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Quercetin and diabetes

Quercetin and diabetes

The involved mechanisms diabetws diabetes-induced diabetic Quercetin and diabetes mainly include oxidative stress, inflammation, Quercetin and diabetes, daibetes damaged retinal vasculature. Diabetes Care — Diabetes Care. Their combination is expected to possess either additive or synergistic action. Metabolism 57 7 Suppl 1 :S39—S Eur J Pharmacol 1—3 — Metabolic Control of Type 2 Diabetes by Targeting the GLUT4 Glucose Transporter: Intervention Approaches. Quercetin and diabetes

Quercetin and diabetes -

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Proteome Res. Saisho, Y. Quercetin is soluble in ethanol, methanol, and ethyl acetate, slightly soluble in petroleum ether, benzene, ether, and chloroform, and nearly insoluble in water [ 14 ]. It is regarded as having a strong antioxidant effect since its molecular arrangement is acknowledged as the optimum one for scavenging free radicals and binding transition metal ions.

Fruits and vegetables contain glycoconjugates of quercetin. The quantity and kind of sugar moiety affect the solubility and absorption of glycoconjugates. It is then delivered to the liver via the portal circulation, where it is digested and bound to albumin in plasma.

After 0. Unabsorbed quercetin is bio-transformed in the intestine by enzymes from the gut microbiota through glucuronidation, hydroxylation, methylation, and sulfonylation.

Quercetin is eliminated from humans through their feces or urine. Quercetin is a promising drug target for treating diabetes. Several mechanisms, including improved insulin sensitivity, promoted glycogen synthesis, and reduced insulin resistance, have been put up to explain quercetin antihyperglycemic effects.

It enhances glucose metabolism and insulin production, which all work together to improve the insulin sensitization effect and also quercetin inhibits the enzymes glucosidase and amylase. In addition, quercetin maintained the mass and functionality of β-cells, hence enhancing the serum insulin effect, and lowered blood glucose in streptozotocin STZ -induced diabetes mice.

acts similarly to rosiglitazone-like drugs such as glycogen phosphorylase GP and peroxisome proliferator-activated receptor γ PPARγ agonist on insulin-receptor signaling and glucose transport to increase the utilization of glucose [ 16 ].

Quercetin might considerably raise plasma insulin levels and lower blood glucose levels by preserving the bulk and activity of cells and enhancing serum insulin action. Additionally, the establishment of the diabetic state in alloxan-diabetic animal models is based on the death of cells brought on by oxidative stress.

It has a variety of ways to harm beta cells. However, by lowering oxidative stress in diabetic patients, the quercetin can lessen islet cell failure, improve cell insulin secretion, and further prevent DM.

In people, quercetin can affect a variety of organs, including the liver, pancreas, small intestine, and muscles. In skeletal muscles, quercetin increases adenosine monophosphate kinase AMPK , which, in turn, stimulates GLUT4 receptors [ 17 ]. Through GLUT4, which facilitates glucose entry into cells, glucose is processed, which controls the glucose level.

Additionally, quercetin stimulates AMPK activity in hepatocytes and blocks glucose 6-phosphatase. The main signaling molecules that control cellular GLUT4 expression are AMPK and CaMKII. Exercise is also an effective GLUT4 expression activator, which enhances insulin action and muscle glycogen synthesis Figure 3.

On the other hand, quercetin administration decreases intestine sodium-dependent glucose absorption and GLUT2 expression [ 18 ]. Quercetin functions similarly to rosiglitazone as a PPAR gamma agonist in that it influences signal transduction and improves the utilization of glucose through affecting glucose transport and insulin-receptor signaling [ 10 ].

Mechanism of quercetin as antidiabetic agent. Pancreatic beta cells secrete insulin, which regulates blood glucose levels when blood sugar levels rise. Reduced viability and functionality of pancreatic cells are frequently linked to diabetic problems.

Quercetin improves glucose metabolism and insulin secretion, has a superior hypoglycemic impact, and has an insulin-sensitizing effect by encouraging pancreatic-cell proliferation [ 19 ]. In INS-1E insulin-secreting rat insulinoma cells, quercetin may help to increase glucose-stimulated insulin secretion and insulin expression.

According to a study, quercetin can prevent the malfunctioning of pancreatic cells brought on by cholesterol, preserving insulin production triggered by glucose and glycemic management [ 19 ].

Additionally, during an oral glucose tolerance test in diabetic rats, quercetin considerably raised the insulin sensitivity index at 30 minutes while significantly lowering the levels of plasma cholesterol, fasting plasma insulin, and postprandial glucose [ 20 ].

Regarding this, the beneficial effects of quercetin on islet cells can be divided into three categories, namely an increase in insulin secretion, protection of -cells, and promotion of islet-cell proliferation.

High levels of fatty acids and glucose promote an excessive buildup of ROS, which can damage cells and lead to insulin resistance in peripheral metabolic tissues [ 10 ]. In other studies, it was discovered that long-term hyperglycemia decreased the binding of the insulin receptor and the substrate IRS-1 , increased the expression of inducible nitric oxide synthase while decreasing endothelial nitric oxide synthase, and ultimately caused insulin resistance in diabetic rats.

Inducible nitric oxide synthase expression was raised as a result of the anti-oxidative protective activity on the pancreatic islets of endothelial nitric oxide synthase, which, in turn, caused insulin resistance in diabetic rats.

These advantageous effects of quercetin may be attained by decreasing the buildup of cyclic adenosine phosphoric acid cAMP and the input of free fatty acids, activating protein kinase A PKA , maintaining cyclic nucleotide-dependent phosphodiesterase 3B PDE3B , and increasing two acyl glycerol DAG [ 21 ].

One of the therapeutic methods is to suppress the carbohydrate hydrolyzing enzymes, amylases and glucosidase, in the human digestive system in order to delay the absorption of glucose [ 22 ]. Consequently, finding glucosidase inhibitors in plants has become a very important endeavor.

The intestinal GLUT2 enzyme is severely inhibited by quercetin, which lowers the absorption of glucose [ 23 ]. According to numerous reports, quercetin inhibits yeast glucosidases more potently than acarbose. Inhibiting amylase and glucosidases may, therefore, be useful in lowering blood glucose levels after consuming a diet high in mixed carbohydrates.

The findings revealed that quercetin had a high ORAC value, reduced glucosidase activity, and may have physiological benefits for the treatment of diabetes despite the need for additional in vivo research. Diabetes patients experience hyperglycemia following a meal as a result of elevated glucosidase and amylase activity.

Inhibiting amylase and glucosidases may, therefore, be useful in lowering blood glucose levels following the administration of a mixed carbohydrate diet.

In conclusion, reducing insulin resistance, influencing glucose metabolism, and safeguarding islet cells all contribute to the mechanism of quercetin hypoglycemic activity Figure 3 [ 24 ]. A growing body of research indicates a clear connection between diabetes and the emergence of liver problems.

Diabetes has been linked to an increase in CYP2E1 in the liver, and the suppression of the enzyme primarily protects the liver from oxidative damage. It was discovered that STZ-induced diabetes in rats resulted in hyperglycemia, body weight loss, altered hepatocyte ultrastructure, elevated protein levels, and enhanced CYP2E1 activity in the liver [ 26 ].

In STZ-induced diabetic rats, the impact of quercetin on liver apoptosis was examined. On experimentally developed diabetic rats, quercetin produced hepatoprotective effects via the anti-apoptosis action. Since oxidative stress is improved and hepatocyte apoptosis is inhibited, differing doses of quercetin may be effective in avoiding diabetic liver damage in part because of these effects [ 25 , 27 ].

The involved mechanisms in diabetes-induced diabetic retinopathy mainly include oxidative stress, inflammation, neurodegeneration, and damaged retinal vasculature.

Diabetes-related alterations to the retina were significantly prevented by quercetin therapy [ 28 ]. Notably, the protective effect of quercetin was significantly reduced by concomitant HO-1 inhibition. Quercetin inhibited high glucose-induced cell proliferation by reducing vascular endothelial growth factor VEGF production, according to an in vitro experiment using human retinal endothelial cells.

Quercetin also had a neuroprotective effect against diabetic retinopathy [ 29 ]. Quercetin protects against neuronal damage in diabetic retina, perhaps by increasing levels of neurotrophic factors and preventing neuronal death. In order to stop neurodegeneration in DR, quercetin may, therefore, be an appropriate therapeutic agent [ 30 ].

One of the main microvascular consequences of diabetes, diabetic nephropathy DN , is marked by high incidence, low diagnosis rate, lengthy duration, expensive treatment, and high rates of disability and fatality.

End-stage renal failure may result from mesangial enlargement and thickening of basement membranes, which cause pathological alterations such as glomerulosclerosis, interstitial fibrosis, and tubular atrophy [ 31 ]. Numerous factors, including abnormalities in lipid synthesis, oxidative stress, changes in renal hemodynamics, and signaling pathways for polyol and mitogen-activated protein kinase, all have a role in the outcome and progression of DN.

Through the inhibition of protein kinase C PKC activity, downregulation of TGF-1 expression, reduction of extracellular matrix production, and delay of renal hypertrophy, quercetin may help the kidney shape that has been affected by hyperglycemia. In addition, quercetin can slow the onset of diabetic nephropathy, prevent degenerative alterations to the kidneys, and enhance glycolipid metabolism in type 2 diabetic rats [ 32 ].

Increased insulin resistance and high blood glucose levels have been associated to the release of pro-inflammatory mediators such as IL-1, IL-6, IL-8, IL-4, TNF-, and histamine in brown adipose tissue Figure 3.

These mediators are inhibited by quercetin, which also reduces oxidative stress. Quercetin decreases blood glucose reabsorption by lowering DPP-IV and cyclooxygenase-2 COX-2 activities in the kidneys Figure 3. Quercetin prevented renal development in diabetic rats with kidney disease by stimulating AMPK phosphorylation and decreasing sterol regulatory element binding protein SREBP -1c in the kidney [ 33 ].

This decreased the tissue dyslipidemia caused by lipid deposits. Quercetin might reduce the oxidative damage brought on by diabetes in the kidney tissues.

Additionally, several investigations revealed that diabetic rats with kidney dysfunction had high lipid accumulation. This reduced the tissue dyslipidemia condition. Male diabetic patients frequently experience clinical issues with diabetes-induced reproductive dysfunction, which negatively impacts their sexual lives and ability to conceive.

The positive effects of quercetin on diabetes-induced reproductive dysfunction processes, such as sexual dysfunction, testicular dysfunction, or infertility, have been demonstrated in animal trials, but the underlying mechanisms are still unknown [ 33 ].

In adult male STZ-induced diabetic SD rats, a recent study examined the effects of quercetin on male sexual behavior and sperm quantity. According to additional research, treating damaged rat testes with an appropriate dosage of quercetin led to a considerable rise in the testis and epididymis weights, SOD activity, and levels of sexual hormones.

On the impaired reproductive system of diabetics, quercetin has protective properties [ 34 , 35 ]. Part of the protective impact of quercetin on sexual behavior, testicular cell damage, and spermatogenic damage brought on by diabetes can be attributed to anti-oxidation, cell proliferation, and anti-apoptosis.

These diseases are a result of changes in the central nervous system. Numerous research on animals has demonstrated the therapeutic effects of antidiabetics, antioxidants, and acetylcholine esterase AChE inhibitors on diabetic neurodegenerative disorders, particularly memory loss and cognitive dysfunction.

In many in vitro and in vivo scenarios, quercetin exhibits neuroprotective or increased neurogenesis effects; however, the underlying processes are still not completely understood [ 36 ]. Quercetin significantly reduced cerebral blood flow CBF and blood glucose levels, avoided memory loss, enhanced antioxidant enzyme activity, and mitigated abnormalities of the cholinergic system, as well as the consumption of brain energy.

Diets high in quercetin should be promoted in order to ward off diabetic vascular and neurological disorders [ 37 ]. BDNF is well known for its ability to protect the brain. It encourages the development of new neurons and supports the survival and functionality of existing ones.

In the context of diabetes, maintaining appropriate BDNF levels may be crucial for shielding nerve cells from harm brought on by oxidative stress and high blood sugar levels [ 38 ].

Quercetin supplementation may raise BDNF levels, which may help with cognitive function and memory, both of which can be affected by diabetes-related diseases, such diabetic neuropathy. The pro-inflammatory cytokines IL-1 and IL, as well as NLRP3, ASC, and cleaved Caspase-1, were all expressed less, while SIRT1 was expressed more in response to quercetin.

It also enhanced the protein expression of SIRT1 and lowered the expression of NLRP3 inflammation-related proteins. One of the most challenging types of pain to manage is diabetic neuropathic pain, a significant micro-vascular consequence of diabetes mellitus DM. There are not many reports on the use of quercetin to treat diabetic neuropathic pain.

The antinociceptive effects of quercetin in normal mice and animals with diabetes caused by STZ. Diabetes patients frequently experience depression, which impairs glucose control and raises the risk of diabetic complications.

Clinical care for diabetics has come to be seen as increasingly dependent on the accurate diagnosis and treatment of concomitant depression [ 40 ]. Malignant diabetic cardiomyopathy has a high incidence and fatality rate. This type of cardiomyopathy causes hypertension and coronary artery disease and is linked to mitochondrion abnormalities, hyperinsulinemia, insulin resistance, and endoplasmic reticulum modifications.

These results indicate that QE and RS promoted the utilization of glucose and ameliorated ketosis and metabolic acidosis. These symptoms were improved by QE, RS, and cotreatment, possibly due to the correction of hyperglycemia and insulin deficiency Go et al.

Finally, the elevated serum levels of ALT, AST, ALP, and GGT, as liver injury markers in diabetic rats indicate the induction of tissue injuries due to the diabetes-induced oxidative stress. These elevations were dramatically prevented by QE, RS, or cotreatment. Therefore, our test compounds may prevent the liver damage due to the diabetes.

Serum CRE and BUN levels which are indicators for diabetic nephropathy Wang et al. Thus, the compounds exhibited the potential to protect the kidney in the diabetic rats. In conclusion, our results suggest that QE, RS, and especially their cotreatment have the potential to improve hyperglycemia, serum glucose dysfunction, and dyslipidemia in STZ-induced diabetic rats.

We also demonstrated that treatment with QE and RS alone and in combination improved the pathological blood conditions of diabetic rats. Therefore, our study provides evidence that cotreatment with QE and RS is a potentially useful strategy for the treatment of diabetes.

Furthermore, cotreatment of QE and RS is worth to evaluate their effects on the type 2 diabetes in the future. This study was supported in part by the Brain Korea 21 Plus program of the National Research Foundation of Korea Grant and the Basic Science Research Program through the National Research Foundation of Korea NRF funded by the Ministry of Education NRFR1D1A3A The authors have declared that there are no conflicts of interest associated with this manuscript.

Effects of quercetin QE , resveratrol RS , and their cotreatment on hematological parameters and blood ions in streptozotocin STZ -induced diabetic rats. Data are means ± standard error of the mean SEM. Effects of quercetin QE , resveratrol RS , and their cotreatment on serum liver and kidney injury markers in streptozotocin STZ -induced diabetic rats.

STZ-treated group, respectively. AST, aspartate aminotransferase; ALT, alanine aminotransferase; ALP, alkaline phosphatase; GGT, gamma glutamyl transferase; BUN, blood urea nitrogen; CRE, creatinine; TP, total protein.

Title Author Keyword Volume Vol. Current Issue Online First Archives Most Cited Most Read. Anti-Diabetic Effect of Cotreatment with Quercetin and Resveratrol in Streptozotocin-Induced Diabetic Rats. Department of Veterinary Pharmacology and Toxicology, College of Veterinary Medicine, Biosafety Research Institute and Korea Zoonosis Research Institute, Center for Poultry Diseases Control, Chonbuk National University, Iksan , Republic of Korea.

E-mail: kang-hs jbnu. Received : December 22, ; Revised : December 29, ; Accepted : January 9, ; Published online : February 21, Keywords : Diabetes, Quercetin, Resveratrol, Streptozotocin, Glucose.

Induction of experimental diabetes mellitus and experimental design Diabetes was induced by intraperitoneally injecting the rats with STZ Sigma-Aldrich, St. Biochemical analysis Blood was collected from the caudal vena cava after all rats were euthanized.

Measurements of hepatic glucose regulating enzymes The rat livers were quickly rinsed and lysed in homogenizing buffer containing 0. Measurement of oxidative stress-related enzymes The serum levels of malondialdehyde MDA were measured using an OXI-TEK thiobarbituric acid reactive substances TBARS kit Enzo Life Sciences Inc.

Statistical analysis All the data are expressed as the mean ± standard error of the mean SEM. Effects of QE, RS, and cotreatments on glucose levels Fig. Effects of QE, RS, and cotreatment on serum insulin, C-peptide, HbA1c, Hb, and Hct levels In the STZ-treated group, the serum insulin, C-peptide, blood Hct and Hb levels significantly decreased compared with those in the normal control group.

Effects of QE, RS, and cotreatment on serum lipid profiles To investigate whether the hypoglycemic effect of the test compounds was mediated through protective actions against dyslipidemia in diabetic rats, we determined the serum lipid profiles.

Effects of QE, RS, and cotreatment on hepatic glucose regulating enzymes To determine the effects of QE, RS, and cotreatment on glucose and lipid metabolism in the liver under diabetic conditions, we investigated the hepatic glucose contents after treating the STZ-induced diabetic rats with the test compounds.

Effects of different treatments on serum levels of tissue injury markers As shown in Table 2 , levels of ALT, AST, ALP, GGT, BUN, and CRE were elevated while the TP level was reduced in the STZ-treated group compared with those of the normal control group. Effects of QE, RS, and cotreatment on serum oxidative stress parameters To investigate the protective actions of our test compounds against oxidative stress in diabetic conditions, we determined the levels of various serum oxidative stress parameters after treatment of STZ-induced diabetic rats.

Histological analysis of pancreatic tissues The STZ-induced diabetic rats exhibited extensive granulation of the β-cells and severe vacuolation of the pancreatic islets, while normal pancreatic-β cells in the islet of Langerhans and the acini were observed in the normal control group.

Effects of quercetin QE , resveratrol RS , and their cotreatment on body weight change and water consumption. A Initial body weight and final body weight at 14th day after compounds treatment of rats in all groups. B Average daily water intake during the experimental period.

Effects of quercetin QE , resveratrol RS , and their cotreatment on blood glucose levels. The blood glucose levels during the experimental period A and oral glucose tolerance test OGTT conducted at 14th day after compounds treatment B.

Effects of quercetin QE , resveratrol RS , and their cotreatment on serum levels of A Insulin, B C-peptide, C glycated hemoglobin HbA1c , D hemoglobin Hb and E hematocrit Hct. Effects of quercetin QE , resveratrol RS , and their cotreatment on serum lipid profiles.

Effects of quercetin QE , resveratrol RS , and their cotreatment on hepatic glucose-regulating enzymes activities. Effects of quercetin QE , resveratrol RS , and their cotreatment on serum oxidative stress-related parameters in streptozotocin STZ -induced diabetic rats. Effects of quercetin QE , resveratrol RS , and their cotreatment on pancreatic tissues.

Scale bar, 50 μm. Table 2. Diagnosis and classification of diabetes mellitus. Diabetes Care. Arias, N, Macarulla, MT, Aguirre, L, Milton, I, and Portillo, MP The combination of resveratrol and quercetin enhances the individual effects of these molecules on triacylglycerol metabolism in white adipose tissue.

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Anticancer Drugs. Friedewald, WT, Levy, RI, and Fredrickson, DS Estimation of the concentration of low-density lipoprotein cholesterol in plasma, without use of the preparative ultracentrifuge.

Clin Chem. Go, HK, Rahman, MM, Kim, GB, Na, CS, Song, CH, Kim, JS, Kim, SJ, and Kang, HS Antidiabetic effects of yam dioscorea batatas and its active constituent, allantoin, in a rat model of streptozotocin-induced diabetes.

Gumaa, KA, and McLean, P The kinetic quantitation of ATP: D-glucose 6-phosphotransferases. FEBS Lett. Gupta, D, Raju, J, Prakash, J, and Baquer, NZ Change in the lipid profile, lipogenic and related enzymes in the livers of experimental diabetic rats: effect of insulin and vanadate. Diabetes Res Clin Pract.

Igura, K, Ohta, T, Kuroda, Y, and Kaji, K Resveratrol and quercetin inhibit angiogenesis in vitro. Cancer Lett.

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Diabetss is a flavonoid, present in various natural Quercetin and diabetes, African Mango seed reviews has demonstrated in vitro and in vivo antidiabetic properties. Xnd improves oral Quercetin and diabetes Querceitn, Quercetin and diabetes well as pancreatic β-cell diahetes to secrete insulin. Quervetin inhibits diabeetes α-glucosidase and DPP-IV enzymes, which prolong the half-life of glucagon-like peptide-1 GLP-1 and glucose-dependent insulinotropic polypeptide GIP. Quercetin also suppresses the release of pro-inflammatory markers such as IL-1β, IL-4, IL-6, and TNF-α. Diabetes mellitus DM is a chronic disease that is one of the leading causes of illness and mortality across the globe. DM is diagnosed as a result of an elevated blood glucose level hyperglycaemia caused by inadequate insulin secretion, defective insulin action, or both. Herein we investigated the Querectin mechanism of Qudrcetin of the citrus flavonoid, quercetin in skeletal muscle cells Diabeyes myotubes. Taking Quecetin of protein kinase inhibitors, Qiercetin proved that the effect of quercetin Quercwtin 2-NBDG uptake Quercetin and diabetes L6 myotubes was Quegcetin through Herbal weight loss tea side effects signaling pathway, but through diabwtes monophosphate kinase AMPK pathway and its downstream target p38 MAPK. An increase in the cellular AMP to ATP ratio on pretreatment may account for AMPK activation which was coupled with a transient change in mitochondrial membrane potential. In addition, quercetin triggered a rise in intracellular calcium suggesting that calcium-calmodulin mediated protein kinase CaMKK may also be involved. Quercetin shared a similar mechanism with the well-known drug metformin, highlighting it as a promising compound for the management of type 2 diabetes. The AMPK signaling pathway could contribute to correction of insulin resistance through bypassing the insulin-regulated system for GLUT4 translocation. Diabetes mellitus is defined as a hyperglycemic condition arising due to insulin resistance or impaired insulin secretion.

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