Cybermedlife - Therapeutic Actions Dietary Modification - Low-Protein Diet

Long-term effects of calorie or protein restriction on serum IGF-1 and IGFBP-3 concentration in humans. 📎

Abstract Title: Long-term effects of calorie or protein restriction on serum IGF-1 and IGFBP-3 concentration in humans. Abstract Source: Thromb Res. 2009 Mar;123(5):740-4. Epub 2008 Sep 10. PMID: 18843793 Abstract Author(s): Luigi Fontana, Edward P Weiss, Dennis T Villareal, Samuel Klein, John O Holloszy Article Affiliation: Division of Geriatrics&Nutritional Sciences, Washington University School of Medicine, St Louis, MO 63110, USA. This email address is being protected from spambots. You need JavaScript enabled to view it. Abstract: Reduced function mutations in the insulin/IGF-I signaling pathway increase maximal lifespan and health span in many species. Calorie restriction (CR) decreases serum IGF-1 concentration by ~40%, protects against cancer and slows aging in rodents. However, the long-term effects of CR with adequate nutrition on circulating IGF-1 levels in humans are unknown. Here we report data from two long-term CR studies (1 and 6 years) showing that severe CR without malnutrition did not change IGF-1 and IGF-1 : IGFBP-3 ratio levels in humans. In contrast, total and free IGF-1 concentrations were significantly lower in moderately protein-restricted individuals. Reducing protein intake from an average of 1.67 g kg(-1) of body weight per day to 0.95 g kg(-1) of body weight per day for 3 weeks in six volunteers practicing CR resulted in a reduction in serum IGF-1 from 194 ng mL(-1) to 152 ng mL(-1). These findings demonstrate that, unlike in rodents, long-term severe CR does not reduce serum IGF-1 concentration and IGF-1 : IGFBP-3 ratio in humans. In addition, our data provide evidence that protein intake is a key determinant of circulating IGF-1 levels in humans, and suggest that reduced protein intake may become an important component of anticancer and anti-aging dietary interventions. Article Published Date : Mar 01, 2009

Treatment of chronic uremic patients with protein-poor diet and oral supply of essential amino acids. I. Nitrogen balance studies. 1

Abstract Title: Treatment of chronic uremic patients with protein-poor diet and oral supply of essential amino acids. I. Nitrogen balance studies. Abstract Source: Clin Nephrol. 1975;3(5):187-94. PMID: 1149343 Abstract Author(s): J Bergström, P Fürst, L O Norée Abstract: Twenty-six nitrogen balance studies were performed in 15 patients with severe uremia (Ccr mean value 5.1, range 2.3-8.5 ml/min) treated with an unselected protein-poor (16-20 g protein/day corresponding to 2.6-3.2 g N/day) diet and oral supply of the essential amino acids including histidine (2.6 g N/day). The general condition improved and the concentration of serum urea nitrogen decreased. The nitrogen balance, corrected for changes in total urea pool, was negative on the diet alone,-1.46 plus or minus 1.15 g N/day (mean plus or minus SD), but was positive when the essential amino acids were supplied, plus 0.84 plus or minus 0.68 g N/day. In four patients studied after 3 to 26 months of diet and amino acid therapy, during which time a further deterioriation of the renal function had occurred, the nitrogen balance was around zero in three and negative in one patient (-1.2 g N/day). The results show that it is possible with our new regimen to attain positive nitrogen balance or nitrogen equilibrium in severely uremic patients without excessive accumulation of urea in the body fluids.   Article Published Date : Jan 01, 1975

Treatment of chronic uremic patients with protein-poor diet and oral supply of essential amino acids. II. Clinical results of long-term treatment.

Abstract Title: Treatment of chronic uremic patients with protein-poor diet and oral supply of essential amino acids. II. Clinical results of long-term treatment. Abstract Source: Clin Nephrol. 1975;3(5):195-203. PMID: 1149344 Abstract Author(s): L O Norée, J Bergström Abstract: Twenty-six uremic patients - serum urea nitrogen (SUN) 110 MG/100 ml plus or minus 22.8 (mean plus or minus SD), serum cretinine (S-Creat) 13.2 mg/100 ml plus or minus 2.27, ratio SUN/S-Creat 8.6 plus or minus 2.26, and endogenous creatinine clearance (Ccr) 3.86 plus or minus 1.41 ml/min - were treated for three months or longer with an unselected protein-poor (16-20 g protein/day) diet with oral supply of the essential amino acids including histidine in high doses as coated tablets. The amino acids were instituted after an initial diet only period (mean 0.4 months). The average treatment time was 8.4 months (range 2.7-33.6). An improvement of the general condition was obtained, persisting for several months. SUN and SUN/S-Creat decreased on the diet alone, continued to decrease after one month, and increased slightly again after three months of treatment, but did not reach the initial levels for several months in spite of an almost doubled nitrogen intake. S-Creat increased after six months indicating a further deterioration of the renal function. In patients with initially low serum total protein (smaller than 6.5 g/100 ml, 9 patients), albumin (smaller than 3.5 g/100 ml, 10 patients), and total iron-binding capacity (smaller than 260 mug/100 ml, 11 patients) the values increased after one month on amino acids and were thereafter stable. No signs of bleeding tendency, progressive muscle atrophy, or progressive peripheral neuropathy were observed. - Five patients died due to cardiovascular maladies. A further 13 patients were withdrawn for medical reasons (overhydration, 4 patients; hypertension, 1 patient; nausea and vomiting, 7 patients; and pericarditis, 1 patient). - The renal function improved in one patient. Four patients received home dialysis training, three a kidney transplant. - The results indicate that it is possible to keep severely uremic patients free from uremic symptoms, counteract protein depletion, and even improve the nutritional status during long-term treatment with an unselected protein-poor diet supplementd with essential amino acids.   Article Published Date : Jan 01, 1975
Therapeutic Actions DIETARY MODIFICATION Low-Protein Diet

NCBI pubmed

Mouse maternal protein restriction during preimplantation alone permanently alters brain neuron proportion and adult short-term memory.

Related Articles Mouse maternal protein restriction during preimplantation alone permanently alters brain neuron proportion and adult short-term memory. Proc Natl Acad Sci U S A. 2018 07 31;115(31):E7398-E7407 Authors: Gould JM, Smith PJ, Airey CJ, Mort EJ, Airey LE, Warricker FDM, Pearson-Farr JE, Weston EC, Gould PJW, Semmence OG, Restall KL, Watts JA, McHugh PC, Smith SJ, Dewing JM, Fleming TP, Willaime-Morawek S Abstract Maternal protein malnutrition throughout pregnancy and lactation compromises brain development in late gestation and after birth, affecting structural, biochemical, and pathway dynamics with lasting consequences for motor and cognitive function. However, the importance of nutrition during the preimplantation period for brain development is unknown. We have previously shown that maternal low-protein diet (LPD) confined to the preimplantation period (Emb-LPD) in mice, with normal nutrition thereafter, is sufficient to induce cardiometabolic and locomotory behavioral abnormalities in adult offspring. Here, using a range of in vivo and in vitro techniques, we report that Emb-LPD and sustained LPD reduce neural stem cell (NSC) and progenitor cell numbers at E12.5, E14.5, and E17.5 through suppressed proliferation rates in both ganglionic eminences and cortex of the fetal brain. Moreover, Emb-LPD causes remaining NSCs to up-regulate the neuronal differentiation rate beyond control levels, whereas in LPD, apoptosis increases to possibly temper neuron formation. Furthermore, Emb-LPD adult offspring maintain the increase in neuron proportion in the cortex, display increased cortex thickness, and exhibit short-term memory deficit analyzed by the novel-object recognition assay. Last, we identify altered expression of fragile X family genes as a potential molecular mechanism for adverse programming of brain development. Collectively, these data demonstrate that poor maternal nutrition from conception is sufficient to cause abnormal brain development and adult memory loss. PMID: 29941596 [PubMed - indexed for MEDLINE]

Replication of a Gene-Diet Interaction at CD36, NOS3 and PPARG in Response to Omega-3 Fatty Acid Supplements on Blood Lipids: A Double-Blind Randomized Controlled Trial.

Related Articles Replication of a Gene-Diet Interaction at CD36, NOS3 and PPARG in Response to Omega-3 Fatty Acid Supplements on Blood Lipids: A Double-Blind Randomized Controlled Trial. EBioMedicine. 2018 May;31:150-156 Authors: Zheng JS, Chen J, Wang L, Yang H, Fang L, Yu Y, Yuan L, Feng J, Li K, Tang J, Lin M, Lai CQ, Li D Abstract BACKGROUND: Modulation of genetic variants on the effect of omega-3 fatty acid supplements on blood lipids is still unclear. METHODS: In a double-blind randomized controlled trial, 150 patients with type 2 diabetes (T2D) were randomized into omega-3 fatty acid group (n = 56 for fish oil and 44 for flaxseed oil) and control group (n = 50) for 180 days. All patients were genotyped for genetic variants at CD36 (rs1527483), NOS3 (rs1799983) and PPARG (rs1801282). Linear regression was used to examine the interaction between omega-3 fatty acid intervention and CD36, NOS3 or PPARG variants for blood lipids. FINDINGS: Significant interaction with omega-3 fatty acid supplements was observed for CD36 on triglycerides (p-interaction = 0.042) and PPAGR on low-density lipoprotein-cholesterol (p-interaction = 0.02). We also found a significant interaction between change in erythrocyte phospholipid omega-3 fatty acid composition and NOS3 genotype on triglycerides (p-interaction = 0.042), total cholesterol (p-interaction = 0.013) and ratio of total cholesterol to high-density lipoprotein cholesterol (p-interaction = 0.015). The T2D patients of CD36-G allele, PPARG-G allele and NOS3-A allele tended to respond better to omega-3 fatty acids in improving lipid profiles. The interaction results of the omega-3 fatty acid group were mainly attributed to the fish oil supplements. INTERPRETATION: This study suggests that T2D patients with different genotypes at CD36, NOS3 and PPARG respond differentially to intervention of omega-3 supplements in blood lipid profiles. PMID: 29703528 [PubMed - indexed for MEDLINE]

Hypomorphic citrullinaemia due to mutated ASS1 with episodic ataxia.

Related Articles Hypomorphic citrullinaemia due to mutated ASS1 with episodic ataxia. BMJ Case Rep. 2018 Apr 25;2018: Authors: Saini AG, Attri S, Sankhyan N, Singhi P Abstract Children with citrullinaemia commonly present in the neonatal period with life-threatening hyperammonaemia and progressive encephalopathy. Less often, 'hypomorphic' or mild late-onset childhood or adult-onset forms may be seen with intermittent neurological symptoms or acute crisis in pregnancy. We describe an 11-year-old boy with late-onset citrullinaemia manifesting as brief episodes of ataxia triggered by minor febrile illnesses, significant citrullinaemia, mild hyperammonaemia, normal neurological examination and mild cerebellar atrophy. Targeted gene sequencing showed a homozygous, missense mutation c.815G>A (p.R272H) in exon 12 of ASS1 gene resulting in the amino acid substitution of histidine for arginine at codon 272. Our case highlights the importance of recognising urea cycle defects as a cause of intermittent neurological symptoms such as ataxia. Type-1 citrullinaemia may remain hypomorphic and needs a high index of suspicion. PMID: 29695388 [PubMed - indexed for MEDLINE]

Efficacy of a Moderately Low Carbohydrate Diet in a 36-Month Observational Study of Japanese Patients with Type 2 Diabetes.

Related Articles Efficacy of a Moderately Low Carbohydrate Diet in a 36-Month Observational Study of Japanese Patients with Type 2 Diabetes. Nutrients. 2018 Apr 24;10(5): Authors: Sanada M, Kabe C, Hata H, Uchida J, Inoue G, Tsukamoto Y, Yamada Y, Irie J, Tabata S, Tabata M, Yamada S Abstract We previously showed that a non-calorie-restricted, moderately low-carbohydrate diet (mLCD) is more effective than caloric restriction for glycemic and lipid profile control in patients with type 2 diabetes. To determine whether mLCD intervention is sustainable, effective, and safe over a long period, we performed a 36-month observational study. We sequentially enrolled 200 patients with type 2 diabetes and taught them how to follow the mLCD. We compared the following parameters pre- and post-dietary intervention in an outpatient setting: glycated hemoglobin (HbA1c), body weight, lipid profile (total cholesterol, low and high-density lipoprotein cholesterol, triglycerides), systolic and diastolic blood pressure, liver enzymes (aspartate aminotransferase, alanine aminotransferase), and renal function (urea nitrogen, creatinine, estimated glomerular filtration rate). Data from 157 participants were analyzed (43 were lost to follow-up). The following parameters decreased over the period of study: HbA1c (from 8.0 ± 1.5% to 7.5 ± 1.3%, p < 0.0001) and alanine aminotransferase (from 29.9 ± 23.6 to 26.2 ± 18.4 IL/L, p = 0.009). Parameters that increased were high-density lipoprotein cholesterol (from 58.9 ± 15.9 to 61.2 ± 17.4 mg/dL, p = 0.001) and urea nitrogen (from 15.9 ± 5.2 to 17.0 ± 5.4 mg/dL, p = 0.003). Over 36 months, the mLCD intervention showed sustained effectiveness (without safety concerns) in improving HbA1c, lipid profile, and liver enzymes in Japanese patients with type 2 diabetes. PMID: 29695055 [PubMed - indexed for MEDLINE]

Dietary Treatment of Metabolic Acidosis in Chronic Kidney Disease.

Related Articles Dietary Treatment of Metabolic Acidosis in Chronic Kidney Disease. Nutrients. 2018 Apr 20;10(4): Authors: Siener R Abstract Chronic kidney disease and reduced glomerular filtration rate are risk factors for the development of chronic metabolic acidosis. The prevention or correction of chronic metabolic acidosis has been found to slow progression of chronic kidney disease. Dietary composition can strongly affect acid⁻base balance. Major determinants of net endogenous acid production are the generation of large amounts of hydrogen ions, mostly by animal-derived protein, which is counterbalanced by the metabolism of base-producing foods like fruits and vegetables. Alkali therapy of chronic metabolic acidosis can be achieved by providing an alkali-rich diet or oral administration of alkali salts. The primary goal of dietary treatment should be to increase the proportion of fruits and vegetables and to reduce the daily protein intake to 0.8⁻1.0 g per kg body weight. Diet modifications should begin early, i.e., even in patients with moderate kidney impairment, because usual dietary habits of many developed societies contribute an increased proportion of acid equivalents due to the high intake of protein from animal sources. PMID: 29677110 [PubMed - indexed for MEDLINE]

Pedunculoside, a novel triterpene saponin extracted from Ilex rotunda, ameliorates high-fat diet induced hyperlipidemia in rats.

Related Articles Pedunculoside, a novel triterpene saponin extracted from Ilex rotunda, ameliorates high-fat diet induced hyperlipidemia in rats. Biomed Pharmacother. 2018 May;101:608-616 Authors: Liu C, Shen YJ, Tu QB, Zhao YR, Guo H, Wang J, Zhang L, Shi HW, Sun Y Abstract Pedunculoside (PE) is a novel triterpene saponin extracted from the dried barks of Ilex rotunda Thunb. The present study aims to explore lipid-lowering effects of PE on hyperlipidemia rat induced by high-fat diet. The rats were fed with the high-fat diet and subjected to intragastric administration of PE at doses of 30, 15, or 5 mg/kg daily for 7 weeks. The results demonstrated that treatment with PE for 7-week dramatically decreased serum total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C) and reduced liver TC in hyperlipidemia rat induced by high-fat diet. Furthermore, the results also showed that PE modulated the expression of enzymes involved in lipid metabolism including peroxisome proliferator-activated receptor α (PPAR-α), sterol regulatory element-binding protein 1 (SREBP-1), fatty acid synthase (FAS) and stearoyl CoA desaturase-1 (SCD-1) mRNA in liver. Besides, PE-treated group decreased weights and diameters of epididymal adipose hyperlipidemia rat. Mechanism study demonstrated that PE regulated PPAR-γ, CCAAT/Enhancer-binding Protein α (C/EBPα)、and SREBP-1 expression as well as inhibited phosphorylation of AMPK in MDI (methylisobutylxanthine, dexamethasone, insulin) induced-3T3L1 cells. Molecular Docking confirmed interaction between PE with proteins involving PPAR-γ, C/EBPα and SREBP-1. In summary, these findings may support that PE is a novel lipid-lowering drug candidate. PMID: 29518607 [PubMed - indexed for MEDLINE]

Assessment of the spectrum of hepatic encephalopathy: A multicenter study.

Related Articles Assessment of the spectrum of hepatic encephalopathy: A multicenter study. Liver Transpl. 2018 05;24(5):587-594 Authors: Reuter B, Walter K, Bissonnette J, Leise MD, Lai J, Tandon P, Kamath PS, Biggins SW, Rose CF, Wade JB, Bajaj JS Abstract Hepatic encephalopathy (HE) is a major cause of morbidity in cirrhosis. However, its severity assessment is often subjective, which needs to be studied systematically. The aim was to determine how accurately trainee and nontrainee practitioners grade and manage HE patients throughout its severity. We performed a survey study using standardized simulated patient videos at 4 US and 3 Canadian centers. Participants were trainees (gastroenterology/hepatology fellows) and nontrainees (faculty, nurse practitioners, physician assistants). We determined the accuracy of HE severity identification and management options between grades <2 or ≥2 HE and trainees/nontrainees. In total, 108 respondents (62 trainees, 46 nontrainees) were included. For patients with grades <2 versus ≥2 HE, a higher percentage of respondents were better at correctly diagnosing grades ≥2 compared with grades <2 (91% versus 64%; P < 0.001). Specialized cognitive testing was checked significantly more often in grades <2, whereas more aggressive investigation for precipitating factors was ordered in HE grades >2. Serum ammonia levels were ordered in almost a third of grade ≥2 patients. For trainees and nontrainees, HE grades were identified similarly between groups. Trainees were less likely to order serum ammonia and low-protein diets, more likely to order rifaximin, and more likely to perform a more thorough workup for precipitating factors compared with nontrainee respondents. There was excellent concordance in the classification of grade ≥2 HE between nontrainees versus trainees, but lower grades showed discordance. Important differences were seen regarding blood ammonia, specialized testing, and nutritional management between trainees and nontrainees. These results have important implications at the patient level, interpreting multicenter clinical trials, and in the education of practitioners. Liver Transplantation 24 587-594 2018 AASLD. PMID: 29457869 [PubMed - indexed for MEDLINE]

Unique case of gyrate atrophy with a well-preserved electroretinogram (ERG).

Related Articles Unique case of gyrate atrophy with a well-preserved electroretinogram (ERG). BMJ Case Rep. 2018 Feb 05;2018: Authors: Jasani KM, Parry NRA, Black G, Kelly SP Abstract Gyrate atrophy is a rare autosomal recessive disorder caused by a mutation in the ornithine-δ-amino transferase gene. We present an interesting case of a 33-year-old woman who presented with increasing myopia, nyctalopia and failing vision. Examination revealed posterior subscapsular cataracts, narrowed peripheral visual fields and scalloped atrophic peripheral chorioretinal lesions. Blood investigations showed a raised plasma ornithine level at 917 μmol/L (normal range: 32-88 μmol/L) confirming the diagnosis of gyrate atrophy. The patient, despite not tolerating dietary treatment, had retained central vision over a follow-up period of 18 years. The electroretinogram, which normally diminishes with disease progression, was still nearly normal when last tested at 16 years follow-up. Genetic testing did not reveal any novel mutation that could account for this variation. PMID: 29437727 [PubMed - indexed for MEDLINE]