RETRACTED ARTICLE: Soy protein prevents renal damage in a fructose-induced model of metabolic syndrome via inhibition of NF-kB in male rats

2011 ◽  
Vol 26 (10) ◽  
pp. 1809-1821 ◽  
Author(s):  
Nallasamy Palanisamy ◽  
Carani Venkataraman Anuradha
Keyword(s):  
Metabolic Syndrome ◽  
Soy Protein ◽  
Renal Damage ◽  
Male Rats ◽  
Retracted Article

Renoprotective and blood pressure-lowering effect of dietary soy protein via protein kinase C βII inhibition in a rat model of metabolic syndrome

2010 ◽  
Vol 88 (1) ◽  
pp. 28-37 ◽  
Author(s):  
Nallasamy Palanisamy ◽  
Periyasamy Viswanathan ◽  
Mambakkam Katchapeswaran Ravichandran ◽  
Carani Venkataraman Anuradha
Keyword(s):  
Oxidative Stress ◽  
Blood Pressure ◽  
Metabolic Syndrome ◽  
Renal Function ◽  
Protein Kinase C ◽  
Insulin Sensitivity ◽  
Protein Kinase ◽  
Soy Protein ◽  
Male Rats ◽  
Kinase C

We studied whether substitution of soy protein for casein can improve insulin sensitivity, lower blood pressure (BP), and inhibit protein kinase C βII (PKCβII) activation in kidney in an acquired model of metabolic syndrome. Adult male rats were fed 4 different diets: (i) starch (60%) and casein (20%) (CCD), (ii) fructose (60%) and casein (20%) (FCD), (iii) fructose (60%) and soy protein (20%) (FSD), and (iv) starch (60%) and soy protein (20%) (CSD). Renal function parameters, BP, pressor mechanisms, PKCβII expression, oxidative stress, and renal histology were evaluated after 60 days. FCD rats displayed insulin resistance and significant changes in body weight, kidney weight, urine volume, plasma and urine electrolytes accompanied by significant changes in renal function parameters compared with CCD rats. Elevated BP, plasma angiotensin-converting enzyme (ACE) activity, renal oxidative stress, and reduced nitrite (NO) and kallikrein activity were observed. Western blot analysis revealed enhanced renal expression of membrane-associated PKCβII in the FCD group. Histology showed fatty infiltration and thickening of glomeruli while urinary protein profile revealed a 5-fold increase in albumin. Substitution of soy protein for casein improved insulin sensitivity, lowered BP and PKCβII activation and restored renal function. Antioxidant action, inhibitory effect on ACE and PKCβII activation, and increased availability of kinins and NO could be contributing mechanisms for the benefits of dietary soy protein.

scholarly journals Kidney Injury Caused by Preeclamptic Pregnancy Recovers Postpartum in a Transgenic Rat Model

2021 ◽  
Vol 22 (7) ◽  
pp. 3762
Author(s):  
Sarah M. Kedziora ◽  
Kristin Kräker ◽  
Lajos Markó ◽  
Julia Binder ◽  
Meryam Sugulle ◽  
...  
Keyword(s):  
Rat Model ◽  
Renal Damage ◽  
Kidney Injury ◽  
Tissue Growth ◽  
Female Rats ◽  
Male Rats ◽  
Renal Diseases ◽  
Transgenic Rat ◽  
Increased Risk ◽  
Before And After

Preeclampsia (PE) is characterized by the onset of hypertension (≥140/90 mmHg) and presence of proteinuria (>300 mg/L/24 h urine) or other maternal organ dysfunctions. During human PE, renal injuries have been observed. Some studies suggest that women with PE diagnosis have an increased risk to develop renal diseases later in life. However, in human studies PE as a single cause of this development cannot be investigated. Here, we aimed to investigate the effect of PE on postpartum renal damage in an established transgenic PE rat model. Female rats harboring the human-angiotensinogen gene develop a preeclamptic phenotype after mating with male rats harboring the human-renin gene, but are normotensive before and after pregnancy. During pregnancy PE rats developed mild tubular and glomerular changes assessed by histologic analysis, increased gene expression of renal damage markers such as kidney injury marker 1 and connective-tissue growth factor, and albuminuria compared to female wild-type rats (WT). However, four weeks postpartum, most PE-related renal pathologies were absent, including albuminuria and elevated biomarker expression. Only mild enlargement of the glomerular tuft could be detected. Overall, the glomerular and tubular function were affected during pregnancy in the transgenic PE rat. However, almost all these pathologies observed during PE recovered postpartum.

The protective effect of carvacrol on acetaminophen-induced renal damage in male rats

2022 ◽  
Author(s):  
Alireza Najafizadeh ◽  
Ayat Kaeidi ◽  
Mohammadreza Rahmani ◽  
Elham Hakimizadeh ◽  
Jalal Hassanshahi
Keyword(s):  
Protective Effect ◽  
Renal Damage ◽  
Male Rats

scholarly journals Resolution of metabolic syndrome parameters in subjects following a Mediterranean‐style, low glycemic load diet in conjunction with a soy protein, plant sterol‐(SPS) supplement

2009 ◽  
Vol 23 (S1) ◽  
Author(s):  
Jennifer Jones ◽  
Daniela Ackermann ◽  
Michael Comperatore ◽  
Jose O Leite ◽  
Jacqueline Barona ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Soy Protein ◽  
Plant Sterol ◽  
Glycemic Load

scholarly journals Age features of metabolic syndrome effects on fetal embryonic development of the male rat offsprings

2016 ◽  
Vol 21 (2) ◽  
pp. 71-75
Author(s):  
O. Tkachenko ◽  
V. Kovalenko
Keyword(s):  
Metabolic Syndrome ◽  
Embryonic Development ◽  
Comparative Study ◽  
Fetal Death ◽  
Total Mortality ◽  
Male Rats ◽  
Male Rat ◽  
Adult Rats ◽  
Juvenile Age ◽  
Age Features

Comparative study of embryo-fetal death in females fertilized by males with metabolic syndrome, induced in adult or juvenile age has shown that the offspring of adult rats did not have significant abnormalities in embrio- and fetogenesis. At the same time it has been revealed 4% postimplantation death of offspring in male rats with metabolic syndrome induced in the juvenile age. The pre-implantation loss in this group was 6 folds higher than in control. Accordingly, the total mortality of the offspring rose 2.4 times in comparison with control.

scholarly journals The Effect of Combined Diet Containing n-3 Polyunsaturated Fatty Acids and Silymarin on Metabolic Syndrome in Rats

2019 ◽  
pp. S39-S50
Author(s):  
M. PORUBA ◽  
P. ANZENBACHER ◽  
Z. RACOVA ◽  
O. OLIYARNYK ◽  
M. HÜTTL ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Metabolic Syndrome ◽  
Fatty Acids ◽  
Polyunsaturated Fatty Acids ◽  
Metabolic Disorders ◽  
Male Rats ◽  
Lipid Homeostasis ◽  
Metabolic Disturbances ◽  
Serum Triglycerides ◽  
Esterified Fatty Acids

The risk of development of metabolic syndrome can be increased by hypertriglyceridemia. A search for effective therapy is a subject of considerable attention. Therefore, our hypothesis is that the fish oil (containing polyunsaturated fatty acids; n-3 PUFA) in a combination with silymarin can more effectively protect against hypertriglyceridemia-induced metabolic disturbances. The study was conducted using a unique non-obese strain of rats with hereditary hypertriglyceridemia an accepted model of metabolic syndrome. Adult male rats were treated with n-3 PUFA (300 mg/kg/day) without or with 1 % micronized silymarin in a diet for 4 weeks. The treatment with the diet containing n-3 PUFA and silymarin significantly reduced concentrations of serum triglycerides (-45 %), total cholesterol (-18 %), non-esterified fatty acids (-33 %), and ectopic lipid accumulation in skeletal muscle (-35 %) compared to controls. In addition, an increase in Abcg5 and Abcg8 mRNA expression (as genes affecting lipid homeostasis) as well as in protein content of ABCG5 (+78 %) and ABCG8 (+232 %) transporters have been determined in the liver of treated rats. Our findings suggest that this combined diet could be used in the prevention of hypertriglyceridemia-induced metabolic disorders.

scholarly journals Comparison of high-fat and high-carbohydrate diets for obtaining an experimental model of metabolic syndrome

2021 ◽  
Vol 15 (1) ◽  
pp. 3-14
Author(s):  
T. S. Petryn ◽  
◽  
M. R. Nagalievska ◽  
N. O. Sybirna ◽  
◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Glucose Tolerance ◽  
Pathological Condition ◽  
Male Rats ◽  
Laboratory Animals ◽  
Atherogenic Dyslipidemia ◽  
Chow Diet ◽  
High Fat ◽  
High Carbohydrate

Introduction. Metabolic syndrome is a cluster of metabolic abnormalities that includes hypertension, central obesity, insulin resistance and atherogenic dyslipidemia. Given the wide geographical distribution and growing number of people suffering from this disease, there is an urgent need in developing animal models that would accurately reproduce the development of all symptoms of human metabolic syndrome (insulin resistance, dyslipidemia, obesity and hypertension). The most cost-effective method related to the real causes of metabolic syndrome is the use of different types of diets. Materials and Methods. The study was performed on white outbred male rats about 6 months old and weighing 300–400 g. The metabolic syndrome was induced by high-fat and high-carbohydrate diets. The lipid-enriched diet involved the consumption of regular chow diet for laboratory animals with additional fat content (40 % by weight of chow). The source of additional lipids was olive oil, which is rich in monounsaturated fatty acids (MUFAs). Animals on the diet enriched in carbohydrates together with regular chow diet for laboratory animals consumed 10 % fructose solution instead of drinking water. Glucose tolerance tests were conducted and areas under the glycemic curves were calculated. We determined the content of glycated hemoglobin and glucose concent­ration, the concentration of low-density lipoproteins (LDL), high-density lipoproteins (HDL), triglycerides and cholesterol in the blood plasma of rats. Results. The development of metabolic syndrome induced by an excessive consumption of carbohydrates and lipids for 42 days was accompanied by impaired glucose tolerance, increased glycosylated hemoglobin, triglycerides and cholesterol concentrations, as well as a decreased HDL content. An increase in the concentrations of LDL and activity of paraoxonase were found due to the induction of the pathological condition by an excessive fat intake, while a high carbohydrate diet caused a decrease in paraoxonase activity. Conclusions. The use of fructose for 42 days causes the most pronounced manifestations of the studied pathology. The use of this model will allow determining the biochemical and molecular changes that accompany the development of this pathological condition. It will also facilitate the development and evaluation of the effectiveness of new therapeutic approaches to the treatment of metabolic syndrome.

scholarly journals Diets Containing Soy Protein Isolate Increase Hepatic CYP3A Expression and Inducibility in Weanling Male Rats Exposed during Early Development

2004 ◽  
Vol 134 (12) ◽  
pp. 3270-3276 ◽  
Author(s):  
Martin J. Ronis ◽  
Ying Chen ◽  
Chan-He Jo ◽  
Pippa Simpson ◽  
Thomas M. Badger
Keyword(s):  
Early Development ◽  
Soy Protein ◽  
Soy Protein Isolate ◽  
Protein Isolate ◽  
Male Rats

Dynamic genetic architecture of metabolic syndrome attributes in the rat

2005 ◽  
Vol 21 (2) ◽  
pp. 243-252 ◽  
Author(s):  
Ondrej Seda ◽  
Frantisek Liska ◽  
Drahomira Krenova ◽  
Ludmila Kazdova ◽  
Lucie Sedova ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Genetic Architecture ◽  
Genetic Model ◽  
Interval Mapping ◽  
Male Rats ◽  
Brown Norway ◽  
Whole Genome ◽  
Morphometric Traits ◽  
Whole Genome Analysis ◽  
Genetic Determination

The polydactylous rat strain (PD/Cub) is a highly inbred (F > 90) genetic model of metabolic syndrome. The aim of this study was to analyze the genetic architecture of the metabolic derangements found in the PD/Cub strain and to assess its dynamics in time and in response to diet and medication. We derived a PD/Cub × BN/Cub (Brown Norway) F2 intercross population of 149 male rats and performed metabolic profiling and genotyping and multiple levels of genetic linkage and statistical analyses at five different stages of ontogenesis and after high-sucrose diet feeding and dexamethasone administration challenges. The interval mapping analysis of 83 metabolic and morphometric traits revealed over 50 regions genomewide with significant or suggestive linkage to one or more of the traits in the segregating PD/Cub × BN/Cub population. The multiple interval mapping showed that, in addition to “single” quantitative train loci, there are more than 30 pairs of loci across the whole genome significantly influencing the variation of particular traits in an epistatic fashion. This study represents the first whole genome analysis of metabolic syndrome in the PD/Cub model and reveals several new loci previously not connected to the genetics of insulin resistance and dyslipidemia. In addition, it attempts to present the concept of “dynamic genetic architecture” of metabolic syndrome attributes, evidenced by shifts in the genetic determination of syndrome features during ontogenesis and during adaptation to the dietary and pharmacological influences.

Sign in / Sign up

Export Citation Format

Share Document