High Amylose Resistant Starch Diet Ameliorates Oxidative Stress, Inflammation, and Progression of Chronic Kidney Disease

Abstract

Inflammation is a major mediator of CKD progression and is partly driven by altered gut microbiome and intestinal barrier disruption, events which are caused by: urea influx in the intestine resulting in dominance of urease-possessing bacteria; disruption of epithelial barrier by urea-derived ammonia leading to endotoxemia and bacterial translocation; and restriction of potassium-rich fruits and vegetables which are common sources of fermentable fiber. Restriction of these foods leads to depletion of bacteria that convert indigestible carbohydrates to short chain fatty acids which are important nutrients for colonocytes and regulatory T lymphocytes. We hypothesized that a high resistant starch diet attenuates CKD progression. Male Sprague Dawley rats were fed a chow containing 0.7% adenine for 2 weeks to induce CKD. Rats were then fed diets supplemented with amylopectin (low-fiber control) or high fermentable fiber (amylose maize resistant starch, HAM-RS2) for 3 weeks. CKD rats consuming low fiber diet exhibited reduced creatinine clearance, interstitial fibrosis, inflammation, tubular damage, activation of NFkB, upregulation of pro-inflammatory, pro-oxidant, and pro-fibrotic molecules; impaired Nrf2 activity, down-regulation of antioxidant enzymes, and disruption of colonic epithelial tight junction. The high resistant starch diet significantly attenuated these abnormalities. Thus high resistant starch diet retards CKD progression and attenuates oxidative stress and inflammation in rats. Future studies are needed to explore the impact of HAM-RS2 in CKD patients.

Dose-dependent deleterious and salutary actions of the Nrf2 inducer dh404 in chronic kidney disease

“…The tissue sections were examined in a blinded fashion and the severity of the lesions quantified as described in in an earlier study [36].…”

Effect of Synbiotic Therapy on Gut–Derived Uremic Toxins and the Intestinal Microbiome in Patients with CKD

“…Rossi et al (20) attributed the observed reduction of PCS level to Bifidobacterium spp.-driven suppression of PCS-forming bacteria. In addition, by lowering the pH of colonic contents, formation of shortchain fatty acids from fermentation of the polysaccharides (prebiotics) inhibits the enzymes involved in generation of PCS and IS precursors (19). Because of the short durations of this trial and previous trials, the effect of therapy on clinical outcomes could not be determined.…”

“…Unfortunately, because of the short duration and possibly inadequate amounts of the prebiotics given, the effect of these treatments on clinical outcomes could not be assessed. However, a recent study showed significant attenuation of oxidative stress, inflammation, restoration of the colonic epithelial tight junction, and delayed CKD progression in rats fed a diet containing close to 50% resistant starch compared with those fed a low-fiber diet (19). Future clinical studies are needed to explore the efficacy of long-term use of high dietary fiber supplementation in the CKD population.…”

“…Because of the short durations of this trial and previous trials, the effect of therapy on clinical outcomes could not be determined. In addition to the duration of therapy, the quantity of prebiotics can play a role in the clinical outcomes and the biochemical parameters (19).…”

Kronik Böbrek Hastalığında Renal İnflamasyon ve Bazı Güncel Diyet Bileşenleri İlişkisi

“…Bu durum diyetin prebiyotik içeriğinin kısıtlı olmasına ve disbiyozise neden olabilmektedir. Ratlarda yüksek dirençli nişastanın oksidatif stres ve inflamasyonu hafifleterek KBH gelişimini yavaşlattığı gösterilmiştir (107). Kronik böbrek hastalarında (3. evre veya daha ileri evre), posa tüketiminin inflamasyon ile ilişkisini değerlendiren ve NHANES III verilerini içeren bir çalışmada; KBH hastalarında toplam posa tüketiminde her 10 g/gün artışla CRP düzeyinin odds oranının %38 oranında düştüğü gösterilmiştir (108).…”