Consumption of Dietary Resistant Starch Partially Corrected the Growth Pattern Despite Hyperglycemia and Compromised Kidney Function in Streptozotocin-Induced Diabetic Rats

Koh, Gar Yee; Rowling, Matthew J.; Schalinske, Kevin L.; Grapentine, Kelly; Loo, Yi Ting

doi:10.1021/acs.jafc.6b03808

Cited by 14 publications

(13 citation statements)

References 43 publications

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“…Whilst RS has been shown to reduce albuminuria in the adenine-induced CKD model [11] and the Zucker diabetic fatty rat, an obesity driven model of diabetes [10], a recent study that utilised the STZ model in Sprague-Dawley rats showed that RS had no protective effect on albuminuria [12]. This is consistent with the findings reported here, that in STZ-induced diabetic mice RS supplementation did not alter albuminuria or blood urea levels.…”

Section: Discussionsupporting

confidence: 89%

“…In addition, in the adenine-induced rat model of chronic kidney disease (CKD), supplementation of 59% HAMS diet (Hi-maize 260, equivalent to 27% RS) for three weeks was associated with improvements in creatinine clearance [11]. Conversely however, a study that supplemented a diet containing 55% HAMS (Amylogel, equivalent to 20% RS) for four weeks in male Sprague-Dawley rats with streptozotocin-induced diabetes did not find any renoprotective benefit with RS supplementation [12]. Whilst these results show promise, the concentrations of HAMS used in these studies are likely to be much greater than could be reasonably expected to be consumed by people.…”

Section: Introductionmentioning

confidence: 99%

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Exploring the role of the metabolite-sensing receptor GPR109a in diabetic nephropathy

Snelson

Tan

Higgins

et al. 2019

Preprint

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25Alterations in gut homeostasis may contribute to the progression of diabetic 26 nephropathy. There has been recent attention on the renoprotective effects of 27 metabolite-sensing receptors in chronic renal injury, including the G-protein-coupled-28 receptor (GPR)109a, which ligates the short chain fatty acid butyrate. However, the role 29 of GPR109a in the development of diabetic nephropathy, a milieu of diminished 30 microbiome-derived metabolites, has not yet been determined. This study aimed to 31 assess the effects of insufficient GPR109a signalling via genetic deletion of GPR109a 32 on the development of renal injury in diabetic nephropathy. Gpr109a-/-mice or their 33 wildtype littermates (Gpr109a+/+) were rendered diabetic with streptozotocin (STZ). 34Mice received a control diet or an isocaloric high fiber diet (12.5% resistant starch) for 35 24 weeks and gastrointestinal permeability and renal injury were determined. Diabetes 36 was associated with increased albuminuria, glomerulosclerosis and inflammation. In 37 comparison, Gpr109a-/-mice with diabetes did not show an altered renal phenotype. 38Resistant starch supplementation did not afford protection from renal injury in diabetic 39 nephropathy. Whilst diabetes was associated with alterations in intestinal morphology, 40 intestinal permeability assessed in vivo using the FITC-dextran test was unaltered. 41GPR109a deletion did not worsen gastrointestinal permeability. Further, 12.5% resistant 42 starch supplementation, at physiological concentrations, had no effect on intestinal 43 permeability or morphology. These studies indicate that GPR109a does not play a 44 critical role in intestinal homeostasis in a model of type 1 diabetes or in the development 45 of diabetic nephropathy. 46 47

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Section: Discussionsupporting

confidence: 89%

Section: Introductionmentioning

confidence: 99%

Exploring the role of the metabolite-sensing receptor GPR109a in diabetic nephropathy

Snelson

Tan

Higgins

et al. 2019

Preprint

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“…Standard diet consisted of 54.61% nitrogen-free extract (mainly represented by starch and hemicellulose), 5.54% fibers, 19.42% protein, 11.09% water, 2.58% lipids, and 6.76% ash (non-organic mineral matter) (3.9 kcal/g; 4RF21, Mucedola, Italy). The percentage of substrate supplementation to standard chow diet was determined based on published literature: 10% (w/w) I ( Van den Abbeele et al, 2011 ; Pattananandecha et al, 2016 ), 10% (w/w) RS ( Koh et al, 2016 ), and 3% (w/w) CP ( Tian et al, 2016 ).…”

Section: Methodsmentioning

confidence: 99%

How to Feed the Mammalian Gut Microbiota: Bacterial and Metabolic Modulation by Dietary Fibers

et al. 2017

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The composition of the gut microbiota of mammals is greatly influenced by diet. Therefore, evaluation of different food ingredients that may promote changes in the gut microbiota composition is an attractive approach to treat microbiota disturbances. In this study, three dietary fibers, such as inulin (I, 10%), resistant starch (RS, 10%), and citrus pectin (3%), were employed as supplements to normal chow diet of adult male rats for 2 weeks. Fecal microbiota composition and corresponding metabolite profiles were assessed before and after prebiotics supplementation. A general increase in the Bacteroidetes phylum was detected with a concurrent reduction in Firmicutes, in particular for I and RS experiments, while additional changes in the microbiota composition were evident at lower taxonomic levels for all the three substrates. Such modifications in the microbiota composition were correlated with changes in metabolic profiles of animals, in particular changes in acetate and succinate levels. This study represents a first attempt to modulate selectively the abundance and/or metabolic activity of various members of the gut microbiota by means of dietary fiber.

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“…During this study, diabetes was induced in a cohort of healthy rats. Evolution of diabetes might induce other diseases including renal dysfunction (Chen et al, 2017) and malnutrition (Koh, Rowling, Schalinske, Grapentine, & Loo, 2016). However, these conditions were not tested in this study and might have influenced wound healing response.…”

Section: Discussionmentioning

confidence: 99%

Diabetes alters the involvement of myofibroblasts during periodontal wound healing

et al. 2020

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Objectives Myofibroblasts constitute a specific cell phenotype involved in connective tissue healing. Diabetes alters the wound healing response. However, it is not clear whether diabetes modifies the involvement of myofibroblasts in periodontal wounds. Materials and Methods Type I diabetes was induced in rats through streptozotocin injection, and periodontal wounds were performed. Wound healing was evaluated histologically at 2, 5, 7, and 15 days by measuring epithelial migration, neutrophil infiltration, and collagen and biofilm formation. Distribution of myofibroblasts was evaluated through immunofluorescence for α‐smooth muscle actin. Data analyses were performed using the Shapiro–Wilk, ANOVA, or Kruskal–Wallis tests. Results Diabetic wounds were characterized by delayed epithelial closure, increased neutrophil infiltration, biofilm formation, and reduced collagen formation. Quantification of the myofibroblasts showed a significant reduction at 5 and 7 days in wounds of diabetic rats and an increase at 15 days when compared to wounds of non‐diabetic rats. Conclusions Diabetic wound healing was associated with decreased epithelial and connective tissue healing, increased levels of inflammation, and biofilm formation. Myofibroblast differentiation was delayed in diabetic periodontal wounds at early time points. However, myofibroblasts persisted at later time points of healing. The present study suggests that diabetes alters the involvement of myofibroblasts during periodontal wound healing.

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Consumption of Dietary Resistant Starch Partially Corrected the Growth Pattern Despite Hyperglycemia and Compromised Kidney Function in Streptozotocin-Induced Diabetic Rats

Cited by 14 publications

References 43 publications

Exploring the role of the metabolite-sensing receptor GPR109a in diabetic nephropathy

Exploring the role of the metabolite-sensing receptor GPR109a in diabetic nephropathy

How to Feed the Mammalian Gut Microbiota: Bacterial and Metabolic Modulation by Dietary Fibers

Diabetes alters the involvement of myofibroblasts during periodontal wound healing

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