Efficacy of increased resistant starch consumption in human type 2 diabetes

Resistant starch (RS) has been shown to beneficially affect insulin sensitivity in healthy individuals and those with metabolic syndrome, but its effects on human type 2 diabetes (T2DM) are unknown. This study aimed to determine the effects of increased RS consumption on insulin sensitivity and glucose control and changes in postprandial metabolites and body fat in T2DM. Seventeen individuals with well-controlled T2DM (HbA1c 46.6±2 mmol/mol) consumed, in a random order, either 40 g of type 2 RS (HAM-RS2) or a placebo, daily for 12 weeks with a 12-week washout period in between. At the end of each intervention period, participants attended for three metabolic investigations: a two-step euglycemic–hyperinsulinemic clamp combined with an infusion of [6,6-2H2] glucose, a meal tolerance test (MTT) with arterio-venous sampling across the forearm, and whole-body imaging. HAM-RS2 resulted in significantly lower postprandial glucose concentrations (P=0.045) and a trend for greater glucose uptake across the forearm muscle (P=0.077); however, there was no effect of HAM-RS2 on hepatic or peripheral insulin sensitivity, or on HbA1c. Fasting non-esterified fatty acid (NEFA) concentrations were significantly lower (P=0.004) and NEFA suppression was greater during the clamp with HAM-RS2 (P=0.001). Fasting triglyceride (TG) concentrations and soleus intramuscular TG concentrations were significantly higher following the consumption of HAM-RS2 (P=0.039 and P=0.027 respectively). Although fasting GLP1 concentrations were significantly lower following HAM-RS2 consumption (P=0.049), postprandial GLP1 excursions during the MTT were significantly greater (P=0.009). HAM-RS2 did not improve tissue insulin sensitivity in well-controlled T2DM, but demonstrated beneficial effects on meal handling, possibly due to higher postprandial GLP1

The relationship between resistant starch and glycemic control: A review on current evidence and possible mechanisms

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Gut microbiota and chronic kidney disease: evidences and mechanisms that mediate a new communication in the gastrointestinal-renal axis

Chronic kidney disease (CKD) represents a growing public health problem associated with loss of kidney function and cardiovascular disease (CVD), the main leading cause of morbidity and mortality in CKD. It is well established that CKD is associated with gut dysbiosis. Over the past few years, there has been a growing interest in studying the composition of the gut microbiota in patients with CKD as well as the mechanisms by which gut dysbiosis contributes to CKD progression, in order to identify possible therapeutic targets to improve the morbidity and survival in CKD. The purpose of this review is to explore the clinical evidence and the mechanisms involved in the gut-kidney crosstalk as well as the possible interventions to restore a normal balance of the gut microbiota in CKD. It is well known that the influence of the gut microbiota on the gut–kidney axis acts in a reciprocal way: on the one hand, CKD significantly modifies the composition and functions of the gut microbiota. On the other hand, gut microbiota is able to manipulate the processes leading to CKD onset and progression through inflammatory, endocrine, and neurologic pathways. Understanding the complex interaction between these two organs (gut microbiota and kidney) may provide novel nephroprotective interventions to prevent the progression of CKD by targeting the gut microbiota. The review is divided into three main sections: evidences from clinical studies about the existence of a gut microbiota dysbiosis in CKD; the complex mechanisms that explain the bidirectional relationship between CKD and gut dysbiosis; and reports regarding the effects of prebiotic, probiotic, and synbiotic supplementation to restore gut microbiota balance in CKD.Fil: Rukavina Mikusic, Natalia Lucía. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Química y Físico-Química Biológicas "Prof. Alejandro C. Paladini". Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Química y Físico-Química Biológicas; Argentina. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Ciencias Biológicas; ArgentinaFil: Kouyoumdzian, Nicolás Martín. Consejo Nacional de Investigaciones Cientificas y Tecnicas. Oficina de Coordinacion Administrativa Houssay. Instituto Alberto C. Taquini de Investigaciones En Medicina Traslacional. - Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Cardiologicas "prof. Dr. Alberto C. Taquini". Instituto Alberto C. Taquini de Investigaciones En Medicina Traslacional.; ArgentinaFil: Choi, Marcelo Roberto. Consejo Nacional de Investigaciones Cientificas y Tecnicas. Oficina de Coordinacion Administrativa Houssay. Instituto Alberto C. Taquini de Investigaciones En Medicina Traslacional. - Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Cardiologicas "prof. Dr. Alberto C. Taquini". Instituto Alberto C. Taquini de Investigaciones En Medicina Traslacional.; Argentina. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Ciencias Biológicas; Argentin

Natural products from plants and microorganisms: Novel therapeutics for chronic kidney disease via gut microbiota regulation

Dysbiosis of gut microbiota plays a fundamental role in the pathogenesis and development of chronic kidney disease (CKD) and its complications. Natural products from plants and microorganisms can achieve recognizable improvement in renal function and serve as an alternative treatment for chronic kidney disease patients with a long history, yet less is known on its beneficial effects on kidney injury by targeting the intestinal microbiota. In this review, we summarize studies on the effects of natural products from plants and microorganisms, including herbal medicines and their bioactive extracts, polysaccharides from plants and microorganisms, and phytochemicals, on the prevention and treatment of chronic kidney disease through targeting gut microflora. We describe the strategies of these anti-CKD effects in animal experiments including remodulation of gut microbiota structure, reduction of uremic toxins, enhancement of short-chain fatty acid (SCFA) production, regulation of intestinal inflammatory signaling, and improvement in intestinal integrity. Meanwhile, the clinical trials of different natural products in chronic kidney disease clinical practice were also analyzed and discussed. These provide information to enable a better understanding of the renoprotective effects of these effective natural products from plants and microorganisms in the treatment of chronic kidney disease. Finally, we propose the steps to prove the causal role of the intestinal microflora in the treatment of chronic kidney disease by natural products from plants and microorganisms. We also assess the future perspective that natural active products from plants and microorganisms can beneficially delay the onset and progression of kidney disease by targeting the gut flora and highlight the remaining challenges in this area. With the continuous deepening of studies in recent years, it has been proved that gut microbiota is a potential target of natural active products derived from plants and microorganisms for chronic kidney disease treatment. Fully understanding the functions and mechanisms of gut microbiota in these natural active products from plants and microorganisms is conducive to their application as an alternative therapeutic in the treatment of chronic kidney disease

Dietary Polysaccharides as Modulators of the Gut Microbiota Ecosystem: An Update on Their Impact on Health

A polysaccharide is a macromolecule composed of more than ten monosaccharides with a wide distribution and high structural diversity and complexity in nature. Certain polysaccharides are immunomodulators and play key roles in the regulation of immune responses during the progression of some diseases. In addition to stimulating the growth of certain intestinal bacteria, polysaccharides may also promote health benefits by modulating the gut microbiota. In the last years, studies about the triad gut microbiota–polysaccharides–health have increased exponentially. In consequence, in the present review, we aim to summarize recent knowledge about the function of dietary polysaccharides on gut microbiota composition and how these effects affect host health.Regional Ministry of Health and Families (Andalucia, Spain)CSyF 2021-Postdoctoral RPS 24665"Fundacion Ramon Areces", Madrid, Spai

HYPOGLYCEMIC EFFECT OF HIGH-RESISTANT STARCH ANALOG RICE THROUGH GLP-1 AND INSULIN OR HIGH-RESISTANT STARCH ANALOG RICE ATTENUATES BLOOD GLUCOSE LEVEL THROUGH ENHANCEMENT OF GLP-1 AND INSULIN

Objective: This study was to investigate the effect of analog rice (AR) on glucagon-like peptide-1 (GLP-1) and insulin serum levels, glucose transporter-2 (GLUT-2) expression, and fasting blood glucose (FBG) level in diabetic rats. Methods: Fifty male Wistar rats divided into the control group (n=10) and the experimental group. High-fat diet and streptozotocin were administered in experimental groups, which then divided into four equal groups (n=10, each) (negative control group, rice group, AR1 and AR2 group, given standard pellet, rice pellet, AR1 and AR2 pellet, respectively, for 6 weeks). GLP-1 and insulin serum levels were measured by enzyme-linked immunosorbent assay. The expression of GLUT-2 and the number of pancreatic β-cells observed using an immunohistochemistry method. Results: FBG levels in the AR1 and AR2 groups decreased, while the rice group remained. GLP-1 serum levels of the negative control and rice groups were not significantly different from the control group, while the AR1 and AR2 groups higher than the control group (p≤0.05). All the treatment groups had insulin serum levels significantly lower than control group (p≤0.05), except the AR1 group. The expression of GLUT-2 and the number of pancreatic β-cells in the treatment groups were less than the control group, but between treatment groups were not significantly different. Conclusion: AR significantly effective in reducing FBG level in diabetic rats through stimulation of increased GLP-1 and insulin serum levels serum levels but AR did not affect on the expression of GLUT-2

Resistant starch: implications in kidney health and vitamin D homeostasis in diabetes mellitus

Diabetic nephropathy has a significant impact on vitamin D status partially due to the role of kidney in maintaining renal uptake of 25-hydroxycholecalciferol (25D) and its subsequent activation to 1,25-dihydroxycholecalciferol (1,25D). We previously reported that feeding high-amylose maize (HAM), a rich source of resistant starch (RS), prevented excretion of 25D-vitamin D-binding protein (DBP) and albumin in Streptozotocin (STZ)-induced type 1 diabetic (T1D) rats. The objectives of the studies described in this dissertation were to: 1) determine if dietary RS could prevent excessive excretion of vitamin D metabolites and maintain serum 25D levels in Zucker diabetic fatty (ZDF) rats, a well characterized animal model of type 2 diabetes (T2D); 2) to conduct dose-response studies to evaluate the renoprotective effect of RS following the induction of T1D; and 3) to determine the impact of RS on cytokines and hormones involved in the inflammatory process and whether the renoprotective actions of RS can be achieved at a lower dose in ZDF rats. In the first study described in this dissertation, Lean Zucker (n = 8) rats were fed a control diet (LC; AIN-93G diet with 550 g/kg of corn starch) and ZDF rats (n = 8/group) were fed either the control diet (DC) or RS diet (DRS; AIN-93G diet with 550 g/kg of HAM) for 6 weeks. RS attenuated hyperglycemia by 41% and prevented albuminuria. Additionally, urinary 25D and 1,25D in DRS were 90% and 97% lower, respectively, resulting in 41% greater serum 25D concentrations (P \u3c 0.001) compared to DC rats. Along with the improved renal histopathologic scoring, our data suggest that dietary RS maintained vitamin D balance through its protection against diabetes-induced kidney damage. In the second study described in this dissertation, we explored the possibility that RS would have a nephroprotective effect following T1D onset. Sprague Dawley (SD) rats (n = 8/ group), after induction of T1D with STZ, were fed with AIN-93G diet containing 550g/kg of corn starch (CS), 550 g/kg of high-amylose maize (HRS), 275 g/kg of high-amylose maize + 275 g/kg of corn starch (MRS), or 138 g/kg of high-amylose maize + 412 g/kg of corn starch (LRS) for 4 weeks. Vehicle-treated SD rats (n = 5) fed AIN-93G diet containing 550 g/kg of corn starch were served as non-diabetic control (NDC). Our results showed that RS, regardless of dose, did not improve fasting blood glucose levels in T1D rats compared to NDC rats. The overall growth rate in NDC rats was 1.7- to 3.3-fold greater than in T1D rats. In comparison with CS rats, MRS- and HRS-rats gained 52% and 72%, respectively, but body weight did not differ between LRS and CS rats. Though RS normalized growth pattern in T1D rats, no differences were observed in urinary albumin or 25D concentrations in these rats regardless of treatments. Despite the improvement of vitamin D status (~15 – 20% greater compared to NDC rats) in T1D rats, interleukin-6 (IL-6) was 9 – 31% greater compared to CS rats which was strongly correlated to hyperglycemia (r = 0.472, P = 0.02). Hence, the potential mechanism by which RS promotes kidney health and reduces inflammation could be contingent on glycemic status and thus future work should focus on a preventative approach with RS to maximize its beneficial effects in diabetes. The objective of the third study included in this dissertation was to examine the mechanism underlying the RS-mediated effects on vitamin D balance of and whether lower intake of dietary RS would promote kidney health and vitamin D balance in ZDF rats. Here, lean Zucker rats (n=5) were used as our control group (LC) and fed a control diet (AIN-93G). For comparison to LC rats, ZDF rats (n = 5/group) were fed the control diet (DC), RS diet (HRS), or a diet containing 275 g/kg of high-amylose maize and 275 g/kg of corn starch (MRS) for 6 weeks. Fasting blood glucose concentrations and hemoglobin A1c% were not affected by HRS or MRS diet. Yet, insulin concentrations were 1.5-fold greater and HOMA-β% was 2-fold greater in HRS rats compared to DC rats, whereas these improvements were not observed in MRS-fed ZDF rats. Additionally, HRS rats, when compared to DC rats, exhibited a 20% increase in serum 25D concentrations and excretion of vitamin D metabolites was blunted. No differences were detected between MRS and DC rats with respect to vitamin D balance. Serum triglycerides were 50% lower and liver triglycerides were 2-fold greater in HRS rats when compared to DC rats. Circulating adiponectin concentrations were 77% greater and serum angiotensin II concentrations were 44% lower in HRS rats than in DC rats. No differences in circulating adiponectin and angiotensin II concentrations were observed in MRS compared to DC rats. Moreover, adiponectin concentrations were highly correlated with vitamin D status (r = 0.815, P \u3c 0.001) and urinary creatinine output (r = 0.818, P \u3c 0.001) and inversely correlated with urinary protein (r = -0.583, P = 0.02). Collectively, though we showed that the effect of 20% RS on promoting kidney function and vitamin D homeostasis in ZDF rats may be influenced by circulating adiponectin concentrations, our studies indicate that a 50% reduction in dietary RS does not produce the same results. Nevertheless, the studies described in this dissertation indicate that HAM could be a part of dietary intervention strategies aiming to prevent or attenuate symptoms of diabetic nephropathy that are independent of blood glucose management. Because the level of dietary RS used in these studies would be difficult to translate to human feeding studies, future work should consider combination strategies with RS and other dietary compounds or medications for the prevention and/or management of diabetic nephropathy and its associated complications

Vegetable-Based Diets for Chronic Kidney Disease? It Is Time to Reconsider

Traditional dietary recommendations to renal patients limited the intake of fruits and vegetables because of their high potassium content. However, this paradigm is rapidly changing due to the multiple benefits derived from a fundamentally vegetarian diet such as, improvement in gut dysbiosis, reducing the number of pathobionts and protein-fermenting species leading to a decreased production of the most harmful uremic toxins, while the high fiber content of these diets enhances intestinal motility and short-chain fatty acid production. Metabolic acidosis in chronic kidney disease (CKD) is aggravated by the high consumption of meat and refined cereals, increasing the dietary acid load, while the intake of fruit and vegetables is able to neutralize the acidosis and its deleterious consequences. Phosphorus absorption and bioavailability is also lower in a vegetarian diet, reducing hyperphosphatemia, a known cause of cardiovascular mortality in CKD. The richness of multiple plants in magnesium and vitamin K avoids their deficiency, which is common in these patients. These beneficial effects, together with the reduction of inflammation and oxidative stress observed with these diets, may explain the reduction in renal patients' complications and mortality, and may slow CKD progression. Finally, although hyperkalemia is the main concern of these diets, the use of adequate cooking techniques can minimize the amount absorbed