scholarly journals Source and Composition in Amino Acid of Dietary Proteins in the Primary Prevention and Treatment of CKD

Nutrients ◽  
2020 ◽  
Vol 12 (12) ◽  
pp. 3892
Author(s):  
Pierre Letourneau ◽  
Stanislas Bataille ◽  
Philippe Chauveau ◽  
Denis Fouque ◽  
Laetitia Koppe
Keyword(s):  
Protein Intake ◽  
Metabolic Disorders ◽  
Dietary Proteins ◽  
Clear Understanding ◽  
Low Protein ◽  
Clinical Benefits ◽  
Underlying Mechanisms ◽  
Protein Diets ◽  
Global Reduction

Nutrition is a cornerstone in the management of chronic kidney disease (CKD). To limit urea generation and accumulation, a global reduction in protein intake is routinely proposed. However, recent evidence has accumulated on the benefits of plant-based diets and plant-derived proteins without a clear understanding of underlying mechanisms. Particularly the roles of some amino acids (AAs) appear to be either deleterious or beneficial on the progression of CKD and its complications. This review outlines recent data on the role of a low protein intake, the plant nature of proteins, and some specific AAs actions on kidney function and metabolic disorders. We will focus on renal hemodynamics, intestinal microbiota, and the production of uremic toxins. Overall, these mechanistic effects are still poorly understood but deserve special attention to understand why low-protein diets provide clinical benefits and to find potential new therapeutic targets in CKD.

scholarly journals A Comprehensive Review Evaluating the Impact of Protein Source (Vegetarian vs. Meat Based) in Hepatic Encephalopathy

Nutrients ◽  
2021 ◽  
Vol 13 (2) ◽  
pp. 370
Author(s):  
Umair Iqbal ◽  
Ravirajsinh N. Jadeja ◽  
Harshit S. Khara ◽  
Sandeep Khurana
Keyword(s):  
Hepatic Encephalopathy ◽  
Protein Intake ◽  
Alternative Therapy ◽  
Case Series ◽  
Current Evidence ◽  
Branch Chain Amino ◽  
The Impact ◽  
Protein Diets

Hepatic encephalopathy (HE) is a common neurological consequence in patients with cirrhosis and has a healthcare burden of USD 5370 to 50,120 per patient annually. HE significantly hampers the quality of life and is a major cause of morbidity and mortality. Patients with cirrhosis are at a high risk for protein-calorie malnutrition due to altered metabolism. Current evidence has changed the old belief of protein restriction in patients with cirrhosis and now 1.2 to 1.5 g/kg/day protein intake is recommended. Case series and studies with small numbers of participants showed that a vegetarian protein diet decreases the symptoms of HE when compared to a meat-based diet, but the evidence is limited and requires further larger randomized controlled trials. However, vegetable or milk-based protein diets are good substitutes for patients averse to meat intake. Branch chain amino acids (BCAA) (leucine, isoleucine and valine) have also been shown to be effective in alleviating symptoms of HE and are recommended as an alternative therapy in patients with cirrhosis for the treatment of HE. In this review, we provide an overview of current literature evaluating the role of protein intake in the management of HE in cirrhosis.

scholarly journals Possible role of available phosphorus in potentiating the use of low-protein diets for broiler chicken production

2020 ◽  
Vol 99 (12) ◽  
pp. 6954-6963
Author(s):  
A.J. Cowieson ◽  
R. Perez-Maldonado ◽  
A. Kumar ◽  
M. Toghyani
Keyword(s):  
Broiler Chicken ◽  
Available Phosphorus ◽  
Low Protein ◽  
Protein Diets

scholarly journals THE ROLE OF HOMOCYSTINE IN PROTECTING PROTEIN-DEPLETED DOGS EXPOSED TO FATAL DOSES OF CHLOROFORM

1955 ◽  
Vol 101 (2) ◽  
pp. 197-204
Author(s):  
George P. Vennart ◽  
Frank W. McKee
Keyword(s):  
Liver Damage ◽  
Methyl Groups ◽  
Histological Changes ◽  
Long Period ◽  
Lethal Action ◽  
Low Protein ◽  
Depletion Period ◽  
Protein Diets ◽  
Cellular Destruction

In dogs maintained on low protein diets and subjected to phlebotomy over a long period of time, the inhalation of chloroform, for 30 minutes, produced uniform fatality within 48 hours. The histological changes of massive hepato-cellular destruction were observed at autopsy. Homocystine, in the amount of 2.0 gm., given orally 2 hours after or 2 hours prior to the administration of chloroform, protected dogs against the lethal action of the toxin. Inconstant changes in fibrinogen and icteric indices were observed in the protected animals, indicating some mild liver damage, but this was not correlated with the length of the previous depletion period, the phase of the experiment, or any other factor. No evidence was obtained that methyl groups are necessary for the protection of the liver by homocystine.

Diet and the progression of chronic kidney disease

2015 ◽  
Author(s):  
Juan Jesús Carrero ◽  
Hong Xu ◽  
Bengt Lindholm
Keyword(s):  
Blood Pressure ◽  
Protein Intake ◽  
Salt Intake ◽  
Angiotensin Converting Enzyme Inhibitors ◽  
High Serum ◽  
Nutritional Epidemiology ◽  
Converting Enzyme Inhibitors ◽  
Early Stages ◽  
Low Protein ◽  
Protein Diets

The dietary management of non-dialysed CKD patients has focused on limiting the intake of substances which lead to accumulation of urea, potassium, phosphorus, and sodium. Recent advances in nutritional epidemiology have given us the opportunity to examine the relationships between diet and CKD. This chapter focuses on evidence relating to retarding progression of renal impairment in the early to mid stages of CKD. Limits may need to change if GFR falls. The hypothesis that a high dietary protein intake leads to progressive CKD through a mechanism of glomerular hyperfiltration has been taught for decades, and it appears effective in animals. However, the evidence that low-protein diets (LPDs) halt CKD progression in patients is weak. Their management is of course likely to include other interventions such as blood pressure control. There is risk to low-protein diets. There is some evidence that high protein intakes are harmful. We therefore recommend moderate protein intake (not low; not high – no protein supplements; around 1g/kg/day). Salt handling is impaired in most patients with CKD, probably even early stages, and hypertension is an early feature, except in salt-losing patients, to whom different rules apply. Salt intake tends to raise blood pressure, worsen proteinuria, and reduce the effects of angiotensin converting enzyme inhibitors on blood pressure and proteinuria. Very low salt intakes are difficult to comply with and limit diet. In early stages of CKD we therefore recommend restriction to moderately low levels (below 6g/day of salt; 100 mmol of sodium). Lower levels may have additional benefits, and these limits may need to be reduced as GFR declines. Potassium is associated with healthy, desirable foods such as fruit and vegetables. It should only be restricted if high serum values make this necessary.

FGF21 prevents low protein diet-induced renal inflammation in aged mice

2021 ◽  
Author(s):  
Han Fang ◽  
Sujoy Ghosh ◽  
Landon Sims ◽  
Kirsten P. Stone ◽  
Cristal M Hill ◽  
...  
Keyword(s):  
Transcriptional Activation ◽  
Renal Damage ◽  
Protective Role ◽  
Wild Type ◽  
Kidney Weight ◽  
Albumin Creatinine Ratio ◽  
Low Protein ◽  
The Impact ◽  
Protein Diets

Low protein diets extend lifespan through a comprehensive improvement in metabolic health across multiple tissues and organs. Many of these metabolic responses to protein restriction are secondary to transcriptional activation and release of FGF21 from the liver. However, the effects of a low protein (LP) diet on the kidney in the context of aging has not been examined. Therefore, the goal of the current study was to investigate the impact of chronic consumption of a LP diet on the kidney in aging mice lacking FGF21. Wild type (WT, C57BL/6J) and FGF21 KO mice were fed a normal protein (NP, 20% casein) or a LP (5% casein) diet ad libitum from 3 to19 months of age. The LP diet led to a decrease in kidney weight and urinary albumin/creatinine ratio in both WT and FGF21 KO mice. Although the LP diet produced only mild fibrosis and infiltration of leukocytes in WT kidneys, the effects were significantly exacerbated by the absence of FGF21. Accordingly, transcriptomic analysis showed that inflammation-related pathways were significantly enriched and upregulated in response to LP diet in FGF21 KO but not WT mice. Collectively, these data demonstrate that the LP diet negatively affected the kidney during aging, but in the absence of FGF21, the LP diet-induced renal damage and inflammation were significantly worse, indicating a protective role of FGF21 in the kidney.

The Role of the Colon in Urea Metabolism in Man

1976 ◽  
Vol 50 (1) ◽  
pp. 51-59 ◽  
Author(s):  
J. A. Gibson ◽  
N. J. Park ◽  
G. E. Sladen ◽  
A. M. Dawson
Keyword(s):  
Dietary Protein ◽  
Colonic Mucosa ◽  
Normal Subjects ◽  
Urea Concentration ◽  
Low Protein ◽  
Urea Content ◽  
Colonic Lumen ◽  
Urea Metabolism ◽  
Protein Diets

1. The urea content of ileostomy effluent has been measured by the urease method as an indirect estimate of the urea concentration in the lumen of the normal ileum. 2. The plasma disappearance of intravenously administered [14C]urea was used to study intestinal urea breakdown. Normal subjects on high and low protein diets and patients with either excised (i.e. with ileostomies) or excluded colons were studied. 3. The 24 h intestinal urea breakdown was considerably greater than the quantity of urea estimated to be entering the colon from the ileum and across the colonic mucosa. 4. Intestinal urea breakdown increased with increase in dietary protein and decreased with, but was not abolished by, exclusion or excision of the colon. 5. Our results suggest that the colonic lumen is not the only site of intestinal ureolysis and that significant quantities of urea must be broken down either at a juxtamucosal site or in the ileum.

Circulating bile acid profiles: a need for further examination

2021 ◽  
Author(s):  
Li Qi ◽  
Yu Tian ◽  
Yongsheng Chen
Keyword(s):  
Metabolic Disorders ◽  
Metabolic Response ◽  
Evidence Synthesis ◽  
Review Literature ◽  
Therapeutic Interventions ◽  
Promising Tool ◽  
Pubmed Search ◽  
Underlying Mechanisms ◽  
Bile Acid Profiles

Abstract Context Bile acids (BAs) are increasingly recognized as metabolic and chronobiologic integrators that synchronize the systemic metabolic response to nutrient availability. Alterations in the concentration and/or composition of circulating BAs are associated with a number of metabolic disorders, such as obesity, type 2 diabetes mellitus (T2DM), insulin resistance (IR), and metabolic-associated fatty liver disease (MAFLD). This review summarizes recent evidence that links abnormal circulating BA profiles to multiple metabolic disorders, and discusses the possible mechanisms underlying the connections to determine the role of BA profiling as a novel biomarker for these abnormalities. Evidence Acquisition The review is based on a collection of primary and review literature gathered from a PubMed search of BAs, T2DM, IR, and MAFLD, among other keywords. Evidence Synthesis Obese and IR subjects appear to have elevated fasting circulating BAs but lower postprandial increase when compared with controls. The possible underlying mechanisms are the disruption in the synchronization between the feeding/fasting cycle and the properties of BA-regulated metabolic pathways. Whether BA alterations are associated per se with MAFLD remains inconclusive. However, increased fasting circulating BAs level was associated with higher risk of advanced fibrosis stage. Thus, for patients with MAFLD, dynamically monitoring the circulating BA profiles may be a promising tool for the stratification of MAFLD. Conclusions Alterations in the concentration, composition, and rhythm of circulating BAs are associated with adverse events in systemic metabolism. Subsequent investigations regarding these aspects of circulating BA kinetics may help predict future metabolic disorders and guide therapeutic interventions.

scholarly journals Inhibitory effect of high protein intake on nephrocalcinogenesis in female rats

1992 ◽  
Vol 67 (2) ◽  
pp. 223-233 ◽  
Author(s):  
J. G. H. Sterck ◽  
J. Ritskes-Hoitinga ◽  
A. C. Beynen
Keyword(s):  
Protein Intake ◽  
Inhibitory Effect ◽  
High Protein ◽  
Female Rats ◽  
High Protein Intake ◽  
Low Protein ◽  
Background Diet ◽  
Calcium Magnesium ◽  
High Protein Diets ◽  
Protein Diets

Increased intakes of protein have been shown to reduce kidney calcification (nephrocalcinosis) in female rats. Two questions were addressed in the present study. First, can protein-induced inhibition of nephrocalcinosis be demonstrated when the diets used are balanced for calcium, magnesium and phosphorus in the added protein? Second, can the protein effect be explained by the frequently observed magnesiuria after giving high-protein diets? Nephrocalcinosis was induced in female rats by giving purified diets containing 151 g casein/kg and either an increased concentration of P (6 v. 2 g/kg) or a decreased concentration of Mg (0·1 v. 0·4 g/kg). To these diets 151 g ovalbumin/kg was added at the expense of glucose, and the diets were balanced for Ca, Mg and P in ovalbumin. The diets were given for 29 d. In rats fed on the diet containing 151 g protein/kg, an increased intake of P or a decreased intake of Mg caused nephrocalcinosis as measured chemically by analysis of kidney Ca as well as histologically by scoring kidney sections stained according to Von Kossa's method. The addition of ovalbumin to the diet prevented the induction of nephrocalcinosis. High P intake and low Mg intake with the low-protein diets induced enhanced loss of albumin in urine, suggesting that nephrocalcinosis caused kidney damage. Increased protein intake with a non-calcinogenic diet also caused increased albumin excretion in urine. Irrespective of the composition of the background diet, increased protein intake caused increased urinary excretion of Mg. When all dietary groups were considered, differences in nephrocalcinosis and urinary Mg output were not proportionally related.Nephrocalcinosis: Phosphorus: Magnesium: Protein: Rat

scholarly journals Emerging insights into the relationship between hyperlipidemia and the risk of diabetic retinopathy

2020 ◽  
Vol 19 (1) ◽  
Author(s):  
Yuyu Chou ◽  
Jin Ma ◽  
Xin Su ◽  
Yong Zhong
Keyword(s):  
Diabetic Retinopathy ◽  
Metabolic Disorders ◽  
Lipid Lowering ◽  
The Novel ◽  
Cardiovascular Morbidity And Mortality ◽  
Protective Strategies ◽  
Underlying Mechanisms ◽  
The Relationship ◽  
Established Role

AbstractHyperlipidemia is correlated with a series of health problems. Notably, aside from its established role in promoting cardiovascular morbidity and mortality, hyperlipidemia has also been considered for modulating the risk and the severity of multiple metabolic disorders. According to the results of epidemiologic investigations, several certain circulating lipoprotein species are correlated with the prevalence of diabetic retinopathy, suggesting that the physiological and pathological role of these lipoproteins is analogous to that observed in cardiovascular diseases. Furthermore, the lipid-lowering treatments, particularly using statin and fibrate, have been demonstrated to ameliorate diabetic retinopathy. Thereby, current focus is shifting towards implementing the protective strategies of diabetic retinopathy and elucidating the potential underlying mechanisms. However, it is worth noting that the relationship between major serum cholesterol species and the development of diabetic retinopathy, published by other studies, was inconsistent and overall modest, revealing the relationship is still not clarified. In this review, the current understanding of hyperlipidemia in pathogenesis of diabetic retinopathy was summarized and the novel insights into the potential mechanisms whereby hyperlipidemia modulates diabetic retinopathy were put forward.

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