scholarly journals Effect of Rosmarinic Acid on the Serum Parameters of Glucose and Lipid Metabolism and Oxidative Stress in Estrogen-Deficient Rats

Nutrients ◽  
2019 ◽  
Vol 11 (2) ◽  
pp. 267 ◽  
Author(s):  
Maria Zych ◽  
Ilona Kaczmarczyk-Sedlak ◽  
Weronika Wojnar ◽  
Joanna Folwarczna

Rosmarinic acid is found in medicinal and spice plants such as rosemary, lemon balm, and mint. The aim of the study was to investigate the effect of rosmarinic acid on parameters of glucose and lipid metabolism and parameters of oxidative stress in rats in the early phase of estrogen deficiency. The study was carried out on mature female Wistar rats divided into the following groups: sham-operated control rats, ovariectomized control rats, and ovariectomized rats treated orally with rosmarinic acid at a dose of 10 mg/kg or 50 mg/kg daily for 28 days. The concentration of sex hormones, parameters related to glucose and lipid metabolism as well as parameters of antioxidant abilities and oxidative damage were determined in the blood serum. In the ovariectomized control rats, the homeostasis model assessment of insulin resistance (HOMA-IR) index and cholesterol concentration increased, the superoxide dismutase activity increased, and the reduced glutathione concentration decreased. Administration of rosmarinic acid at both doses induced decreases in the fructosamine concentration and HOMA-IR, an increase in the concentration of reduced glutathione, and a decrease in the concentration of advanced oxidation protein products in ovariectomized rats. Moreover, rosmarinic acid at a dose of 50 mg/kg induced a decrease in the total cholesterol and triglyceride concentrations. The results indicate that rosmarinic acid may be useful in the prevention of metabolic disorders associated with estrogen deficiency, however further studies are necessary.

Nutrients ◽  
2019 ◽  
Vol 11 (4) ◽  
pp. 803 ◽  
Author(s):  
Maria Zych ◽  
Weronika Wojnar ◽  
Sławomir Dudek ◽  
Ilona Kaczmarczyk-Sedlak

Oxidative stress is believed to be associated with both postmenopausal disorders and cataract development. Previously, we have demonstrated that rosmarinic and sinapic acids, which are diet-derived antioxidative phenolic acids, counteracted some disorders induced by estrogen deficiency. Other studies have shown that some phenolic acids may reduce cataract development in various animal models. However, there is no data on the effect of phenolic acids on oxidative stress markers in the lenses of estrogen-deficient rats. The study aimed to investigate whether administration of rosmarinic acid and sinapic acid affects the antioxidative abilities and oxidative damage parameters in the lenses of estrogen-deficient rats. The study was conducted on three-month-old female Wistar rats. The ovariectomized rats were orally treated with rosmarinic acid at doses of 10 and 50 mg/kg or sinapic acid at doses of 5 and 25 mg/kg, for 4 weeks. The content of reduced glutathione (GSH), oxidized glutathione and amyloid β1-42, as well as products of protein and lipid oxidation, were assessed. Moreover, the activities of superoxide dismutase, catalase, and some glutathione-related enzymes in the lenses were determined. Rosmarinic and sinapic acids in both doses resulted in an increase in the GSH content and glutathione reductase activity. They also improved parameters connected with protein oxidation. Since GSH plays an important role in maintaining the lens transparency, the increase in GSH content in lenses after the use of rosmarinic and sinapic acids seems to be beneficial. Therefore, both the investigated dietary compounds may be helpful in preventing cataract.


2012 ◽  
Vol 167 (4) ◽  
pp. 569-578 ◽  
Author(s):  
Francisco J Ortega ◽  
Mónica Sabater ◽  
José M Moreno-Navarrete ◽  
Neus Pueyo ◽  
Patricia Botas ◽  
...  

ObjectiveIncreased circulating calprotectin has been reported in obese subjects but not in association with measures of insulin resistance and type 2 diabetes (T2D). The main aim of this study was to determine whether calprotectins in plasma and urine are associated with insulin resistance.DesignWe performed both cross-sectional and longitudinal (diet-induced weight loss) studies.MethodsCirculating calprotectin concentrations (ELISA), other inflammatory markers, homeostasis model assessment of insulin resistance (HOMA-IR), and parameters of glucose and lipid metabolism were evaluated in 298 subjects (185 with normal (NGT) and 62 with impaired (IGT) glucose tolerance and 51 T2D subjects). Calprotectin was also evaluated in urine samples from 71 participants (50 NGT and 21 subjects with IGT). Insulin sensitivity (SI, Minimal Model) was determined in a subset of 156 subjects, and the effects of weight loss were investigated in an independent cohort of obese subjects (n=19).ResultsCirculating calprotectin was significantly increased in IGT–T2D (independently of BMI) and positively associated with HOMA-IR, obesity measures, inflammatory markers, and parameters of glucose and lipid metabolism. Similar findings were reported for calprotectin concentrations in urine. In the subset of subjects, the association of calprotectin withSIwas independent of BMI and age. In fact,SItogether with C-reactive protein contributed to 27.4% of calprotectin variance after controlling for age and blood neutrophils count. Otherwise, weight loss led to decreased circulating calprotectin in parallel to fasting glucose and HOMA-IR.ConclusionThese findings suggest that circulating and urinary concentrations of calprotectin are linked to chronic low-grade inflammation and insulin resistance beyond obesity.


Antioxidants ◽  
2020 ◽  
Vol 9 (12) ◽  
pp. 1201
Author(s):  
Claudio Pirozzi ◽  
Adriano Lama ◽  
Chiara Annunziata ◽  
Gina Cavaliere ◽  
Clara Ruiz-Fernandez ◽  
...  

Lines of evidence have shown the embryogenic and transgenerational impact of bisphenol A (BPA), an endocrine-disrupting chemical, on immune-metabolic alterations, inflammation, and oxidative stress, while BPA toxic effects in adult obese mice are still overlooked. Here, we evaluate BPA’s worsening effect on several hepatic maladaptive processes associated to high-fat diet (HFD)-induced obesity in mice. After 12 weeks HFD feeding, C57Bl/6J male mice were exposed daily to BPA (50 μg/kg per os) along with HFD for 3 weeks. Glucose tolerance and lipid metabolism were examined in serum and/or liver. Hepatic oxidative damage (reactive oxygen species, malondialdehyde, antioxidant enzymes), and mitochondrial respiratory capacity were evaluated. Moreover, liver damage progression and inflammatory/immune response were determined by histological and molecular analysis. BPA amplified HFD-induced alteration of key factors involved in glucose and lipid metabolism, liver triglycerides accumulation, and worsened mitochondrial dysfunction by increasing oxidative stress and reducing antioxidant defense. The exacerbation by BPA of hepatic immune-metabolic dysfunction induced by HFD was shown by increased toll-like receptor-4 and its downstream pathways (i.e., NF-kB and NLRP3 inflammasome) amplifying inflammatory cytokine transcription and promoting fibrosis progression. This study evidences that BPA exposure represents an additional risk factor for the progression of fatty liver diseases strictly related to the cross-talk between oxidative stress and immune-metabolic impairment due to obesity.


2021 ◽  
Vol 22 (11) ◽  
pp. 6149
Author(s):  
Nathan Favalier ◽  
Vincent Véron ◽  
Michael Marchand ◽  
Anne Surget ◽  
Patrick Maunas ◽  
...  

Rainbow trout are considered as a poor user of dietary carbohydrates, displaying persistent postprandial hyperglycaemia when fed a diet containing high amounts of carbohydrates. While this phenotype is well-described in juveniles, less attention was given to broodstock. Our objective was to assess for the first time the short-term consequences of feeding mature female and male, and neomale trout with a low-protein high-carbohydrate diet on glucose and lipid metabolism. Fish were fed for two days with a diet containing either no or 32% of carbohydrates. We analysed plasma metabolites, mRNA levels and enzymatic activities of glycolysis, gluconeogenesis, de novo lipogenesis and β-oxidation in the liver. Results demonstrated that the glucose and lipid metabolism were regulated by the nutritional status in all sexes, irrespective of the carbohydrate intake. These data point out that carbohydrate intake during a short period (5 meals) at 8 °C did not induce specific metabolic changes in broodstock. Finally, we demonstrated, for the first time, sex differences regarding the consequences of two days of feeding on glucose and lipid metabolism.


Cholesterol ◽  
2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
Hirokazu Kakuda ◽  
Junji Kobayashi ◽  
Mio Nakato ◽  
Noboru Takekoshi

Introduction. The objective of this study was to clarify how pitavastatin affects glucose and lipid metabolism, renal function, and oxidative stress. Methods. Ten Japanese men (average age of 33.9 years) were orally administered 2 mg of pitavastatin for 4 weeks. Postprandial glucose, lipoprotein metabolism, and oxidative stress markers were evaluated at 0 and 4 weeks of pitavastatin treatment (2 mg once daily) with a test meal consisting of total calories: 460 kcal, carbohydrates: 56.5 g (226 kcal), protein: 18 g (72 kcal), lipids: 18 g (162 kcal), and NaCl: 1.6 g. Metabolic parameters were measured at 0, 60, and 120 minutes after test meal ingestion. Results. After administration of pitavastatin, serum total cholesterol, low-density lipoprotein cholesterol, apolipoprotein B, arachidonic acid, insulin, and adjusted urinary excretion of uric acid decreased, whereas creatinine clearance (CCr) and uric acid clearance (CUA) increased. And postprandial versus fasting urine 8-hydroxydeoxyguanosine remained unchanged, while postprandial versus fasting isoprostane decreased after pitavastatin treatment. Next, we compared postprandial glucose and lipid metabolism after test meal ingestion before and after pitavastatin administration. Incremental areas under the curve significantly decreased for triglycerides (P<0.05) and remnant-like particle cholesterol (P<0.01), while those for apolipoprotein E (apoE), glucose, insulin, and high-sensitivity C-reactive protein remained unchanged. Conclusion. Pitavastatin improves postprandial oxidative stress along with hyperlipidemia.


2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Saisai Li ◽  
Linjuan Ma ◽  
Yang Song ◽  
Jiehong Zheng ◽  
Yuqun Cai ◽  
...  

Abstract Background Previous studies have indicated that women with a history of menstrual disorders have an increased risk of metabolic and cardiovascular diseases. This has been attributed to the high proportion of polycystic ovary syndrome (PCOS) among this group. The favorable effects of hormone replacement therapy (HRT) on serum lipid profiles and glucose homeostasis in postmenopausal women is widely accepted. Whether HRT can also show positive effects on metabolic homeostasis in menopausal women with prior menstrual disorders (a putative PCOS phenotype) has not been reported yet. The aim of the study was to compare the effects of HRT on glucose and lipid metabolism in peri- and postmenopausal women with prior menstrual disorders and controls who did not have prior menstrual disorders. Methods A retrospective multicenter study was conducted including 595 peri- and postmenopausal women who received HRT at four hospitals in the Zhejiang Province from May 31, 2010 to March 8, 2021. Participants were divided into the Normal menstruation group and the Menstrual disorders group according to their prior usual menstrual cycle pattern. Glucose and lipid metabolism indicators were assessed at baseline and after HRT. The results were compared between and within the groups, and data from peri- and postmenopausal women were analyzed separately. Results HRT significantly decreased fasting insulin and homeostasis model assessment of insulin resistance in perimenopausal users, and fasting plasma glucose levels in postmenopausal users with prior menstrual disorders, compared with baseline. Furthermore, HRT decreased low-density lipoprotein cholesterol, total cholesterol, fasting insulin, fasting plasma glucose and homeostasis model assessment of insulin resistance in both peri- and postmenopausal controls, compared with baseline. Nevertheless, no significant differences were observed in any of the glucose or lipid metabolism indicators at baseline and follow-up, as well as changes from baseline levels between menopausal women with and without prior menstrual disorders. Conclusions HRT shows more obvious within-group improvements in glucose and lipid metabolism in controls, but there is no significant between-group difference. Further prospective studies are required for confirmation.


2017 ◽  
Vol 102 (2) ◽  
pp. e706-e717 ◽  
Author(s):  
Z.-P. Lv ◽  
Y.-Z. Peng ◽  
B.-B. Zhang ◽  
H. Fan ◽  
D. Liu ◽  
...  

2020 ◽  
Vol 21 (18) ◽  
pp. 6902
Author(s):  
Adam Włodarski ◽  
Justyna Strycharz ◽  
Adam Wróblewski ◽  
Jacek Kasznicki ◽  
Józef Drzewoski ◽  
...  

Oxidative stress (OxS) is the cause and the consequence of metabolic syndrome (MetS), the incidence and economic burden of which is increasing each year. OxS triggers the dysregulation of signaling pathways associated with metabolism and epigenetics, including microRNAs, which are biomarkers of metabolic disorders. In this review, we aimed to summarize the current knowledge regarding the interplay between microRNAs and OxS in MetS and its components. We searched PubMed and Google Scholar to summarize the most relevant studies. Collected data suggested that different sources of OxS (e.g., hyperglycemia, insulin resistance (IR), hyperlipidemia, obesity, proinflammatory cytokines) change the expression of numerous microRNAs in organs involved in the regulation of glucose and lipid metabolism and endothelium. Dysregulated microRNAs either directly or indirectly affect the expression and/or activity of molecules of antioxidative signaling pathways (SIRT1, FOXOs, Keap1/Nrf2) along with effector enzymes (e.g., GPx-1, SOD1/2, HO-1), ROS producers (e.g., NOX4/5), as well as genes of numerous signaling pathways connected with inflammation, insulin sensitivity, and lipid metabolism, thus promoting the progression of metabolic imbalance. MicroRNAs appear to be important epigenetic modifiers in managing the delicate redox balance, mediating either pro- or antioxidant biological impacts. Summarizing, microRNAs may be promising therapeutic targets in ameliorating the repercussions of OxS in MetS.


2020 ◽  
Vol 0 (0) ◽  
pp. 0
Author(s):  
Hsin-Hsueh Shen ◽  
Zheng-Zong Lai ◽  
Hsiang-Yu Yang ◽  
Ping-Nan Chen ◽  
Wei-Jou Shih ◽  
...  

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