Polycystic kidney disease (PKD) is a genetic disorder characterized by multiple cyst formation that increases renal size, structural damage, and loss of function. Studies showed soy protein isolate (SPI) protective against chronic kidney disease and omega‐3 polyunsaturated fatty acids (n‐3 PUFAs) decrease inflammation. Few studies have examined the role of diet in PKD. The study objective was to investigate whether SPI and/or n‐3 PUFA supplementation attenuates PKD progression. Young (age 28 d) female pck rats were randomly assigned (n=12/group) to diets consisting of casein + corn oil (Casein + CO), casein + soybean oil (casein + SO), SPI + soybean oil (SPI + SO) or SPI + 1:1 soybean/salmon oil (SPI + BLEND) for 12‐weeks. Kidney weights were highest in the SPI + BLEND group. Histology showed interstitial inflammation, fibrotic changes, interstitial matrix deposition, and structural effacement due to cyst growth in all groups. Cortical cyst obstruction indicating more extensive nephron damage was only observed in the SPI + BLEND group. The SPI +BLEND group had the highest (11.78 + 0.60 mg/dL, P=0.01) and Casein + SO group the lowest (9.28 + 0.81, P=0.01) serum blood urea nitrogen. Urinary calcium and phosphorus was higher in the casein than SPI groups. There were no significant differences in serum calcium, phosphorus, uric acid, total protein or albumin. Based on the results, diet did not attenuate PKD progression.Grant Funding Source: WVU Hatch Grant H459
Studies have reported that high fructose intake promotes de novo lipogenesis (DNL). In turn, DNL stimulation can promote non‐alcoholic fatty liver disease (NAFLD), a metabolic condition that can progress to cirrhosis and liver failure. A frequent alternative to sucrose in calorically sweetened beverages, high fructose corn syrup‐55 (HFCS‐55) contains a higher percentage of free fructose (55%) compared to sucrose (50%, all of which is combined with glucose as a disaccharide). The objective of this study was to determine the effect of HFCS‐55 sweetened solution intake on hepatic lipid metabolism and risk of developing NAFLD in a rodent model. Female Sprague‐Dawley rats (age 28 days) were randomly assigned (n=7/group) to one of four treatment groups consisting of distilled deionized water (ddH2O) or ddH2O sweetened with sucrose, fructose or HFCS‐55 for 8 weeks. Caloric sweeteners were administered at a concentration of 13% w/v, the level typically found in sugar‐sweetened beverages. Gene expression of key transcription factors and enzymes involved in DNL including sterol regulatory element‐binding protein 1c (SREBP‐1c), fatty acid synthase (FAS), and stearoyl‐CoA desaturase 1 (SCD1) as well as peroxisome proliferator‐activated receptor alpha (PPARα), a transcription factor activating lipolysis, were measured using real‐time quantitative polymerase chain reactions (RT‐qPCR). Liver fatty acid composition was determined using gas chromatography and serum clinical markers were measured by enzymatic assays. Expression of SREBP‐1c (P=0.02) and FAS (P=0.001), molecular markers of DNL, were up‐regulated in all caloric sugar treatment groups compared to the ddH2O group. Transcript abundance of SCD1, which is involved in synthesizing palmitoleate (C16:1n‐7) and oleate (C18:1n‐9) from palmitate (C16:0) and stearate (C18:0), was also induced in all caloric sugar treatment groups compared to the ddH2O group (P=0.001). Hepatic palmitoleate content was higher in the sucrose and HFCS‐55 groups compared to the ddH2O group (P<0.001), and hepatic oleate content was highest in the HFCS‐55 group (P<0.001). PPARα expression was lower in the sucrose and HFCS‐55 groups (P=0.002). Altogether, we show evidence that HFCS‐55 intake had a greater effect on fatty acid metabolism than sucrose by promoting DNL, which was not compensated for by increased lipolysis. Rats drinking HFCS‐55 solution had highest hepatic triglyceride content (P=0.03) among all treatment groups and higher low density lipoprotein (P=0.02) than rats drinking ddH2O, indicating NAFLD. Thus, HFCS‐55 intake in healthy growing rats resulted in higher risk of NAFLD indicated by hepatic lipid accumulation and dyslipidemia.Support or Funding InformationThis research was sponsored in part by the West Virginia Research Challenge Fund through a grant from the Davis College of Agriculture, West Virginia University.
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