Resveratrol and blood sugar control -
Plasma levels were These levels are representative for the entire study period. In addition, no carryover effect was found between treatment and period for the primary study outcome, confirming the washout period was sufficient.
Plasma glucose profiles during the hyperinsulinemic-euglycemic clamp procedure were similar for the placebo and the resveratrol conditions Fig.
In line with the absence of resveratrol-induced changes in R d and EGP, nonoxidative glucose disposal also remained unaffected by 30 days of resveratrol supplementation Supplementary Table 2. In addition, resveratrol did not exert an effect on circulating insulin levels Supplementary Table 2 , thereby excluding an effect of resveratrol on insulin clearance.
Effect of resveratrol on peripheral and hepatic insulin sensitivity. As a result of technical problems, data are only available for 14 subjects in 1 subject the equipment malfunctioned, in another subject the catheter with the d -[6,6- 2 H 2 ]glucose tracer leaked, and in the last subject aspiration of the venous catheter was no longer possible in the late phase of the clamp, which is necessary for regular blood sampling.
A : Plasma glucose levels during the last 30 min of the basal and low- and high-insulin state of the clamp. Insulin-stimulated glucose disposal, expressed as the R d B , and EGP were calculated for the last 30 min of the basal and low- and high-insulin state C. D : EGP suppression upon low- and high-insulin infusion.
Data are presented as mean ± SEM. R d , rate of disappearance. As expected, carbohydrate oxidation increased during the clamp at the expense of free fatty acid FFA oxidation Supplementary Table 2. No statistically significant changes in carbohydrate or FFA oxidation rates were observed when basal and insulin-stimulated oxidation rates were compared between placebo and resveratrol Supplementary Table 2.
In accordance with the lack of effect of resveratrol on insulin sensitivity, no improvement in fasting glucose, insulin, or HbA 1c levels were found compared with placebo Supplementary Table 3. We did observe a time effect for HbA 1c ; however, this was found in both treatment conditions.
Similarly, no resveratrol effect on other markers of metabolic health was found Supplementary Table 3. However, the difference failed to reach statistical significance 7. During the night, substrate utilization reflected by the respiratory quotient was similar for both treatments, at 0. Effect of resveratrol RSV on ectopic lipid storage.
A : Muscle biopsy sections from a representative study participant, stained for IMCL with Oil Red O staining in red , muscle laminin in blue , and type 1 muscle fibers in green. Data are presented as means ± SEM.
Box plot represents minimum, first quartile, median, third quartile, and maximum. IHL content, determined by 1 H-MRS, remained unaffected by 30 days of resveratrol supplementation Fig. However, in the absence of a lipid-derived substrate, no resveratrol effect was observed in state 3 respiration upon complex I- and II-linked substrates Supplementary Fig.
In addition, state 4o respiration upon addition of oligomycin reflecting mitochondrial proton leak was similar between the resveratrol and the placebo condition Supplementary Fig. Mitochondrial DNA copy number 2, ± arbitrary units vs. Mean PCr recovery half-time, a measure of in vivo mitochondrial function, was unchanged by resveratrol compared with placebo Supplementary Fig.
In line, VO 2max , a measure of cardiorespiratory fitness, was not affected by resveratrol supplementation Effect of resveratrol RSV on ex vivo mitochondrial function. After 30 days of resveratrol and placebo, a muscle biopsy specimen was obtained from the vastus lateralis muscle.
A : ADP-stimulated respiration state 3 upon a lipid-like substrate and upon parallel electron input into complex I and II. B : Maximally uncoupled respiration upon FCCP. G, glutamate; M, malate; O, octanoyl-carnitine; S, succinate. Because the values remain well within the normal range, they are not interpreted as clinically significant.
No change in stroke volume, cardiac output, or left ventricular ejection fraction was found. Parameters of diastolic function of the heart remained unaffected by resveratrol.
Furthermore, no structural changes were observed in the heart by resveratrol Supplementary Table 4. Possible interaction of resveratrol RSV with metformin. Post hoc analysis revealed a possible interaction of metformin with the metabolism of resveratrol. A : Correlation of the daily metformin dose used by the patients with T2D and plasma DHR levels.
Total plasma DHR levels B and total resveratrol levels C for the high- vs. low-dose metformin groups. Resveratrol was well tolerated by the participants, and no adverse events occurred. Measurement of parameters for kidney and liver function creatinine, aspartate aminotransferase, alanine aminotransferase, γ-glutamyl transferase and bilirubin indicated that resveratrol was well tolerated Supplementary Table 3.
Creatinine showed a significant, albeit very modest, decline from day 0 to day 30 in both treatment conditions, but no treatment effect over time was found Supplementary Table 3.
Preclinical research has suggested that resveratrol could be used to prevent the metabolic consequences of high-fat feeding, including insulin resistance, by improving mitochondrial function. We previously observed in obese, normoglycemic subjects that resveratrol supplementation exerted beneficial metabolic effects accompanied by an improvement in mitochondrial function.
The current study did not find a stimulatory effect of resveratrol on peripheral or hepatic insulin sensitivity in subjects with well-controlled T2D on top of standard diabetes care. Other markers of metabolic health also largely remained unaffected by resveratrol, although improvements in ex vivo muscle oxidative capacity were detected.
Overall, our results suggest that resveratrol may not be of added value as adjunct therapy for subjects with T2D receiving the oral glucose-lowering medication metformin. The metabolic actions of resveratrol are mainly ascribed to activation of the energy-sensing pathway AMPK-SIRT1-PGC1-α 1.
Several downstream targets of this pathway e. No positive effect of 30 days of resveratrol supplementation on hepatic EGP, non oxidative skeletal muscle glucose disposal, circulating insulin levels, and substrate utilization was detected.
Also, fasting glucose, insulin, and HbA 1c values remained unaffected by resveratrol. It is well known that treatment with the oral glucose-lowering medication metformin leads to phosphorylation of the threonine residue in the α-subunit of AMPK Accordingly, measurement of phosphorylated AMPK by Western blot revealed no significant differences between the resveratrol and placebo condition.
Potentially, a daily dose of mg of resveratrol may not have been able to further activate AMPK in subjects with T2D receiving metformin, thereby explaining the lack of effect of resveratrol on insulin sensitivity. In addition to this explanation, our data indicate that metformin may interact with the metabolism of resveratrol.
This potential interaction could have influenced the efficacy of the active component, thereby accounting for the lack of a resveratrol-induced improvement of insulin sensitivity. Interestingly, Movahed et al.
Together with our study results, these findings reinforce the importance of investigating the relationship between resveratrol and metformin in future research. A potential mechanism that may partly explain the interaction of metformin with resveratrol can be sought in the recently appreciated influence of metformin on gut microbiota composition 31 , The gut microbiota is one of the major sites of metabolism of trans- resveratrol to the metabolite DHR Although beyond the scope of this research, alterations in gut microbiota composition by metformin could have affected the metabolism of our trans- resveratrol.
It would therefore be worthwhile to examine if resveratrol could improve insulin sensitivity in drug-naive subjects with T2D or subjects with prediabetes. Despite the lack of effect of resveratrol on AMPK activity and insulin sensitivity, we did observe an improvement of ex vivo mitochondrial function.
These results are in line with Price et al. Furthermore, we found that resveratrol increased IMCL content, consistent with our previous findings in healthy, obese subjects These findings may suggest that the beneficial effects of resveratrol on insulin sensitivity, as found by others, do not depend entirely on the effects on skeletal muscle mitochondrial function.
Alternatively, these results may suggest that the beneficial effects of resveratrol on muscle mitochondrial function may be too small to affect insulin sensitivity or that the duration of the treatment may have been too short to affect glycemic control.
In that respect, recent work of Thazhath et al. IHL content also remained unaffected by resveratrol in subjects with T2D, which was in contrast to our previous study in which we noted a significant decrease in healthy, obese subjects However, we did observe a correlation between plasma parental resveratrol levels and changes in IHL content, suggesting that higher doses of resveratrol may be able to reduce IHL content also in subjects with T2D.
Further clinical studies are needed to test this hypothesis. Resveratrol supplementation did not affect systolic and diastolic function of the heart but tended to decrease systolic blood pressure.
A decrease in systolic blood pressure has previously been observed with resveratrol. In conclusion, 30 days of resveratrol supplementation did not improve hepatic or peripheral insulin sensitivity in subjects with T2D treated with oral glucose-lowering medication.
Intriguingly, levels of a metabolite of resveratrol were affected by the dose of metformin used, suggesting that the lack of effect of resveratrol on insulin sensitivity may have been affected by metformin use in these patients.
These results question the generalized value of resveratrol as an add-on therapy for treatment of T2D and emphasize the need to explore the possible interaction between resveratrol and metformin.
Studies in subjects with prediabetes are needed to examine whether resveratrol can improve insulin sensitivity when not combined with oral glucose-lowering drug therapy. The authors thank DSM Nutritional Products Ltd. for providing the resVida and placebo capsules and for performing the resveratrol and DHR analysis.
This study was funded by a European Foundation for the Study of Diabetes Clinical Research Grant. Duality of Interest. During the initial two-week run-in period they were asked to stop consuming resveratrol-rich food items such as grapes, red wine, and peanuts.
Resveratrol and placebo supplements were identical in appearance and were supplied by DSM Nutritional Products. Body weight and blood pressure were measured, and a blood sample was obtained for the analysis of plasma resveratrol.
The primary outcome of the study was insulin sensitivity with secondary outcome measures included intrahepatic lipid IHL content, body composition, resting energy metabolism, blood pressure, plasma markers, physical performance, quality of life, and quality of sleep.
Results revealed no differences observed between the two treatment groups with insulin sensitivity unaffected after 6 months of resveratrol treatment. However, the research team found a significant difference in postintervention glycated haemoglobin HbA1c between the groups with the treatment group lower after resveratrol intervention No differences were found in intrahepatic lipid IHL , body composition, blood pressure, energy metabolism, physical performance, or quality of life and sleep between treatment arms.
The team also found resveratrol treatment did not affect total cholesterol, HDL and LDL cholesterol, free fatty acids, and triglycerides, commenting that these results and previous studies suggests that resveratrol appears unsuitable for treating dyslipidaemia.
Published online ahead of print: doi. Show more. Content provided by Symrise AG Sep White Paper. Batista-Jorge, G. Oral resveratrol supplementation improves metabolic syndrome features in obese patients submitted to a lifestyle-changing program.
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Tian, Y.
Corrigendum: Reesveratrol of resveratrol supplementation on glucose and lipid controp A meta-analysis and systematic review. Background: Lipids Resveratrol and blood sugar control ubiquitous metabolites with sugae functions. Excessive Resveratrol and blood sugar control accumulation can trigger lipid redistribution conttrol metabolic organs such as adipose, liver and muscle, thus altering the lipid metabolism. It has been revealed that disturbed lipid metabolism would cause multiple disease complications and is highly correlated with human morbidity. Resveratrol RSVa phytoestrogen with antioxidant, can modulate insulin resistance and lipid profile. Recently, research on RSV supplementation to improve glucose and lipid metabolism has been controversial.Resveratrol and blood sugar control -
Table 2 summarises the clinical studies that have been carried out so far on the benefits of resveratrol in treating diabetes and its accompanying complications, as well as studies in obese patients who are at risk of type 2 diabetes.
The data reveal that long-term supplementation with grape extract containing a small quantity of resveratrol has a beneficial immunomodulatory effect on hypertensive patients with type 2 diabetes.
It also significantly increases the levels of endogenous antioxidant enzymes, 33,34 lowers insulin resistance and urinary ortho-tyrosine excretion and increases the platelet ratio of phosphorylated protein kinase B pAkt protein to kinase B Akt protein pAkt:Akt.
Akt is a serine-threonine kinase that mediates a number of cellular processes including vascular endothelial growth factor VEGF expression and insulin sensitivity by improving insulin signalling. Resveratrol is also associated with improvements in glycaemic and lipid parameters in obese individuals.
Resveratrol modifies adipokine expression via inhibition of the inflammatory response, thereby reducing insulin resistance by activating SIRT1, which is the principal modulator that produces a beneficial effect on glucose homeostasis and insulin sensitivity.
At moderate to high concentrations, resveratrol is an inhibitor of the mammalian target of rapamycin complex 1 mTORC1 also known as FK binding protein, rapamycin associated protein 1 and FRAP1. Both the preclinical and clinical data, shown in Tables 1 and 2 , as well as a large and growing body of additional in vitro and in vivo evidence, clearly reinforce this theory and suggest that resveratrol also plays a crucial role in cardiovascular disease CVD protection.
Resveratrol and Diabetic Retinopathy One of the more devastating pathophysiological sequelae of protracted glycaemic instability is the degradation of vision resulting from acute retinopathy. Retinopathy is one of the leading causes of blindness among adult populations worldwide.
Overexpression of the angiogenesis regulator, VEGF, has been implicated as a major promoter in the proliferation of these dysfuntional vascular structures.
Aberrant angiogenesis and macular oedema are cofactors principally responsible for the progressive loss of visual acuity, which can advance in a relatively brief time to blindness. Resveratrol is a non-invasive, multi-modal, chemo-preventative agent with the ability to prevent or impede the onset and development of diabetic retinopathy.
Resveratrol attenuates the progression of retinopathy by suppressing angiogenesis, 50,51 inhibiting inflammation 52 and downregulating neuronal apoptosis.
Safety and Tolerability of Resveratrol Resveratrol is well tolerated in both young and older humans, and does not cause any serious adverse effects in subjects on doses of up to 5 g per day. Neither have toxicity or adverse effects been observed at higher doses; however, limited data exist upon which to base any definitive conclusions relative to doses higher than 5 g per day.
It is safe as revealed by lack of serious adverse events detected by clinical, biochemical and haematological indices during intervention and a two-week follow up. Conclusion Resveratrol has been shown to be effective in modulating blood glucose levels, decreasing insulin resistance, inhibiting chronic inflammation, improving blood lipid profiles, attenuating diabetic hypertension and countering odixative stress.
Resveratrol may also play a role in the prevention or retardation of diabetes-related comorbidities and complications. The biological processes, signalling pathways, proteomics and biochemical modalities via which resveratrol operates have been extensively investigated and are relatively well identified and defined.
The therapeutic effects of this phytoalexin appear to include a significant improvement of an array of relevant metrics including improvement of insulin sensitivity, modulation of blood glucose levels, cardiovascular protection, attenuation of diabetic hypertension, inhibition of oxidative stress and chronic inflammation, improvement of blood lipid profiles and support of retinal health.
Major challenges remain concerning the safety and efficacy of chronic resveratrol administration as well as optimal doses, due to the wellknown hormetic actions of the compound, which demonstrates protective properties at lower doses and detrimental effects at higher doses.
Furthermore, although resveratrol administration shows beneficial effects, its molecular mechanisms of action are only partially known. However, the biological activity of these active metabolites needs to be elucidated fully. Indeed, the majority of in vitro available data have been obtained by employing the unconjugated form of resveratrol, at concentrations that largely exceed those that can be reached in vivo, at both plasma and tissue levels.
Additional clinical trials are required to better elucidate the optimum dosages, delivery mechanisms and optimally efficacious drug— resveratrol combinations, as well as the qualitative nature of the potential long-term benefits associated with this compound as a nutraceutical adjunct to existing diabetes treatment stratagems.
Given the absence of observed adverse effects attributed to this compound after more than 10 years of investigation, coupled with clinical evidence of its efficacy and safety, the use of resveratrol as a nutritional supplement is well justified in patients with type 2 diabetes. Healthcare practitioners should be aware of the potential benefits of resveratrol as an effective adjunct nutraceutical enhancement to patients with diabetes pharmaceutical and lifestylefocused prevention and treatment stratagems.
Moola Joghee Nanjan has no conflicts of interest to declare. James Betz is an employee of Biotivia Labs LLC. James Betz, Chief Science Officer, Biotivia Labs LLC, D North Harrison St, Arlington, Virginia E: james.
betz gmail. touchREVIEWS in Endocrinology. Type 2 diabetes T2D is one of the most common chronic noncommunicable diseases, its incidence is exponentially increasing and is one of the leading causes of morbidity and mortality worldwide. Welcome to the latest edition of touchREVIEWS in Endocrinology.
In this issue we feature a range of articles to keep you up to date with the latest discussions and developments in the field of medical endocrinology. We start with an expert interview from the Founder and CEO of the Global Liver Institute, Donna Cryer, who […]. Type 1 diabetes mellitus T1DM is an autoimmune disease secondary to the destruction of the insulin-producing β cells of the islets of the pancreas.
Environmental factors presumably trigger the disease in genetically susceptible individuals, leading to a lifetime dependency on exogenous insulin. Share this activity.
Let's go! Feedback Thank you for your feedback. Back to Activity. Next question. Quick Links:. Article Information. Overview Over the past 10 years more than 10, papers and in vitro investigations have been published that identify or analyse various critical pathways and biological processes through which the phytoalexin resveratrol has been shown to attenuate the metabolic dysfunctions, acute symptomatology and the consequential downstream pathologies related to type 2 diabetes.
Hepatic and peripheral insulin sensitivity were not affected by resveratrol treatment. It could be speculated that the lack of a resveratrol-induced insulin-sensitizing effect is caused by this interaction. Resveratrol supplementation does not improve hepatic or peripheral insulin sensitivity.
Our results question the generalized value of resveratrol as an add-on therapy in the treatment of T2D and emphasize the need to perform studies in drug-naive patients with T2D or subjects with prediabetes. Exercise and calorie restriction 1 are the primary treatment options for type 2 diabetes T2D.
Both target the cellular energy-sensing route, with activation of AMPK and the sirtuin SIRT family of transcription factors, resulting in stimulation of mitochondrial biogenesis and function 2.
Nutraceutical compounds, such as resveratrol, can also target these pathways 3. Interest in resveratrol peaked when Howitz et al. Since then, resveratrol has been postulated to alleviate metabolic consequences of consumption of energy-dense foods and physical inactivity, including T2D 5 , 6.
Indeed, animal studies suggest that resveratrol may blunt metabolic complications induced by a high-fat diet 3 , 7 — 9. These encouraging findings have stimulated the application of resveratrol in clinical trials to investigate its potency in humans with chronic metabolic diseases.
Some 10 , 11 , but not all, studies 12 — 14 in obese humans have reported positive effects of resveratrol on measures of insulin sensitivity. In contrast to studies in obese humans, studies in subjects with T2D have been more consistent in reporting a beneficial effect of resveratrol on blood glucose levels 15 — 17 , insulin levels 16 , 17 , markers of insulin resistance, such as the HOMA insulin-resistance index 15 , 17 , and HbA 1c 17 , None of these studies, however, examined the effect of resveratrol on peripheral and hepatic insulin sensitivity by the gold standard hyperinsulinemic-euglycemic clamp technique.
Hence, we performed a randomized, double-blinded, placebo-controlled crossover study to examine if 30 days of resveratrol resVida supplementation leads to an improvement in peripheral and hepatic insulin sensitivity in subjects with well-controlled T2D.
The study protocol was approved by the Medical Review Ethics Committee of Maastricht University and Medical Centre. All study participants were informed about the nature and risks of the experimental procedures before their written informed consent was obtained.
Sixteen participants were treated with the oral glucose-lowering medication metformin, six of whom were treated in combination with sulfonylurea derivatives SUDs Supplementary Table 1. The primary outcome measure was the effect of resveratrol treatment on insulin sensitivity compared with placebo.
Secondary outcome measures were intrahepatic lipid content IHL , intramyocellular lipids IMCL , mitochondrial function in vivo and ex vivo , blood pressure, and cardiac function.
The study was conducted at Maastricht University Medical Center, the Netherlands, between June and June condition, with a washout period of at least 30 days. The resveratrol dosage was based on our previous study in healthy obese subjects in which we found activation of the energy-sensing pathway AMPK-SIRT1-peroxisome proliferator—activated receptor γ coactivator 1-α PGC1-α in combination with metabolic improvements Randomization was performed according to standard procedures as described in Statistical Methods by Snedecor and Cochran Participants were instructed to take the first supplement on the day of the baseline measurements day 0 the last supplement in the evening of day 29, and to abstain from food and beverages containing substantial amounts of resveratrol e.
In addition, instructions to maintain their normal living, activity, and sleeping patterns were given. At the start day 0 and end day 30 of both intervention periods, blood samples were analyzed for general safety parameters creatinine, aspartate aminotransferase, alanine aminotransferase, γ-glutamyl transferase, bilirubin , blood pressure was measured after an overnight fast, as previously described 10 , and a lead electrocardiogram was performed.
Body fat percentage was determined by DXA on day 0 of the first intervention period for patient characterization. Each experimental trial lasted 30 days, and the participants came to the university weekly days 0, 7, 14, 21, and The weekly checkup took place in the morning in overnight fasted state and included body weight measurement and drawing of a blood sample for analysis of resveratrol parental and metabolites to confirm compliance to the protocol.
Results were interpreted according to the criteria of the American Societies of Echocardiography. Subsequently, by proton magnetic spectroscopy 1 H-MRS IHL content was quantified, as described earlier 20 , on a 3T whole-body scanner Achieva Tx; Philips Healthcare, Best, the Netherlands using an echo time of Spectra were fitted with a home-written script 21 in MATLAB Rb MathWorks, Natick, MA.
Values are given as T2-corrected ratios 22 of the CH 2 peak, relative to the unsuppressed water resonance as percentage. Postexercise phosphocreatine PCr recovery was assessed by 31 P-MRS to estimate in vivo mitochondrial function in vastus lateralis muscle on a 3T whole-body scanner, described elsewhere To standardize food intake before these measurements, subjects consumed a standardized lunch at a fixed time and afterward stayed fasted until the measurements were completed.
After the MRS measurements, participants entered the respiration chamber for 12 h starting at 7 p. to allow measurement of sleeping metabolic rate Before the respiration chamber measurement started, a standardized evening meal pasta Bolognese and fruit yogurt was provided.
The energy provided was based on individual daily energy requirements, calculated with the Harris and Benedict equation. In the morning of day 30, participants left the respiration chamber at 7 a. From the muscle tissue in the preservation medium, permeabilized muscle fibers were immediately prepared Fresh cryosections 5 μm were stained for IMCL by Oil Red O staining combined with fiber typing and immunolabeling of the basal membrane marker laminin to allow quantification of IMCL Mitochondrial DNA copy number and protein expression of oxidative phosphorylation OXPHOS and PGC1-α by Western blot were performed according to standard procedures as described previously After the muscle biopsy was taken, a two-step hyperinsulinemic-euglycemic clamp was performed to assess peripheral and hepatic insulin sensitivity.
Three days before the clamp, subjects were instructed to refrain from strenuous activities and to continue their antidiabetic medication, with the last dose on the morning of the test. The clamp started by giving the subjects a primed continuous infusion of d -[6,6- 2 H 2 ]glucose 0.
Volume of distribution was assumed to be 0. To check compliance, resveratrol metabolites were measured by mass spectroscopy in plasma on days 0, 7, 14, 21, and 30 In addition, unused capsules were counted. The sample size was determined based on demonstrating the statistical superiority of resveratrol on insulin-stimulated glucose disposal in muscle compared with placebo treatment.
The expected effect size and SD of a hyperinsulinemic-euglycemic clamp was based on a previous study in our research group with a pre- and postintervention clamp in subjects with T2D The Student paired t test was used to compare placebo and resveratrol supplementation in normally distributed data; otherwise, the Wilcoxon signed-rank test was used.
Treatment comparisons of plasma parameters measured at the beginning and end intervention were assessed by two-way repeated-measures ANOVA. Linear regression analyses were conducted to identify correlations between variables. On normally distributed data Pearson correlation was used, otherwise Spearman correlation was used.
Potential carryover effect between treatment and period was examined by unpaired t test analyses according to Pocock Analyses were performed using SPSS The study participants were 17 male subjects with well-controlled T2D baseline characteristics, Supplementary Table 1. Although no resveratrol or DHR could be detected during the placebo treatment, both compounds were present in the plasma of all resveratrol-supplemented subjects.
Plasma levels were These levels are representative for the entire study period. In addition, no carryover effect was found between treatment and period for the primary study outcome, confirming the washout period was sufficient.
Plasma glucose profiles during the hyperinsulinemic-euglycemic clamp procedure were similar for the placebo and the resveratrol conditions Fig. In line with the absence of resveratrol-induced changes in R d and EGP, nonoxidative glucose disposal also remained unaffected by 30 days of resveratrol supplementation Supplementary Table 2.
In addition, resveratrol did not exert an effect on circulating insulin levels Supplementary Table 2 , thereby excluding an effect of resveratrol on insulin clearance.
Effect of resveratrol on peripheral and hepatic insulin sensitivity. As a result of technical problems, data are only available for 14 subjects in 1 subject the equipment malfunctioned, in another subject the catheter with the d -[6,6- 2 H 2 ]glucose tracer leaked, and in the last subject aspiration of the venous catheter was no longer possible in the late phase of the clamp, which is necessary for regular blood sampling.
A : Plasma glucose levels during the last 30 min of the basal and low- and high-insulin state of the clamp. Insulin-stimulated glucose disposal, expressed as the R d B , and EGP were calculated for the last 30 min of the basal and low- and high-insulin state C.
D : EGP suppression upon low- and high-insulin infusion. Data are presented as mean ± SEM. R d , rate of disappearance. As expected, carbohydrate oxidation increased during the clamp at the expense of free fatty acid FFA oxidation Supplementary Table 2.
No statistically significant changes in carbohydrate or FFA oxidation rates were observed when basal and insulin-stimulated oxidation rates were compared between placebo and resveratrol Supplementary Table 2. In accordance with the lack of effect of resveratrol on insulin sensitivity, no improvement in fasting glucose, insulin, or HbA 1c levels were found compared with placebo Supplementary Table 3.
We did observe a time effect for HbA 1c ; however, this was found in both treatment conditions. Similarly, no resveratrol effect on other markers of metabolic health was found Supplementary Table 3. However, the difference failed to reach statistical significance 7.
During the night, substrate utilization reflected by the respiratory quotient was similar for both treatments, at 0. Effect of resveratrol RSV on ectopic lipid storage. A : Muscle biopsy sections from a representative study participant, stained for IMCL with Oil Red O staining in red , muscle laminin in blue , and type 1 muscle fibers in green.
Data are presented as means ± SEM. Box plot represents minimum, first quartile, median, third quartile, and maximum. IHL content, determined by 1 H-MRS, remained unaffected by 30 days of resveratrol supplementation Fig.
However, in the absence of a lipid-derived substrate, no resveratrol effect was observed in state 3 respiration upon complex I- and II-linked substrates Supplementary Fig. Results revealed no differences observed between the two treatment groups with insulin sensitivity unaffected after 6 months of resveratrol treatment.
However, the research team found a significant difference in postintervention glycated haemoglobin HbA1c between the groups with the treatment group lower after resveratrol intervention No differences were found in intrahepatic lipid IHL , body composition, blood pressure, energy metabolism, physical performance, or quality of life and sleep between treatment arms.
The team also found resveratrol treatment did not affect total cholesterol, HDL and LDL cholesterol, free fatty acids, and triglycerides, commenting that these results and previous studies suggests that resveratrol appears unsuitable for treating dyslipidaemia.
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Resveratrol is a Resvertarol compound that blpod found Resveratrol and blood sugar control Resveratrok than 70 plant sugaar, including nuts, grapes, pine trees, and certain vines, as Resveratrrol as Resveratrol and blood sugar control red wine. It is thought to play Raw energy bars role in preventing heart disease. Early studies have shown that resveratrol has antioxidant, anticancer, antifungal, antiviral, and antibacterial effects. Since resveratrol is found in grapes and wines, early research focused on linking resveratrol to the potential heart health benefits of moderate wine drinking. However, this research has expanded to examine the effects of resveratrol on many medical conditions, including cancer, bacterial and viral infections, Alzheimer's disease, and Parkinson's disease.
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