scholarly journals Osthol Ameliorates Kidney Damage and Metabolic Syndrome Induced by a High-Fat/High-Sugar Diet

2021 ◽  
Vol 22 (5) ◽  
pp. 2431
Author(s):  
Fernando E. García-Arroyo ◽  
Guillermo Gonzaga-Sánchez ◽  
Edilia Tapia ◽  
Itzel Muñoz-Jiménez ◽  
Lino Manterola-Romero ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Metabolic Syndrome ◽  
Western Diet ◽  
Kidney Damage ◽  
Kidney Cortex ◽  
Tubular Damage ◽  
Related Factor ◽  
Lipogenic Enzymes ◽  
High Fat ◽  
High Sugar

Excessive intake of fructose results in metabolic syndrome (MS) and kidney damage, partly mediated by its metabolism by fructokinase-C or ketohexokinase-C (KHK-C). Osthol has antioxidant properties, is capable of regulating adipogenesis, and inhibits KHK-C activity. Here, we examined the potential protective role of osthol in the development of kidney disease induced by a Western (high-fat/high-sugar) diet. Control rats fed with a high-fat/high-sugar diet were compared with two groups that also received two different doses of osthol (30 mg/kg/d or 40 mg/kg/d body weight BW). A fourth group served as a normal control and received regular chow. At the end of the follow-up, kidney function, metabolic markers, oxidative stress, and lipogenic enzymes were evaluated. The Western diet induced MS (hypertension, hyperglycemia, hypertriglyceridemia, obesity, hyperuricemia), a fall in the glomerular filtration rate, renal tubular damage, and increased oxidative stress in the kidney cortex, with increased expression of lipogenic enzymes and increased kidney KHK expression. Osthol treatment prevented the development of MS and ameliorated kidney damage by inhibiting KHK activity, preventing oxidative stress via nuclear factor erythroid 2-related factor (Nrf2) activation, and reducing renal lipotoxicity. These data suggest that the nutraceutical osthol might be an ancillary therapy to slow the progression of MS and kidney damage induced by a Western diet.

scholarly journals Pregnant rats treated with a high-fat/prooxidant Western diet with ANG II and TNF-α are resistant to elevations in blood pressure and renal oxidative stress

2015 ◽  
Vol 308 (11) ◽  
pp. R945-R956 ◽  
Author(s):  
Mark W. Cunningham ◽  
Crystal A. West ◽  
Xuerong Wen ◽  
Aihua Deng ◽  
Chris Baylis
Keyword(s):  
Oxidative Stress ◽  
Western Diet ◽  
Kidney Cortex ◽  
Ang Ii ◽  
Sprague Dawley ◽  
High Fat ◽  
Redox Systems ◽  
Plasma Protein Concentration ◽  
Pregnant Rats ◽  
Tnf Α

Oxidative stress and inflammation are risk factors for hypertension in pregnancy. Here, we examined the 24-h mean arterial pressure (MAP) via telemetry and the nitric oxide (NO) and redox systems in the kidney cortex, medulla, and aorta of virgin and pregnant rats treated with a high-fat/prooxidant Western diet (HFD), ANG II, and TNF-α. Female Sprague-Dawley rats were given a normal diet (ND) or a HFD for 8 wk before mating. Day 6 of pregnancy and age-matched virgins were implanted with minipumps infusing saline or ANG II (150 ng·kg−1·min−1) + TNF-α (75 ng/day) for 14 days. Groups consisted of Virgin + ND + Saline (V+ND) ( n = 7), Virgin + HFD +ANG II and TNF-α (V+HFD) ( n = 7), Pregnant + ND + Saline (P+ND) ( n = 6), and Pregnant + HFD + ANG II and TNF-α (P+HFD) ( n = 8). After day 6 of minipump implantation, V+HFD rats displayed an increase in MAP on days 7, 8, and 10–15 vs. V+ND rats. P+HFD rats, after day 6 of minipump implantation, showed an increase in MAP only on day 7 vs. P+ND rats. P+HFD rats had a normal fall in 24-h MAP, hematocrit, plasma protein concentration, and osmolality at late pregnancy. No change in kidney cortex, medulla, or aortic oxidative stress in P+HFD rats. P+HFD rats displayed a decrease in nNOSβ abundance, but no change in kidney cortex NOxcontent vs. P+ND rats. Pregnant rats subjected to a chronic HFD and prooxidant and proinflammatory insults have a blunted increase in 24-h MAP and renal oxidative stress. Our data suggest renal NO bioavailability is not altered in pregnant rats treated with a HFD, ANG II, and TNF-α.

scholarly journals Cardiovascular function in male and female JCR:LA-cp rats: effect of high-fat/high-sucrose diet

2017 ◽  
Vol 312 (4) ◽  
pp. H742-H751 ◽  
Author(s):  
Ian Hunter ◽  
Amanda Soler ◽  
Gregory Joseph ◽  
Brenda Hutcheson ◽  
Chastity Bradford ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Metabolic Syndrome ◽  
Cardiovascular Function ◽  
Western Diet ◽  
Female Rats ◽  
Male Rats ◽  
High Fat ◽  
Male And Female ◽  
Normal Chow ◽  
High Sucrose

Thirty percent of the world population is diagnosed with metabolic syndrome. High-fat/high-sucrose (HF/HS) diet (Western diet) correlates with metabolic syndrome prevalence. We characterized effects of the HF/HS diet on vascular (arterial stiffness, vasoreactivity, and coronary collateral development) and cardiac (echocardiography) function, oxidative stress, and inflammation in a rat model of metabolic syndrome (JCR rats). Furthermore, we determined whether male versus female animals were affected differentially by the Western diet. Cardiovascular function in JCR male rats was impaired versus normal Sprague-Dawley (SD) rats. HF/HS diet compromised cardiovascular (dys)function in JCR but not SD male rats. In contrast, cardiovascular function was minimally impaired in JCR female rats on normal chow. However, cardiovascular function in JCR female rats on the HF/HS diet deteriorated to levels comparable to JCR male rats on the HF/HS diet. Similarly, oxidative stress was markedly increased in male but not female JCR rats on normal chow but was equally exacerbated by the HF/HS diet in male and female JCR rats. These results indicate that the Western diet enhances oxidative stress and cardiovascular dysfunction in metabolic syndrome and eliminates the protective effect of female sex on cardiovascular function, implying that both males and females with metabolic syndrome are at equal risk for cardiovascular disease. NEW & NOTEWORTHY Western diet abolished protective effect of sex against cardiovascular disease (CVD) development in premenopausal animals with metabolic syndrome. Western diet accelerates progression of CVD in male and female animals with preexisting metabolic syndrome but not normal animals. Exacerbation of baseline oxidative stress correlates with accelerated progression of CVD in metabolic syndrome animals on Western diet.

Lepidium Meyenii Supplemented Diet Modulates Neurobehavioral and Biochemical Parameters in Mice Fed High-Fat-High-Sugar Diet

2020 ◽  
Vol 20 ◽  
Author(s):  
Anthony T. Olofinnade ◽  
Abiola Alawode ◽  
Adejoke Y. Onaolapo ◽  
Olakunle J. Onaolapo
Keyword(s):  
Oxidative Stress ◽  
Metabolic Syndrome ◽  
Body Weight ◽  
Inflammatory Markers ◽  
Acetylcholinesterase Activity ◽  
Standard Diet ◽  
High Fat ◽  
Lepidium Meyenii ◽  
High Sugar ◽  
Increased Risk

Background: Metabolic syndrome has been associated with increased risk of cardiovascular disease, diabetes mellitus, and neurodegenerative disorders. Known side-effects of currently-available drugs necessitate the search for possibly better treatment options. Objective: This study examined the effects of dietary lepidium meyenii (MACA) supplementation on neurobehaviour, metabolic profile, levels of inflammatory markers, and oxidative stress parameters in a mouse model of metabolic syndrome. Methodology: Mice were randomly-assigned into 8 groups of ten animals each. Groups consist of standard diet (SD) control, high fat/high sugar (HFHS) control and three groups each of lepidium meyenii incorporated into either SD or HFHS diet at 0.1, 0.2 and 0.4 %. Mice were fed for seven weeks, and body weight was measured weekly. Open-field behaviors and radial-arm/Y-maze spatial memory were scored at the end of the study. Twenty-four hours after the last behavioral test, fasting blood glucose levels were estimated. Animals were then euthanized, and blood taken for estimation of serum lipid profile. Whole brains were excised, weighed and homogenized for the estimation of levels of lipid peroxidation, inflammatory markers, antioxidant status, and acetylcholinesterase activity. Results: MACA-supplemented diet was associated with a decrease in body weight gain, an increase in food intake (at lower concentrations), suppression of grooming behavior, and decrease in acetylcholinesterase activity. MACA-supplement also reversed HFHS-induced memory impairment, anxiety, hyperglycaemia, lipid derangement, oxidative stress, and derangement of inflammatory markers. Conclusion: Dietary supplementation with MACA shows beneficial effects in mitigating the effects of metabolic syndrome on the brain in mice.

scholarly journals Metabolic Effects of the Sweet Protein MNEI as a Sweetener in Drinking Water. A Pilot Study of a High Fat Dietary Regimen in a Rodent Model

Nutrients ◽  
2019 ◽  
Vol 11 (11) ◽  
pp. 2643
Author(s):  
Rosa Cancelliere ◽  
Serena Leone ◽  
Cristina Gatto ◽  
Arianna Mazzoli ◽  
Carmine Ercole ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Lipid Profile ◽  
Western Diet ◽  
Metabolic Effects ◽  
High Fat ◽  
Metabolic Derangement ◽  
Dietary Regimen ◽  
Sweet Proteins ◽  
Sweet Protein ◽  
Typical Western Diet

Sweeteners have become integrating components of the typical western diet, in response to the spreading of sugar-related pathologies (diabetes, obesity and metabolic syndrome) that have stemmed from the adoption of unbalanced dietary habits. Sweet proteins are a relatively unstudied class of sweet compounds that could serve as innovative sweeteners, but their introduction on the food market has been delayed by some factors, among which is the lack of thorough metabolic and toxicological studies. We have tried to shed light on the potential of a sweet protein, MNEI, as a fructose substitute in beverages in a typical western diet, by studying the metabolic consequences of its consumption on a Wistar rat model of high fat diet-induced obesity. In particular, we investigated the lipid profile, insulin sensitivity and other indicators of metabolic syndrome. We also evaluated systemic inflammation and potential colon damage. MNEI consumption rescued the metabolic derangement elicited by the intake of fructose, namely insulin resistance, altered plasma lipid profile, colon inflammation and translocation of lipopolysaccharides from the gut lumen into the circulatory system. We concluded that MNEI could represent a valid alternative to fructose, particularly when concomitant metabolic disorders such as diabetes and/or glucose intolerance are present.

The combination of maternal and offspring high-fat diets causes marked oxidative stress and development of metabolic syndrome in mouse offspring

Life Sciences ◽  
2016 ◽  
Vol 151 ◽  
pp. 70-75 ◽  
Author(s):  
Junya Ito ◽  
Kiyotaka Nakagawa ◽  
Shunji Kato ◽  
Taiki Miyazawa ◽  
Fumiko Kimura ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Metabolic Syndrome ◽  
High Fat ◽  
High Fat Diets ◽  
Fat Diets

Sleep apnoea and nutrition

2009 ◽  
Vol 302 ◽  
pp. 1-3
Keyword(s):  
Oxidative Stress ◽  
Metabolic Syndrome ◽  
Clinical Trials ◽  
Weight Reduction ◽  
High Fat Diet ◽  
Sleep Apnoea ◽  
High Fat ◽  
Nutritional Treatment ◽  
Nutritional Influences

In a nutshellPotential nutritional influences on sleep apnoea include: overweight, oxidative stress, inflammation, metabolic syndrome and high fat diet.However, so far weight reduction is the only nutritional treatment stemming from this list that is well supported by clinical trials.

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