High-fructose Diet-induced Metabolic Syndrome Research Articles

Aronia melanocarpa fruit juice prevents hepatic impairment in rats subjected to metabolic syndrome

AbstractThis study evaluated the effects of Aronia melanocarpa fruit juice (AMFJ) on the liver in a model of high-fat, high-fructose (HFHF) diet-induced metabolic syndrome (MS). Fifty rats were allocated to five groups – Control, MS, MS+AMFJ2.5, MS+AMFJ5, and MS+AMFJ10. The control group was fed a standard diet, while the other groups were provided a HFHF diet. During MS induction, daily oral treatment was performed. Control and MS groups received 10.0 mL kg−1 distilled water, while the other three groups received AMFJ at doses of 2.5, 5.0, and 10.0 mL kg−1, respectively. After 10 weeks, liver samples were collected and inspected histologically as well as immunohistochemically to determine the expression of Bax, Bcl-2, and MAC387. Bax/Bcl-2 ratio was calculated. In MS rats, steatotic, inflammatory and degenerative alterations of the liver were detected, Bax and MAC387 were markedly elevated, while Bcl-2 was non-significantly reduced. The Bax/Bcl-2 ratio significantly increased. The histopathological alterations were prevented by the AMFJ treatment. Compared to MS group, Bax and MAC387 values were significantly lower and Bcl-2 value was higher resulting in significantly lower (P < 0.001) Bax/Bcl-2 ratio in all AMFJ-treated groups. AMFJ, administered during MS induction in rats, prevented the occurrence of inflammatory, steatotic, degenerative, and pro-apoptotic changes in the liver.

Investigation of Lupinus angustifolius Extracts against High-Fructose Diet-Induced Metabolic Syndrome in Male Wistar Rats Articles

Investigation of Lupinus angustifolius Extracts against High-Fructose Diet-Induced Metabolic Syndrome in Male Wistar Rats Articles

Beneficial Effects of 6-Gingerol on Fatty Pancreas Disease in High-Fat High-Fructose Diet-Induced Metabolic Syndrome Rat Model.

To examine the effects of 6-gingerol (6-G) in overcoming fatty pancreas disease of high-fat high-fructose (HFHF) diet-induced metabolic syndrome in rats. Male Sprague-Dawley rats were randomly divided into 5 groups. The healthy-control group (normal diet, n = 5) received a standard diet. The HFHF group (HFHF; n = 20) received an HFHF diet and a single-dose intraperitoneal injection of streptozotocin (22 mg/kgBW) at week 8. Metabolic syndrome-confirmed rats received 6-G at doses of 50 (6-G 50, n = 5), 100 (6-G 100, n = 5), and 200 (6-G 200, n = 5) mg/kgBW, respectively, for 8 weeks. All rats were killed at week 16. Pancreatic tissue and blood samples were obtained for histological and amylase analysis. The serum amylase, MDA, mRNA of TNF-α, and IL-6 significantly increased, whereas GPx decreased in the HFHF group as compared with the normal diet group, respectively. Rats in the HFHF group showed pancreatic lipid accumulation and a decreased mean number of α- and β-cells in the pancreas. Meanwhile, all rats in 6-G at all dose groups showed improvement in all parameters and histopathological scores for lipid accumulation. 6-Gingerol could attenuate pancreatic lipid accumulation and improve the cell number of α- and β-cells in the pancreas, leading to improvements in fatty pancreas disease.

Influence of bacterial lipopolysaccharide on the degradation of the components of the extracellular matrix of rat biceps femoris muscle during high fructose diet-induced metabolic syndrome

Metabolic syndrome is an epidemic of non-infectious origin, which is associated with the consumption of a large amount of high-calorie food and a sedentary lifestyle. It is not excluded that bacterial lipopolysaccharides (LPS) may enter the body during metabolic syndrome. The purpose of this work is to study the combined effect of bacterial lipopolysaccharide and high fructose diet on the concentration of glycosaminoglycans and their individual fractions, the content of free L-oxyproline and sialic acids in rat biceps femoris muscle. Bacterial LPS was injected intraperitoneally at a dose of 0.4 μg/kg. Metabolic syndrome was modelled by using 20% fructose solution as only source of drinking water. In the test group of animals total concentration of glycosaminoglycans increased by 22.53%, the heparin-heparan and keratan-dermatan fraction concentrations raised by 26.18 and 35.91%, but concentration of the chondroitin fraction did not change compared to the control. The concentrations of free L-oxyproline and sialic acids increased by 120.71 and 156.78%, respectively. Thus, high fructose diet, stimulation of the organism with bacterial lipopolysaccharide and their combination lead to increased degradation of glycoproteins and proteoglycans and intensify collagenolysis in the biceps femoris muscle of rats.

Effect of High-Fructose Diet-Induced Metabolic Syndrome on the Pituitary-Gonadal Axis in Male Rats.

Plasma testosterone levels have been found to decrease in older insulin-resistant male patients. Both lower total testosterone levels and a higher incidence of metabolic syndrome have also been reported. The aim of this study was to investigate the effects of high-fructose diet-induced diabetes on both the testosterone release by Leydig cells and the activity of the hypothalamus-pituitary-gonadal (HPG) axis in male rats. Male rats were fed with either standard chow (control group) or a high-fructose diet (fructose-fed group) for 21 weeks. Hyperglycemia, hyperinsulinemia, and hypertension were observed in the fructose-fed group. Moreover, plasma testosterone and LH levels decreased in the fructose-fed group compared to the control group. Sperm motility was also reduced by 15% in the fructose-fed rats. In contrast, the basal release of testosterone from rat Leydig cells was not altered by fructose feeding. Moreover, in vitro studies showed that the testosterone release, in response to different stimulants, including forskolin (an adenylyl cyclase activator, 10-5 M), 8-Br-cAMP (a permeable analog of cAMP, 10-5 M), A23187 (a calcium ionophore, 10-5 M), or 25-hydroxy-cholesterol (water-soluble cholesterol, 10-5 M), did not significantly differ between the fructose-fed and control groups. Interestingly, the release of testosterone in response to human chorionic gonadotropin (hCG, 0.05 IU/mL) was enhanced by eightfold in the control group, but elevenfold in the fructose-fed group. LH receptor expression in rat Leydig cells was also increased. Moreover, LH secretion from the anterior pituitary was altered in the fructose diet-fed group. These results suggest that fructose diet-fed rats have lower plasma testosterone levels, which can lead to a higher sensitivity of hCG in Leydig cells.

Rosuvastatin and co-enzyme Q10 improve high-fat and high-fructose diet-induced metabolic syndrome in rats via ameliorating inflammatory and oxidative burden

The prevalence of metabolic syndrome (MetS) has been rising alarmingly and it has now become a global concern causing an enormous economic burden on the health care system. MetS is generally linked to complications in lipid metabolism, oxidative stress and low grade inflammation. The aim of the current study was to evaluate the effect of rosuvastatin, co-enzyme Q10 (CoQ10), and their combination on blood pressure, blood sugar, dyslipidemia, and liver function in rats with MetS induced by high fructose and high fat diet (HF-HFD) and the possible underlying mechanism. Oral administration of rosuvastatin (10 mg/kg/day), CoQ10 (10 mg/kg/day) and their combination for 4 weeks in HF-HFD-fed rats elevated serum high density lipoprotein and reduced glutathione. On the other hand, treatment with rosuvastatin, CoQ10 or their combination decreased the serum levels of malondialdehyde, triglycerides, total cholesterol, and low density lipoprotein-cholesterol as well as systolic blood pressure, body weight and fasting blood glucose level. In addition, the drugs or their combination declined serum pro-inflammatory cytokines, namely tumor necrosis factor-α and interleukin-1β. In conclusion, our results showed that rosuvastatin or CoQ10 protected against HF-HFD-induced MetS through the regulation of dyslipidemia, elevated blood glucose, elevated blood pressure, antioxidant defenses and inflammatory response. Rosuvastatin or CoQ10 also alleviated the impairment of liver function that was induced by HF-HFD. Interestingly, CoQ10 augmented rosuvastatin's effect in ameliorating MetS, via exerting synergistic modulatory effects on oxidative stress and inflammation. Thus, rosuvastatin and CoQ10 combination therapy may have possible applications in ameliorating metabolic disorders.

Recent Developments in Rodent Models of High-Fructose Diet-Induced Metabolic Syndrome: A Systematic Review.

Metabolic syndrome (MetS) is the physiological clustering of hypertension, hyperglycemia, hyperinsulinemia, dyslipidemia, and insulin resistance. The MetS-related chronic illnesses encompass obesity, the cardiovascular system, renal operation, hepatic function, oncology, and mortality. To perform pre-clinical research, it is imperative that these symptoms be successfully induced and optimized in lower taxonomy. Therefore, novel and future applications for a disease model, if proven valid, can be extrapolated to humans. MetS model establishment is evaluated based on the significance of selected test parameters, paradigm shifts from new discoveries, and the accessibility of the latest technology or advanced methodologies. Ultimately, the outcome of animal studies should be advantageous for human clinical trials and solidify their position in advanced medicine for clinicians to treat and adapt to serious or specific medical situations. Rodents (Rattus norvegicus and Mus musculus) have been ideal models for mammalian studies since the 18th century and have been mapped extensively. This review compiles and compares studies published in the past five years between the multitude of rodent comparative models. The response factors, niche parameters, and replicability of diet protocols are also compiled and analyzed to offer insight into MetS-related disease-specific modelling.

Effect of high-fructose diet-induced metabolic syndrome on the pituitary-gonadal axis from adolescence through adulthood in male albino rats and the possible protective role of ginger extract. A biochemical, histological and immunohistochemical study.

This work was designed to clarify, for the first time up to our knowledge, the effects of high-fructose diet (HFrD)-induced metabolic syndrome (MetS) on the pituitary-gonadal axis of adolescent male rats continuing through adulthood period and to evaluate the possible role of ginger extract in ameliorating these effects. Forty 4-week-old male albino rats, treated for 8 weeks, were randomly divided into four equal groups; control (fed standard diet), ginger extract-treated (500 mg/kg once daily orally by gavage), HFrD-induced MetS (fed a diet containing 60% fructose), HFrD and ginger groups. The assessment methods included biochemical, histological and immunohistochemical studies. High-fructose diet-fed rats exhibited a picture similar to MetS in the form of increased body weight and serum levels of glucose and insulin with an elevated HOMA-IR reflecting insulin resistance as well as dyslipidaemia. Lipid peroxidation (increased malondialdehyde) and oxidative stress (decreased superoxide dismutase) were implicated in this syndrome. This group exhibited a significant decrease in testicular weight and the levels of reproductive hormones (LH, FSH and testosterone). The pituitary gonadotrophs showed electron dense nuclei, large cytoplasmic vacuoles, destructed organelles in addition to decreased number of secretory granules. Furthermore, testicular specimens presented marked alterations. There were disorganised shrunken tubules with irregular basement membranes, reduced germinal epithelial thickness, vacuolations and degenerated mitochondria in the spermatogenic cells. Beclin 1 and proliferating cell nuclear antigen immunoexpressions were significantly downregulated with HFrD-induced MetS. Ginger extract supplementation proved to be a potent protective agent against these harmful effects through its antioxidant, hypoglycaemic, insulinotropic, androgenic and hypolipidaemic effects in addition to its ability to induce testicular autophagy. Consumption of HFrD induced MetS and proved to have harmful effects on the pituitary-testicular axis. Moreover, this work provided a new insight into the possible use of ginger extract to alleviate the main features of MetS and protect the pituitary-gonadal axis from the damaging effects of HFrD-induced MetS.

Roles of sarcoplasmic reticulum Ca2+ ATPase pump in the impairments of lymphatic contractile activity in a metabolic syndrome rat model

The intrinsic lymphatic contractile activity is necessary for proper lymph transport. Mesenteric lymphatic vessels from high-fructose diet-induced metabolic syndrome (MetSyn) rats exhibited impairments in its intrinsic phasic contractile activity; however, the molecular mechanisms responsible for the weaker lymphatic pumping activity in MetSyn conditions are unknown. Several metabolic disease models have shown that dysregulation of sarcoplasmic reticulum Ca2+ ATPase (SERCA) pump is one of the key determinants of the phenotypes seen in various muscle tissues. Hence, we hypothesized that a decrease in SERCA pump expression and/or activity in lymphatic muscle influences the diminished lymphatic vessel contractions in MetSyn animals. Results demonstrated that SERCA inhibitor, thapsigargin, significantly reduced lymphatic phasic contractile frequency and amplitude in control vessels, whereas, the reduced MetSyn lymphatic contractile activity was not further diminished by thapsigargin. While SERCA2a expression was significantly decreased in MetSyn lymphatic vessels, myosin light chain 20, MLC20 phosphorylation was increased in these vessels. Additionally, insulin resistant lymphatic muscle cells exhibited elevated intracellular calcium and decreased SERCA2a expression and activity. The SERCA activator, CDN 1163 partially restored lymphatic contractile activity in MetSyn lymphatic vessel by increasing phasic contractile frequency. Thus, our data provide the first evidence that SERCA2a modulates the lymphatic pumping activity by regulating phasic contractile amplitude and frequency, but not the lymphatic tone. Diminished lymphatic contractile activity in the vessels from the MetSyn animal is associated with the decreased SERCA2a expression and impaired SERCA2 activity in lymphatic muscle.

Neonatal zingerone protects against the development of high-fructose diet-induced metabolic syndrome in adult Sprague-Dawley rats.

During the early postnatal period, dietary manipulations can alter the developmental trajectory of the growing offspring, causing beneficial or adverse health outcomes later in adult life. We investigated the potential preventive effects of neonatal zingerone intake on the development of fructose-induced metabolic derangements in rats.Four-day old male and female Sprague-Dawley rat pups (n=79) were randomly grouped and administered: 10ml/kg body weight (bwt) of distilled water (W), 10ml/kg bwt 20% fructose solution (FS), 10ml/kg bwt fructose solution+40mg/kg bwt of zingerone in distilled water (ZF) or 40mg/kg bwt of zingerone in distilled water (ZW) pre-weaning. After weaning, W and ZW continued on unlimited tap water, while FS and ZF continued on unlimited fructose solution for 10 weeks. Body mass and food and fluid intake were evaluated, plasma was collected for metabolic assays and visceral fat was quantified.Food intake was decreased, fructose and overall caloric intake were increased due to fructose feeding in both sexes (P<0.05). When compared with the controls, the high-fructose diet significantly raised the terminal body masses of females (P<0.0001), concentrations of triglycerides, total cholesterol, LDL-c, TG:HDL-c ratio and visceral fat mass relative to bwt in both sexes (P<0.05). Zingerone prevented (P<0.05) the fructose-induced increase in body mass (females) and hypercholesterolemia (both sexes). Levels of HDL-c, glycaemic parameters and adiponectin were not affected by the interventions (P>0.05). Sex-related differences were observed in food, fluid and caloric intake, terminal mass, cholesterol subtypes and visceral fat percentage (P<0.05).Zingerone could be used strategically in the neonatal phase as a prophylatic management of high-fructose diet-induced metabolic syndrome.

Effects of the administration of brewed Robusta coffee leaves on total antioxidant status in rats with high-fat, high-fructose diet-induced metabolic syndrome

Robusta coffee (Coffea canephora) leaves contain phytochemical compounds and have antioxidant and anti-diabetic effects. This study investigated the effect of brewed Robusta coffee leaves on the total antioxidant status in metabolic syndrome rats. Metabolic syndrome in rats was induced by high-fat-fructose diet containing pork oil (20%), cholesterol (1.5%), cholic acid (0.5%), standard feed (80%), and fructose (1 mL per 200 g BW). The animals were categorized into normal control group (K1), metabolic syndrome control group without treatment (K2), mangiferin treatment group (X1), brewed Robusta coffee leaves 0.09 g per 200 BW group (X2), brewed Robusta coffee leaves 0.18 g per 200 BW group (X3), and brewed Robusta coffee leaves 0.36 g per 200 BW group (X4). Each dose of the coffee leaves was brewed with 3.6 mL of water at 70 °C for 10 min. The intervention was administered for 28 days. There was a significant increase in the total antioxidant status (p &lt;0.000) in all the groups. In conclusion, the administration of brewed Robusta coffee leaves increased the total antioxidant status in metabolic syndrome rats.

High fructose diet-induced metabolic syndrome and the functional abnormalities in the liver and kidney of Wistar albino rats

Background: Metabolic syndrome is the combination of several medical conditions that increase the risk of developing heart diseases, stroke, cancer, non-alcoholic fatty liver, and diabetes mellitus. Different varieties of animal models have been used for the therapeutic studies of diabetes, hyperlipidemia, and kidney diseases. The establishment of appropriate experimental animal models of metabolic syndrome is very important for evaluating the pathophysiology of the disease in humans. Aim and Objective: The aim of the study was to assess the functional abnormalities associated with high fructose diet (HFrD)-induced metabolic syndrome in Wistar albino rats. Materials and Methods: Metabolic syndrome is induced in adult male Wistar albino rats by feeding a combination of HFrD (55%) and fructose enriched water (15%) for 75 days and kept as Group 2 or HFrD group. Normal male Wistar albino rats were kept as normal control. During the entire course of study, weight gain was monitored once a week in both groups. Biochemical investigations such as lipid profile, liver function test, and renal function test were carried out using standard methods. The obtained data were statistically analyzed by students “t-test” and the values were considered statistically significant at p < 0.05. Results: Chronic administration of HFrD resulted in obesity, abnormal hepatic, and renal functions in Wistar rats. Conclusion: Chronic consumption of HFrD produces functional abnormalities in liver and kidney of Wistar rats.

Betulinic acid improves insulin sensitivity, hyperglycemia, inflammation and oxidative stress in metabolic syndrome rats via PI3K/Akt pathways

This study investigated the influence of betulinic acid on high-fructose diet-induced metabolic syndrome in rats. Oral administration of betulinic acid significantly reversed high-fructose diet-mediated increase in body mass index and blood glucose. Furthermore, betulinic acid restored high-fructose diet-mediated alterations in metabolic hormones (insulin, leptin and adiponectin). Betulinic acid-mediated upregulation of protein kinase B (Akt) and phosphoinositde-3 kinase (PI3K) anulled high-fructose diet mediated depletion. Also, elevated tumour necrosis factor-α, interleukin-6 and -8 were significantly lowered. Administration of betulinic acid restored high-fructose diet-mediated increase in the levels of lipid profile parameters and indices of atherosclerosis, cardiac and cardiovascular diseases. High-fructose diet-mediated decrease in activities of antioxidant enzymes (superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase and glucose 6-phosphate dehydrogenase) and increase in oxidative stress biomarkers (reduced glutathione, lipid peroxidation products, protein oxidation and fragmented DNA) were significantly restored by the phenolic acids. Conclusively, betulinic acid improves insulin sensitivity, elevated blood glucose, inflammation and dyslipidaemia and oxidative stress in high-fructose diet-induced metabolic syndrome through the PI#Kand Akt pathways .

In vitro antioxidant activity, α-glucosidase inhibitory potential and in vivo protective effect of Asparagus stipularis Forssk aqueous extract against high-fructose diet-induced metabolic syndrome in rats

The study was carried out to evaluate the in vitro antioxidant, α-glucosidase inhibitory potential and the protective effect of Asparagus stipularis Forssk aqueous extract against high-fructose diet (HFD; 10% fructose solution for 5 months) induced metabolic syndrome in rats. An A. stipularis shoots decoction (ASD) was administered orally (100 and 300 mg/kg body weight), daily for 4 weeks. Controls were performed using metformin (150 mg/kg) as a standard drug. HPLC-MS analysis showed hydroxycinnamoyl derivatives and flavonoid glycosides as the major constituents of ASD. Fructose fed rats showed hyperglycemia, dyslipidemia, impaired glucose tolerance and an increase of inflammation markers (alkaline phosphatase, aspartate transaminase and alanine transaminase) together with higher values of lipid peroxidation and lowered activities of antioxidants enzymes in liver. Hepatic histopathological examinations were performed. Variable sized fat vacuoles and diffuse lymphocytic infiltration were observed. ASD treatment prevented these abnormalities, demonstrating its protective effect against HFD-induced metabolic syndrome in rats.

Dietary phenolic acids reverse insulin resistance, hyperglycaemia, dyslipidaemia, inflammation and oxidative stress in high-fructose diet-induced metabolic syndrome rats

This study investigated the influence of caffeic, ferulic, gallic and protocatechuic acids on high-fructose diet-induced metabolic syndrome in rats. Oral administration of the phenolic acids significantly reversed high-fructose diet-mediated increase in body mass index and blood glucose. Furthermore, phenolic acids restored high-fructose diet-mediated alterations in metabolic hormones (insulin, leptin and adiponectin). Similarly, elevated tumour necrosis factor-α, interleukin-6 and -8 were significantly lowered. Administration of phenolic acids restored High-fructose diet-mediated increase in the levels of lipid parameters and indices of atherosclerosis, cardiac and cardiovascular diseases. High-fructose diet-mediated decrease in activities of antioxidant enzymes (superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase and glucose 6-phosphate dehydrogenase) and increase in oxidative stress biomarkers (reduced glutathione, lipid peroxidation products, protein oxidation and fragmented DNA) were significantly restored by the phenolic acids. The result of this study shows protective influence of caffeic acid, ferulic acid, gallic acid and protocatechuic acid in high-fructose diet-induced metabolic syndrome.

Effect of thymoquinone on high fructose diet-induced metabolic syndrome in rats

Effect of thymoquinone on high fructose diet-induced metabolic syndrome in rats

Regulatory landscape of AGE-RAGE-oxidative stress axis and its modulation by PPAR\u03b3 activation in high fructose diet-induced metabolic syndrome

BackgroundThe AGE-RAGE-oxidative stress (AROS) axis is involved in the onset and progression of metabolic syndrome induced by a high-fructose diet (HFD). PPARγ activation is known to modulate metabolic syndrome; however a systems-level investigation looking at the protective effects of PPARγ activation as related to the AROS axis has not been performed.The aim of this work is to simultaneously characterize multiple molecular parameters within the AROS axis, using samples taken from different body fluids and tissues of a rat model of HFD-induced metabolic syndrome, in the presence or absence of a PPARγ agonist, Rosiglitazone (RGZ).MethodsRats were fed with 60% HFD for the first half of the treatment duration (21 days) then continued with either HFD alone or HFD plus RGZ for the second half.ResultsRats receiving HFD alone showed metabolic syndrome manifestations including hypertension, dyslipidemia, increased glucose levels and insulin resistance, as well as abnormal kidney and inflammatory parameters. Systolic blood pressure, plasma triglyceride and glucose levels, plasma creatinine, and albuminuria were significantly improved in the presence of RGZ. The following molecular parameters of the AROS axis were significantly upregulated in our rat model: carboxymethyl lysine (CML) in urine and liver; carboxyethyl lysine (CEL) in urine; advanced glycation end products (AGEs) in plasma; receptor for advanced glycation end products (RAGE) in liver and kidney; advanced oxidation protein products (AOPP) in plasma; and 4-hydroxynonenal (HNE) in plasma, liver, and kidney. Conversely, with RGZ administration, the upregulation of AOPP and AGEs in plasma, CML and CEL in urine, RAGE in liver as well as HNE in plasma and liver was significantly counteracted/prevented.ConclusionsOur data demonstrate (i) the systems-level regulatory landscape of HFD-induced metabolic syndrome involving multiple molecular parameters, including HNE, AGEs and their receptor RAGE, and (ii) attenuation of metabolic syndrome by PPARγ modulation.

Aqueous seed extract of Hunteria umbellata (K. Schum.) Hallier f. (Apocynaceae) palliates hyperglycemia, insulin resistance, dyslipidemia, inflammation and oxidative stress in high-fructose diet-induced metabolic syndrome in rats

Ethnopharmacological relevanceHunteria umbellata is used in the management and treatment of diabetes and obesity in Nigeria. This study evaluates the effect of aqueous seed extract of Hunteria umbellata on insulin resistance, dyslipidemia, inflammation and oxidative stress in high-fructose diet-induced metabolic syndrome Materials and methodsRats were randomized into seven groups (A-G). Control (group A) and group C rats received control diet for nine weeks while rats in groups B, D – G were placed on high-fructose diet for 9 weeks. In addition to the diets, groups C – F rats orally received 400, 100, 200 and 400mg/kg body weight aqueous seed extract of Hunteria umbellata for 3 weeks starting from 6th – 9th week. ResultsHigh-fructose diet (when compared to control rats) mediated a significant (p<0.05) increase in body weight, body mass index and abdominal circumference. Similarly, levels of blood glucose, insulin, leptin, adiponectin and insulin resistance were increased. It also caused a significant increase in the levels of cholesterol, triglycerides, low-density lipoprotein cholesterol, very low-density lipoprotein cholesterol, atherogenic index, cardiac index and coronary artery index while high-density lipoprotein cholesterol was decreased significantly. Levels of proinflammatory factor, tumour necrosis factor-α, interleukin-6 and 8 were also increased by the high fructose diet. Moreover, it mediated decrease in activities of superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, glucose 6-phosphate dehydrogenase and level of glutathione reduced. Conversely, levels of malondialdehyde, conjugated dienes, lipid hydroperoxides, protein carbonyl and fragmented DNA were elevated. Aqueous seed extract of Hunteria umbellata significantly ameliorated the high fructose diet-mediated alterations. ConclusionsFrom this study, it is concluded that aqueous seed extract of Hunteria umbellata possesses hypoglycemic, hypolipidemic and antioxidants abilities as evident from its capability to extenuate insulin resistance, dyslipidemia, inflammation and oxidative stress in high-fructose diet-induced metabolic syndrome rats.

α-Amyrin attenuates high fructose diet-induced metabolic syndrome in rats.

This study investigated the effect of α-amyrin (a pentacyclic triterpene) on high-fructose diet (HFD)-induced metabolic syndrome in rats. Male Wistar rats were randomly distributed into different groups. The control group was fed normal rat chow diet. The HFD group was fed HFD (60%; w/w) for 42 days. Pioglitazone (10 mg/kg, orally, once daily) was used as a standard drug. α-Amyrin was administered in 3 doses (50, 100, and 200 mg/kg, orally, once daily along with HFD). Plasma glucose, total cholesterol, triglycerides, and high-density lipoprotein cholesterol (HDL-C) were estimated. Changes in blood pressure, oral glucose tolerance, and insulin tolerance were measured. Hepatic oxidative stress as well as messenger RNA (mRNA) and protein levels of peroxisome proliferator-activated receptor alpha (PPAR-α) were analyzed. A significant increase in systolic blood pressure, plasma glucose, total cholesterol, and plasma triglycerides and a significant decrease in HDL-C were observed in HFD rats as compared with control rats. Glucose tolerance and insulin tolerance were also significantly impaired with HFD. α-Amyrin prevented these changes in a dose-dependent manner. Hepatic oxidative stress as well as micro- and macrovesicular fatty changes in hepatocytes caused by HFD were also attenuated by α-amyrin. α-Amyrin preserved the hepatic mRNA and protein levels of PPAR-α, which was reduced in HFD group. This study thus demonstrates that α-amyrin attenuates HFD-induced metabolic syndrome in rats.

Dioscoreophyllum cumminsii (Stapf) Diels leaves halt high-fructose induced metabolic syndrome: Hyperglycemia, insulin resistance, inflammation and oxidative stress

Ethnopharmacological relevanceDioscoreophyllum cumminsii is widely used in the management and treatment of diabetes and obesity in Nigeria. This study evaluates the effect of aqueous leaf extract of D. cumminsii on high-fructose diet-induced metabolic syndrome. MethodsSeventy male rats were randomized into seven groups. All rats were fed with high-fructose diet for 9 weeks except groups A and C rats, which received control diet. In addition to the diet treatment, groups A and B rats received distilled water for 3 weeks starting from the seventh week of the experimental period. Rats in groups C–F orally received 400, 100, 200 and 400mg/kg body weight of aqueous leaf extract of D. cumminsii respectively, while group G received 300mg/kg bodyweight of metformin for 3 weeks starting from the seventh week. ResultsThere was significant (p<0.05) reduction in high-fructose diet-mediated increase in body weight, body mass index, abdominal circumference, blood glucose, insulin, leptin and insulin resistance by aqueous leaf extract of D. cumminsii. Conversely, high-fructose diet-mediated decrease in adiponectin was reversed by the extract. Increased levels of cholesterol, triglycerides, low-density lipoprotein cholesterol, very low-density lipoprotein cholesterol, atherogenic index, cardiac index and coronary artery index were significantly lowered by the extract, while high-fructose diet mediated decrease in high-density lipoprotein cholesterol was increased by the extract. Tumour necrosis factor-α, interleukin-6 and interleukin-8 levels increased significantly in high-fructose diet-fed rats, which were significantly reversed by the extract. High-fructose mediated-decrease in superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, glucose 6-phosphate dehydrogenase and glutathione reduced were significantly reversed by aqueous leaf extract of D. cumminsii. Conversely, elevated levels of malondialdehyde, conjugated dienes, lipid hydroperoxides, protein carbonyl and fragmented DNA were significantly lowered by the extract. ConclusionData generated in this study further laid credence to the hypoglycemic activity of aqueous leaf extract of D. cumminsii as evident from the reversal of hyperglycemia, insulin resistance, dyslipidemia, inflammation and oxidative stress in high-fructose diet-induced metabolic syndrome rats.