Adenosine Receptor Transcriptomic Profile in Cardiac Tissue of a Zucker Rat Model

Abstract Objectives The correlation of short-term metformin treatment and specific alterations to the gut microbiota in obese models is less known. So, the objectives of this experiment was to investigate the effects of short-term metformin treatment on population of gut microbiota profile in obese rat model. Methods Five week old obese (n = 16) female Zucker rats after one week of acclimation, received AIN-93 G diet for 8 weeks and then rats were randomly assigned 8 rats/group): to 1) obese without metformin (ObC), or 2) obese with metformin (ObMet). Metformin were mixed with AIN-93G diet at 1000 mg/kg of diet. Rats were weighed twice per week. All rats were sacrificed 10 weeks post-metformin treatment and fecal samples were collected and kept at − 80c. Total microbial DNA were collected directly from the fecal samples using a PowerSoil® DNA isolation kit. Isolated DNA were used for shotgun-metagenomics data collection using Illumina NextSeq500 and analyzed using MetaPlAn and HUMAnN. DEICODE and Songbird used calculate log-ratios and differential ranks of taxa and functional pathways associated with metformin treatment respectively. The were then visualized using Qurro. Results There was no significant difference between ObC vs. ObMet group body weight (P = 0.20). Overall microbial beta-diversity (DEICODE), showed significant separation between the obese control and metformin samples (P = 0.0007). Differential ranking (Songbird) of Bacteroides dorei and B. massiliensis vs. all other Bacteroides spp., revealed that B. dorei and B. massiliensis were enriched in the obese metformin group, while the remaining Bacteroides spp. where enriched in the obese control group (P = 0.002). The differential ranking of pathway diversity contributed by the Bacteroides were also associated with treatment group (P = 0.008). Conclusions In summary, in the obese zucker rat model, short-term metformin treatment changes the gut microbiota profile. Funding Sources Arkansas Biosciences Institute.

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Reduced skeletal muscle microvascular network branching and length density in the obese Zucker rat model of non‐insulin dependent diabetes mellitus

The FASEB Journal ◽

10.1096/fasebj.21.6.a1214-a ◽

2007 ◽

Vol 21 (6) ◽

Author(s):

Kelly Fair Benedict ◽

Thomas Cooper Skalak

Keyword(s):

Diabetes Mellitus ◽

Skeletal Muscle ◽

Rat Model ◽

Insulin Dependent Diabetes Mellitus ◽

Insulin Dependent Diabetes ◽

Dependent Diabetes Mellitus ◽

Zucker Rat ◽

Microvascular Network ◽

Obese Zucker Rat ◽

Insulin Dependent

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Effects of Diet Containing Soy Protein Isolate on Liver Metabolic Methylation Status Using Obese Zucker Rat Model (P08-033-19)

Current Developments in Nutrition ◽

10.1093/cdn/nzz044.p08-033-19 ◽

2019 ◽

Vol 3 (Supplement_1) ◽

Author(s):

Reza Hakkak ◽

Soheila Korourian ◽

Oleksandra Pavliv ◽

Stepan Melnyk

Keyword(s):

Rat Model ◽

Soy Protein ◽

Methylation Status ◽

Liver Steatosis ◽

Soy Protein Isolate ◽

The United States ◽

Protein Isolate ◽

Zucker Rats ◽

Zucker Rat ◽

Obese Zucker Rat

Abstract Objectives The obesity epidemic is continuing to grow in the United States and world for past two decades. There is a link between obesity and chronic diseases development such as diabetes, cardiovascular disease, certain types of cancer and liver diseases. Previously, we reported that obesity caused a significant increase liver steatosis and feeding soy protein isolate (SPI) reduced liver steatosis. The mechanism of SPI protection against liver steatosis is less known. We hypothesize that soy protein diet will reduce development of liver steatosis caused by obesity in part by changing methylation status. The objective of the present study was to investigate the effects of SPI feeding on liver metabolic methylation status using obese zucker rat model. Methods After one week of acclimation, five weeks old female lean and obese Zucker rats (n = 8/group) were randomly fed AIN-93-G diet with either casein (CAS as control) or SPI as source of protein for 22 weeks. Rats were weighted twice per week. Liver sample metabolites concentrations were measured using HPLC with Electrochemical Detection and LC-MS. Results Our results shows that; 1) obesity increased body weight significantly (P < 0.001) for both CAS and SPI diets; 2) Obese SPI-fed rats significantly (P < 0.001) reduced liver steatosis compared to obese CAS-fed rats. Also, our results show that liver metabolic profile in lean SPI-fed rats significantly (P < 0.025) increased SAM/SAH ratio (methylation ratio) compare to CAS-fed rats. Obese SPI-fed rats significantly (P < 0.001) decrease level of Homocysteine in liver and increase significantly (P < 0.001) Methionine/Homocysteine ratio. Conclusions In summary we showed that SPI diet can reduce liver steatosis by changing methylation status and improved metabolism of Homocysteine, toxic intracellular compound, through remethylation to Methionine. Funding Sources Arkansas Children's Research Institute's University Medical Group Fund grant program and Arkansas.

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