Rat Model Of Metabolic Syndrome Research Articles

Visseral Lipectomy Improves Metabolic Syndrome Parameters and Adipokines in a Rat Model of Metabolic Syndrome Induced by Monosodium Glutamate.

Metabolic syndrome (MetS) includes abdominal obesity, hypertension, insulin resistance, and dyslipidemia. Research has indicated that reducing excess visceral fat has positive effects on inflammation and insulin resistance. We examined whether visceral lipectomy modifies the effects of MetS parameters and adipocytokine levels. Each group included 15 newborn male rats: control+sham (C+S), metabolic syndrome+sham (MetS+S), and metabolic syndrome+visceral lipectomy (MetS+VL). On postnatal days 0, 2, 4, 6, 8, and 10, subcutaneous injections of monosodium glutamate (MSG) (4g/mg) were administered to induce MetS. The control group received saline injection. The rats underwent sham surgery or lipectomy on the 120th day of life. Two months post-surgery, tests were performed to check lipid and insulin levels as well as the Lee index, HOMA-IR, serum adiponectin (ADP), resistin, interleukin-6 (IL6), leptin, tumor necrosis factor-alpha (TNF-α), and C-reactive protein (CRP) levels. These findings showed that the Lee index (p = 0.001), insulin resistance (p = 0.002), and hyperinsulinemia (p = 0.009) were significantly improved in the MetS+VL group compared to those in the MetS+S group. The lipid profile was unaffected by visceral lipectomy. Furthermore, visceral lipectomy normalized MetS-induced adipokine imbalance. The decrease in the Lee index and improvement in hyperinsulinemia suggest that visceral lipectomy may benefit impaired glucose metabolism. Although visceral lipectomy has no apparent effect on the lipid profile, positive effects on adipokine levels by reducing various inflammatory markers including resistin, IL6, leptin, TNF-α, and CRP. These findings indicate that visceral lipectomy may have therapeutic potential for MetS. This journal requires that authors assign a level of evidence to each submission to which Evidence-Based Medicine rankings are applicable. This excludes Review Articles, Book Reviews, and manuscripts that concern Basic Science, Animal Studies, Cadaver Studies, and Experimental Studies. For a full description of these Evidence-Based Medicine ratings, please refer to the Table of Contents or the online Instructions to Authors www.springer.com/00266 .

The possible protective effect of luteolin on cardiovascular and hepatic changes in metabolic syndrome rat model.

The metabolic syndrome, or MetS, is currently a global health concern. The anti-inflammatory, anti-proliferative, and antioxidant properties of luteolin are some of its advantageous pharmacological characteristics. This research was designed to establish a MetS rat model and investigate the possible protective effect of luteolin on cardiovascular, hepatic, and metabolic changes in diet-induced metabolic syndrome in rats. Forty adult male albino rats were split into four groups: a negative control group, a group treated with luteolin, a group induced MetS (fed 20% fructose), and a group treated with luteolin (fed 20% fructose and given luteolin). Following the experiment after 8weeks, biochemical, histological (light and electron), and immunohistochemistry analyses were performed on liver and heart tissues. Serum levels of cTnI, CK-MB, and LDH were significantly elevated in response to the cardiovascular effect of MetS. Furthermore, compared to the negative control group, the MetS group showed a marked increase in lipid peroxidation in the cardiac and hepatic tissues, as evidenced by elevated levels of MDA and a decline in the antioxidant defense system, as demonstrated by lower activities of GSH and SOD. The fatty liver-induced group exhibited histological alterations, including disrupted hepatic architecture, dilated and congested central veins, blood sinusoids, and portal veins. In addition to nuclear structural alterations, most hepatocytes displayed varying degrees of cytoplasmic vacuolation, mitochondrial alterations, and endoplasmic reticulum dilatation. These alterations were linked to inflammatory cellular infiltrations, collagen fiber deposition, active hepatic stellate cells, and scattered hypertrophied Kupffer cells, as demonstrated by electron microscopy and validated by immunohistochemical analysis. It is interesting to note that eosinophils were seen between the liver cells and in dilated blood sinusoids. Moreover, the biochemical (hepatic and cardiac) and histological (liver) changes were significantly less severe in luteolin-treated raton a high-fructose diet.These results suggested that luteolin protects against a type of metabolic syndrome that is produced experimentally.

Effects of Aerobic Exercise on Leukocyte-Mediated Liver Destruction in a Rat Model of Metabolic Syndrome

Effects of Aerobic Exercise on Leukocyte-Mediated Liver Destruction in a Rat Model of Metabolic Syndrome

Evaluation of Peripheral Neuropathy in Rat Models of Metabolic Syndrome and Diabetes Mellitus.

The dynamics of nephropathy development in rats with type 2 diabetes mellitus, caused by a high-fat diet and the streptozotocin administration (25 mg/kg), and metabolic syndrome, caused by addition of 20% fructose solution to the diet, was evaluated during the experiment. Models with moderate severity of metabolic changes without significant changes in body weight were obtained after 24 weeks. To study neuropathy severity, the method of electroneuromyography was used; the velocities of motor and sensory excitation propagation along the caudal nerve fibers were measured. In modeled diabetes mellitus against the background of hyperglycemia, a marked decrease in motor and sensory propagation rates was observed, and an increase in the response durations was noted from week 12 to week 24, indicating pronounced neuropathy. In the fructose model, the motor response duration increased from week 12, which possibly indicates the development of peripheral neuropathy.

Green Tea and Green Coffee Therapy for Aortic Calcification Prevention in Metabolic Syndrome Model Rats: Effects on Expression of AKT, mTOR, RUNX2, and Osteopontin Levels

Metabolic syndrome (METS) consists of several independent risk factors for cardiovascular disease (CVD), one of which is vascular calcification (VC). Increased oxidative stress is essential in the pathogenesis of CVD in METS. One of the pathways involved in the pathogenesis of VC is the AKT pathway. Green tea and green coffee have many health benefits, including treating METS risk factors. Although several benefits of green tea and green coffee are known, there is not much information regarding the effects of these 2 extracts for treating heart disease, which is often found in METS sufferers. This research explores the benefits of green tea and green coffee extracts in preventing VC in METS through the AKT/MTOR mechanism. This research focuses on the mechanism of CVD in the AKT-mTOR, RUNX activity, and osteopontin (OPN) expression as one of the downstream pathogenesis of CVD in METS. The research was conducted on METS model rat treated with metformin and green tea with green coffee extracts. Male Sprague-Dawley rats were given a diet high in fat and sugar until they met METS for 4 months, then given treatment for 9 weeks. After 9 weeks, the rat had their aortas isolated for staining with specific antibodies to AKT1, MTOR, RUNX2, and serum OPN levels were measured using ELISA-sandwich methods. There was an increase in the expression of AKT1 and MTOR and a decrease in RUNX2 and OPN2, which was better than rat not treated with green tea and green coffee (p < 0.05). A significant reduction was found in the green tea and green coffee therapy group, which was better than when given metformin alone (p < 0.05). The results of this research showed that there is good potential for therapy using green tea and green coffee extracts to prevent VC in metabolic syndrome models. HIGHLIGHTS Metabolic syndrome consists of several independent risk factors for cardiovascular disease, one of which is vascular calcification. Increased oxidative stress is essential in the pathogenesis of cardiovascular disease in metabolic syndrome. This study explores the benefits of green tea and green coffee extracts in preventing vascular calcification in the metabolic syndrome model through the AKT/MTOR mechanism. This research focuses on the mechanism of CVD in the AKT-mTOR, RUNX activity, and osteopontin (OPN) expression as one of the downstream patogenesis of CVD in METS. The research was conducted on METS model rats treated with metformin and green tea with green coffee extracts. In conclusion, this study showed the potential for therapeutic use of green tea and green coffee extracts to prevent vascular calcification in rat models of metabolic syndrome by increasing AKT1 expression, decreasing MTOR and RUNX2, with the main implication of reducing the circular protein product, osteopontin. GRAPHICAL ABSTRACT

Single high-dose intravenous injection of Wharton’s jelly-derived mesenchymal stem cell exerts protective effects in a rat model of metabolic syndrome

BackgroundMetabolic syndrome (MetS) is a significant epidemiological problem worldwide. It is a pre-morbid, chronic and low-grade inflammatory disorder that precedes many chronic diseases. Wharton’s jelly-derived mesenchymal stem cells (WJ-MSCs) could be used to treat MetS because they express high regenerative capacity, strong immunomodulatory properties and allogeneic biocompatibility. This study aims to investigate WJ-MSCs as a therapy against MetS in a rat model.MethodsTwenty-four animals were fed with high-fat high-fructose (HFHF) diet ad libitum. After 16 weeks, the animals were randomised into treatment groups (n = 8/group) and received a single intravenous administration of vehicle, that is, 3 × 106 cells/kg or 10 × 106 cells/kg of WJ-MSCs. A healthy animal group (n = 6) fed with a normal diet received the same vehicle as the control (CTRL). All animals were periodically assessed (every 4 weeks) for physical measurements, serum biochemistry, glucose tolerance test, cardiovascular function test and whole-body composition. Post-euthanasia, organs were weighed and processed for histopathology. Serum was collected for C-reactive protein and inflammatory cytokine assay.ResultsThe results between HFHF-treated groups and healthy or HFHF-CTRL did not achieve statistical significance (α = 0.05). The effects of WJ-MSCs were masked by the manifestation of different disease subclusters and continuous supplementation of HFHF diet. Based on secondary analysis, WJ-MSCs had major implications in improving cardiopulmonary morbidities. The lungs, liver and heart show significantly better histopathology in the WJ-MSC-treated groups than in the untreated CTRL group. The cells produced a dose-dependent effect (high dose lasted until week 8) in preventing further metabolic decay in MetS animals.ConclusionsThe establishment of safety and therapeutic proof-of-concept encourages further studies by improving the current therapeutic model.

Proteolytic cleavage of insulin receptor in the skeletal muscle of a wistar rat model of metabolic syndrome

Proteolytic cleavage of insulin receptor in the skeletal muscle of a wistar rat model of metabolic syndrome

Effects of CBD on the Phosphorylation of Cardiac Insulin Receptor in Rat Model of Metabolic Syndrome

Metabolic syndrome (MetS) comprises a cluster of conditions that include obesity, insulin resistance, dyslipidemia, hypertension, pro-inflammation, and pro-thrombosis. In the United States, approximately one in three adults is afflicted with MetS. If left unmanaged, it can lead to type 2 diabetes (T2D), which would increase the risk of cardiovascular diseases (CVD). The insulin signaling pathway is critical to regulate glucose homeostasis in the body. During insulin resistance, the pathway is downregulated, and glucose remains in the bloodstream leading to a hyperglycemic state. Recent studies on the benefits of cannabidiol (CBD) have shown it can mitigate CVD risk factors, but its impact on glucose metabolism within the heart remains unclear. To investigate this, the Otsuka Long Evans Tokushima Fatty (OLETF) rat, a model of MetS, and its healthy strain-control, the Long Evans Tokushima Otsuka (LETO) rat, were used. Rats were assigned to three groups (n=8/group): (1) untreated LETO, (2) untreated OLETF, and (3) OLETF + H4CBD (200mg/kg/day x 4 weeks). CBD treatment did not impact the nascent insulin receptor nor the nascent protein kinase B, but the effects of CBD on the phosphorylation and activation of these insulin signaling components have yet to be determined (analyses ongoing). Because CBD has been shown to improve glucose homeostasis previously, we anticipate it is by increasing the activation by phosphorylation of the insulin receptor. A better examination of the effects of CBD on the insulin signaling pathway in the heart will provide greater insight on its therapeutic potential during diabetic cardiomyopathy. USDA Hispanic Education Training Program, Center for Medical Cannabis Research. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Dihydroquercetin regulates HIF-1α/AKT/NR2B signalling to improve impaired brain function in rats with metabolic syndrome

Dihydroquercetin (DHQ) is commonly used as a dietary additive, but its activity in improving brain injury with metabolic syndrome (MS) remains known. In present study, the MS rat model was induced using 10 % fructose water. The apoptosis rate of primary brain cells was detected. The HIF-1α/AKT/NR2B signalling pathway, levels of KEAP1/NRF2, HO-1 and NQO-1 were detected. In vitro experiments were performed using H2O2-stimulated PC-12 cells. The effect of DHQ on rates of cell survival and apoptosis were detected. After silencing HIF-1α, we further elucidate the mechanism of action of DHQ. The results indicated that DHQ reduced the hyperactivity and inhibited oxidative stress via increasing the levels of HIF-1α/AKT/NR2B signalling pathway, whereas regulated KEAP1/NRF2 pathway. In vitro experiments showed that the HIF-1α plays an important role in this process. Overall, DHQ may improve impaired brain function in rats with metabolic syndrome by regulating the HIF-1α/AKT/NR2B signalling pathway.

Fennel seeds extract prevents fructose-induced cardiac dysfunction in a rat model of metabolic syndrome via targeting abdominal obesity, hyperuricemia and NF-κβ inflammatory pathway

BackgroundMetabolic syndrome (MetS) is commonly associated with increased risk of cardiac disease that affects a large number of world populations. ObjectiveThis research attempted to investigate the efficacy of fennel seeds extract (FSE) in preventing development of cardiac dysfunction in rats on fructose enriched diet for 3 months, as a model of MetS. Materials & methodsThirty adult Wistar male rats (160–170 g) were assigned into 5 groups including control, vehicle, FSE (200 mg/kg BW) and fructose (60%) fed rats with and without FSE. Following the last treatment, blood pressure, ECG and heart rate were measured. Next, blood and cardiac tissues were taken for biochemical and histological investigations. ResultsFeeding fructose exhibited characteristic features of MetS involving, hypertension, abnormal ECG, elevated heart rate, serum glucose, insulin, lipids and insulin resistance, accompanied by abdominal obesity, cardiac hypertrophy and hyperuricemia. Fructose fed rats also showed significant reduction in cardiac antioxidants (GSH, SOD, CAT) with elevation in oxidative stress indices (NADPH oxidase, O2.-, H2O2, MDA, PCO), NF-κβ, pro-inflammatory cytokines (TNF-α, IL-1β, IL-6), adhesion molecules (ICAM-1, VCAM-1) and serum cardiac biomarkers (AST, LDH, CK-MB, cTn-I). Histopathological changes evidenced by destruction of cardiac myofibrils, cytoplasmic vacuolization, and aggregation of inflammatory cells were also detected. Consumption of FSE showed high ability to alleviate fructose-induced hypertension, ECG abnormalities, cardiac hypertrophy, metabolic alterations, oxidative stress, inflammation and histological injury. ConclusionFindings could suggest FSE as a complementary supplement for preventing MetS and associated cardiac outcomes. However, well controlled clinical studies are still needed.

Fasudil, a Rho kinase inhibitor, attenuates cardiovascular changes in an experimental rat model of metabolic syndrome via modulation of PCSK9 and BNP.

Fasudil, a Rho kinase inhibitor, attenuates cardiovascular changes in an experimental rat model of metabolic syndrome via modulation of PCSK9 and BNP.

Effect of Ketogenic Diet on the Hypothalamic-Pituitary-Gonadal Axis and Weight loss in Induced Metabolic Syndrome Rat model

Effect of Ketogenic Diet on the Hypothalamic-Pituitary-Gonadal Axis and Weight loss in Induced Metabolic Syndrome Rat model

Quinoa seed: A source of lipophilic nutraceuticals for the prevention of metabolic syndrome in a rat model

Metabolic syndrome (MS) is a cluster of metabolic changes including hypertriglyceridemia, elevated glucose tolerance and fatty liver. The aim of this research was to study the bioactivity of petroleum ether extracts prepared from quinoa 1 and Hualhuas quinoa in a MS rat model. Fatty acids and α-tocopherol were assessed in the extracts. MS was induced by feeding a high fructose-high fat diet (HFFD). Four groups of rats were assigned: the control group, fed a balanced diet; the control group, fed a HFFD diet; and two test groups, fed on a HFFD diet and treated by either quinoa 1 or hualhuas extract. The Glucose tolerance, plasma lipids, oxidative stress biomarkers, liver lipids and histopathology of the liver and heart were assessed. The results showed that extracts from both quinoa varieties had the potential to prevent MS; although quinoa 1 was more effective. In both varieties, the major fatty acid was linoleic. Hualhuas showed a higher percentage of linolenic acid than quinoa 1; while more alpha-tocopherol was present in quinoa1.

Hesperidin alleviates inflammation in the metabolic syndrome model

In metabolic syndrome, activated inflammatory signaling pathways trigger the release of proinflammatory cytokines. Nowadays, the use of natural bioactive compounds is trending as an alternative method for the treatment and management of metabolic syndrome. This study aimed to assess the potential effects of hesperidin in the metabolic syndrome model by analyzing the proinflammatory and anti-inflammatory cytokines in serum and liver. Rats were divided into 4 groups: Control (Rats were fed a standard chow diet and water ad libitum), hesperidin [Rats were fed hesperidin supplemented standard chow diet (1%, 10 g/kg feed) and water ad libitum] metabolic syndrome (Rats were fed standard chow diet with 10% fructose-added-drinking-water), and metabolic syndrome + hesperidin (Rats were fed a hesperidin-added standard chow diet (1%, 10 g/kg) with 10% fructose-added-drinking-water). Rats were sacrificed under ketamine/xylazine anesthesia, blood was obtained and liver tissues were removed. Tumor necrosis factor-alpha, interleukin-1 beta, interleukin-6, interleukin-10, and transforming growth factor-beta in the serum and liver were measured by enzyme-linked immunosorbent assay. In the metabolic syndrome group, higher tumor necrosis factor-alpha, interleukin-1 beta, and interleukin-6, but lower serum and liver interleukin-10 and transforming growth factor-beta were found in the serum and liver compared to the control group. In addition, in the metabolic syndrome + hesperidin group lower interleukin-1 beta and interleukin-6 but higher serum interleukin-10 and transforming growth factor-beta were found in the serum and liver compared to the metabolic syndrome groups. Consequently, hesperidin suppressed the serum and liver proinflammatory cytokine response and stimulated the anti-inflammatory cytokine response in the metabolic syndrome rat model.

Cardioprotective effect of green tea and green coffee extract as metformin’s add-on to prevent cardiac fibrosis in a rat model of metabolic syndrome

Cardioprotective effect of green tea and green coffee extract as metformin’s add-on to prevent cardiac fibrosis in a rat model of metabolic syndrome

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.

Preventive and Therapeutic Effects of Silybum marianum Seed Extract Rich in Silydianin and Silychristin in a Rat Model of Metabolic Syndrome.

Metabolic syndrome (MetS) has become an increasing global health problem, which leads to cardiovascular diseases and type 2 diabetes. Silybum marianum extracts have been reported to possess several biological activities. In this study, an ethyl acetate extract prepared from S. marianum seeds of the Iraqi Kurdistan region was analyzed to identify its chemical constituents. Subsequently, its potential for the prevention and treatment of MetS was studied in a rat model induced by a high-fat/high-fructose diet (HFD/F). Silydianin and silychristin were the most abundant flavonolignan constituents (39.4%) identified in the S. marianum extract (SMEE). HFD/F-induced rats treated with SMEE exhibited preventive effects including reduced serum triglyceride levels (TG), decreased glucose levels in an oral glucose tolerance test (p < 0.001), attenuated weight gain, and reduced blood pressure compared to the untreated control group. Therapeutic application of SMEE after inducing MetS led to lowering of TG (p < 0.001) and glucose levels, in addition to reducing weight gain and normalizing blood pressure (p < 0.005). Thus, S. marianum extract rich in silydianin and silychristin may be useful for preventing and attenuating MetS, and further research and clinical trials are warranted.

Benefits of Chronic Administration of a Carbohydrate-Free Diet on Biochemical and Morphometric Parameters in a Rat Model of Diet-Induced Metabolic Syndrome.

Carbohydrate intake restriction positively affects markers related to metabolic syndrome (MS). However, the effects of long-term carbohydrate-free diets (CFD) have yet to be studied. The main objective of this study was to report the effects on biochemical and morphometric parameters in a rat model of MS. Male Wistar rats were initially divided into two groups: the standard diet group (SD, n = 20); and the MS group (n = 30) fed a high-glucose diet. Ten animals from each group were sacrificed after 20 weeks on their respective diets to verify MS development. The remaining MS animals were divided into two subgroups: one continued with the MS diet (n = 10); and the other transitioned to a carbohydrate-free diet (MS + CFD group, n = 10) for 20 more weeks. At week 40, parameters, including glucose, insulin, lipid profile, ketone bodies, C-reactive protein (CRP), aspartate aminotransferase (AST), alanine aminotransferase (ALT), urea, creatinine, liver and muscle glycogen, and serum, hepatic, renal, and pancreatic malondialdehyde (MDA) levels were assessed. Transitioning to CFD resulted in decreased caloric intake and body weight, with normalized parameters including MDA, insulin, lipid profile, ALT, liver glycogen, creatinine, and CRP levels. This shift effectively reversed the MS-induced alterations, except for glycemia and uremia, likely influenced by the diet's high protein content stimulating gluconeogenesis. This research underscores the potential benefits of long-term carbohydrate restriction in mitigating MS-related markers.

Effects of epicatechin on cardiovascular function in middle-aged diet-induced obese rat models of metabolic syndrome.

The current study aimed to investigate the cardiovascular effects of epicatechin, a flavonoid found in green tea and cocoa, in attenuating complications associated with metabolic syndrome in diet-induced obese rats. Male Wistar-Kyoto (WKY) rats aged 16 weeks were fed either standard rat chow or given a high-fat-high-carbohydrate (HFHC) diet for 20 weeks. Epicatechin treatment (5 mg/kg/d) was administered to a subset of WKY rats commencing at week 8 of the 20 week HFHC feeding period. Body weights, food, water and energy intakes, blood pressure, heart rate and glucose tolerance were measured throughout the treatment period. Oxidative stress and inflammatory markers, lipid levels, cardiac collagen deposition, cardiac electrical function, aortic and mesenteric vessel reactivity were examined after the treatment. Twenty weeks of HFHC feeding in WKY rats resulted in the development of metabolic syndrome indicated by the presence of abdominal obesity, dyslipidaemia, glucose intolerance and increased blood pressure. Epicatechin treatment was found to enhance the oxidative stress status in HFHC groups through an increase in serum nitric oxide levels and a decrease in 8-isoprostane concentrations. Furthermore, WKY-HFHC rats displayed a decrease in IL-6 levels. The lipid profiles in HFHC groups showed improvement, with a decrease in LDL-cholesterol and TAG and an increase in HDL-cholesterol levels observed in WKY-HFHC rats. However, epicatechin was not effective in preventing weight gain, glucose intolerance or hypertension in HFHC fed rats. Overall, the results of this study suggest that epicatechin has the potential to improve the underlying mechanisms associated with metabolic syndrome in obese rats.

Effect of Hibiscus sabdariffa L. on the Metabolism of Arachidonic Acid in the Isolated Kidney of a Rat Model of Metabolic Syndrome.

The renal system is engaged in metabolic syndrome (MS) and metabolites of arachidonic acid (AA) participate in renal homeostasis and disruption of functionality. Hibiscus sabdariffa L (HSL) is used as a diuretic and could improve renal function. The aim of this study was to assess if treatment with HSL at 2% improves renal function in MS through the metabolites of AA. A total of 24 male Wistar rats were divided into four groups: Group 1, control (C); Group 2, MS with 30% sucrose in drinking water, Group 3, MS plus HSL infusion at 2% (MS+HSL); and Group 4, C+HSL. We evaluated the perfusion pressure changes (∆-PP), the activities of cyclooxygenases (COXs), the percentage of AA, the expressions of PLA2, COX2, COX1, 5-LOX, TAXS and CYP450, and the concentrations of prostaglandins in the kidney from rats with MS. There was a decrease in the ∆-PP, in the activities of COXs, and the expressions of COX2 and CYP450 (p ≤ 0.03, respectively)as well asPGE2, TxB2, and LKB4 (p ≤ 0.01, respectively). However, the percentage of AA and expressions of PLA2 and PGE1 (p = 0.01, respectively) were increased in C and MS+HSL. The HSL treatment improved the function and anatomical structure of the kidneys in the MS rats, through antioxidant molecules, and inhibited the pathways that metabolize the AA including that of PLA2, COX2, 5-LOX, TAXS, and CYP450 while favoring the COX1 pathway. This improves the vascular resistance of renal arterioles.