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

Oral administration of visceral adipose tissue antigens ameliorates metabolic disorders in mice and elevates visceral adipose tissue-resident CD4+CD25+Foxp3+ regulatory T cells.

Related Articles Oral administration of visceral adipose tissue antigens ameliorates metabolic disorders in mice and elevates visceral adipose tissue-resident CD4+CD25+Foxp3+ regulatory T cells. Vaccine. 2017 08 16;35(35 Pt B):4612-4620 Authors: Chen X, Zhang D, Chen X, Meng G, Zheng Q, Mai W, Wu Y, Ye L, Wang L Abstract Obesity and type 2 diabetes are linked with chronic, low-grade inflammation in visceral adipose tissue (VAT). A unique population of VAT-resident CD4+Foxp3+ Tregs plays a crucial role in regulating VAT inflammation and metabolic homeostasis. VAT-resident Tregs display a highly restricted TCR repertoire, suggesting they recognize certain autoantigen(s) in VAT. A dramatic reduction of VAT-resident Tregs has been shown to closely correlate with obesity-related VAT chronic inflammation and metabolic disorders. Oral tolerance strategy may modulate inflammatory response to autoantigens by several mechanisms including induction of autoantigen-specific Tregs. Here, we explored the effects and cellular mechanism of oral administration of VAT pooled antigens on high-fat diet (HFD)-induced metabolic disorders in mice. Indeed, we found that oral treatment of VAT mixture antigens effectively inhibited gain in body weight and fat mass, ameliorated serum lipid parameters, and improved insulin sensitivity in HFD mice. This strategy was shown to significantly restore HFD-induced decrease of VAT-resident Tregs, accompanied by a hampered M2-type to M1-type macrophages phenotypic switch as well as decreased CD8+ T cells infiltration in VAT. Thus, oral administration of VAT antigens may be a novel and safe strategy against obesity and its related metabolic disorders. PMID: 28736203 [PubMed - indexed for MEDLINE]

Anti-obesity effects of yellow catfish protein hydrolysate on mice fed a 45% kcal high-fat diet.

Related Articles Anti-obesity effects of yellow catfish protein hydrolysate on mice fed a 45% kcal high-fat diet. Int J Mol Med. 2017 Sep;40(3):784-800 Authors: Kim MR, Kim JW, Park JB, Hong YK, Ku SK, Choi JS Abstract Obesity contributes to the etiologies of a variety of comorbid conditions, such as type 2 diabetes, hypertension and cardiovascular disease. In the present study, the anti-obesity effects of yellow catfish protein hydrolysate (YPh) were observed in mice fed a 45% kcal high-fat diet (HFD) compared with those of mice treated with simvastatin. The HFD-fed control mice exhibited noticeable increase in body weight, and whole-body and abdominal fat densities, periovarian and abdominal wall-deposited fat pad weight, as well as in the levels of triglycerides (TG), blood total cholesterol (TC), low-density lipoprotein, alanine aminotransferase, aspartate aminotransferase, creatinine, blood urea nitrogen, and in the fecal TG and TC contents. However, they exhibited a decrease in serum high-density lipoprotein levels. In addition, an increase was detected in periovarian and dorsal abdominally deposited fat pad thickness, adipocyte hypertrophy, the number of steatohepatitis regions, hepatocyte hypertrophy and lipid droplet deposition-related renal tubular vacuolation degenerative lesions, along with increased hepatic lipid peroxidation and a deteriorated endogenous antioxidant defense system (glutathione, catalase and superoxide dismutase). However, all the above-mentioned obesity-related complications were dose-dependently and significantly inhibited after 84 days of thye consecutive oral administration of 125, 250 and 500 mg/kg YPh. In addition, YPh dose-dependently depleted the liver endogenous antioxidant defense system and inhibited hepatic lipid peroxidation. Overall, the effects of 250 mg/kg YPh on HFD-induced obesity and related complications were similar or more potent than those of 10 mg/kg simvastatin. These results indicate that YPh is a promising new potent medicinal ingredient for possible use in the treatment of obesity and related complications. PMID: 28713910 [PubMed - indexed for MEDLINE]

Evaluation of the sub-chronic toxicity profile of the corm of Xanthosoma sagittifolium on hematology and biochemistry of alloxan-induced diabetic Wistar rats.

Related Articles Evaluation of the sub-chronic toxicity profile of the corm of Xanthosoma sagittifolium on hematology and biochemistry of alloxan-induced diabetic Wistar rats. J Complement Integr Med. 2017 Mar 10;14(2): Authors: Oridupa OA, Folasire OF, Owolabi AJ Abstract Background Hematological and biochemical changes associated with diabetes mellitus and probable reversal were assessed in alloxan-induced diabetic Wistar rats fed with varied percentages of Xanthosoma sagittifolium corm feed (Xs). The changes were compared to normoglycemic rats and diabetic rats treated with glibenclamide. Methods The study had eight groups in all with group 8 (control) consisting of five normoglycemic rats fed with normal rat pellets (Nrp). Diabetes was experimentally induced by intraperitoneal injection of alloxan to normoglycemic rats. Diabetic rats (serum glucose >200 mg/dL) at 48 h postinjection were randomly divided into the seven groups, each diabetic group consisting of five rats. One group was untreated and fed with Nrp, four groups were fed with 25 %, 50 %, 75 % or 100 % Xs, one group was fed with 100 % Xs and administered with glibenclamide, while a 7th group was fed with Nrp and administered with glibenclamide. Results This study shows that treatment of diabetes with corm of X. sagittifolium increases cellular response to inflammation which is required for body defense against assaulting agents. Decreased serum protein levels observed in untreated diabetic rats were restored in diabetic rats fed with X. sagittifolium corm with particular increase in serum albumin levels but depression of globulin fraction, except in rats fed with X. sagittifolium feed and administered with glibenclamide. X. sagittifolium showed a potent antihyperglycemic effect and corrected the dyslipidemia in a manner comparable to that observed for glibenclamide. Although HDL levels were still low, significant (p<0.05) decrease of LDL levels was a positive indicator of reduced risk for development of cardiovascular and/or coronary heart disease. Conclusions X. sagittifolium corm can be recommended for inclusion in diets of diabetics without causing further deterioration of health of the diabetic patients. PMID: 28306532 [PubMed - indexed for MEDLINE]

The efficacy of protein supplementation during recovery from muscle-damaging concurrent exercise.

Related Articles The efficacy of protein supplementation during recovery from muscle-damaging concurrent exercise. Appl Physiol Nutr Metab. 2017 Jul;42(7):716-724 Authors: Eddens L, Browne S, Stevenson EJ, Sanderson B, van Someren K, Howatson G Abstract This study investigated the effect of protein supplementation on recovery following muscle-damaging exercise, which was induced with a concurrent exercise design. Twenty-four well-trained male cyclists were randomised to 3 independent groups receiving 20 g protein hydrolysate, iso-caloric carbohydrate, or low-calorific placebo supplementation, per serve. Supplement serves were provided twice daily, from the onset of the muscle-damaging exercise, for a total of 4 days and in addition to a controlled diet (6 g·kg-1·day-1 carbohydrate, 1.2 g·kg-1·day-1 protein, remainder from fat). Following the concurrent exercise session at time-point 0 h, comprising a simulated high-intensity road cycling trial and 100 drop-jumps, recovery of outcome measures was assessed at 24, 48, and 72 h. The concurrent exercise protocol was deemed to have caused exercise-induced muscle damage (EIMD), owing to time effects (p < 0.001), confirming decrements in maximal voluntary contraction (peaking at 15% ± 10%) and countermovement jump performance (peaking at 8% ± 7%), along with increased muscle soreness, creatine kinase, and C-reactive protein concentrations. No group or interaction effects (p > 0.05) were observed for any of the outcome measures. The present results indicate that protein supplementation does not attenuate any of the indirect indices of EIMD imposed by concurrent exercise, when employing great rigour around the provision of a quality habitual diet and the provision of appropriate supplemental controls. PMID: 28199799 [PubMed - indexed for MEDLINE]

Selective protein depletion impairs bone growth and causes liver fatty infiltration in female rats: prevention by Spirulina alga.

Related Articles Selective protein depletion impairs bone growth and causes liver fatty infiltration in female rats: prevention by Spirulina alga. Osteoporos Int. 2016 Nov;27(11):3365-3376 Authors: Fournier C, Rizzoli R, Bouzakri K, Ammann P Abstract Chronic protein malnutrition leads to child mortality in developing countries. Spirulina alga (Spi), being rich in protein and growing easily, is a good candidate as supplementation. We showed that Spi completely prevents bone growth retardation and liver disturbances observed in young rats fed a low protein diet. This supports Spi as a useful source of vegetable protein to fight against protein malnutrition. INTRODUCTION: Chronic malnutrition is a main factor of child mortality in developing countries. A low protein diet impairs whole-body growth and leads to fatty liver in growing rats. Spi has great potential as a supplementation as it has a 60 % protein content and all essential amino acids. However, its specific impact on bone growth and the related secretion of hepatokines have not yet been studied. METHODS: To address this question, 6-week-old female rats were fed isocaloric diets containing 10 % casein, 5 % casein, or 5 % casein + 5 % protein from Spi during 9 weeks. Changes in tibia geometry, microarchitecture, BMC, BMD, and biomechanical properties were analyzed. Serum IGF-I, FGF21, follistatin, and activin A were assessed as well as their hepatic gene expressions in addition to those of Sirt1, Ghr, and Igf1r. Hepatic fat content was also assessed. RESULTS: A low protein diet altered bone geometry and reduced proximal tibia BMD and trabecular bone volume. In addition, it increased hepatic fat content and led to hepatic GH resistance by decreasing serum IGF-I and increasing serum FGF21 without altering serum activin A and follistatin. Spi prevented low protein diet-induced bone, hepatic, and hormonal changes, and even led to higher biomechanical properties and lower hepatic fat content in association with specific InhbA and Follistatin expression changes vs. the 10 % casein group. CONCLUSIONS: Altogether our results demonstrate the preventive impact of Spi on bone growth delay and hepatic GH resistance in conditions of isocaloric dietary protein deficiency. PMID: 27341811 [PubMed - indexed for MEDLINE]

Dietary fat may modulate adipose tissue homeostasis through the processes of autophagy and apoptosis.

Related Articles Dietary fat may modulate adipose tissue homeostasis through the processes of autophagy and apoptosis. Eur J Nutr. 2017 Jun;56(4):1621-1628 Authors: Camargo A, Rangel-Zúñiga OA, Alcalá-Díaz J, Gomez-Delgado F, Delgado-Lista J, García-Carpintero S, Marín C, Almadén Y, Yubero-Serrano EM, López-Moreno J, Tinahones FJ, Pérez-Martínez P, Roche HM, López-Miranda J Abstract PURPOSE: Obesity increases the risk of cardiovascular disease, type 2 diabetes mellitus and cancer development. Autophagy and apoptosis are critical processes for development and homeostasis in multicellular organisms and have been linked to a variety of disorders. We aimed to investigate whether the quantity and quality of dietary fat can influence these processes in the adipose tissue of obese people. METHODS: A randomized, controlled trial within the LIPGENE study assigned 39 obese people with metabolic syndrome to 1 of 4 diets: (a) a high-saturated fatty acid diet, (b) a high-monounsaturated fatty acid (HMUFA) diet, and (c, d) two low-fat, high-complex carbohydrate diets supplemented with long-chain n-3 polyunsaturated fatty acids (LFHCC n-3) or placebo (LFHCC), for 12 weeks each. RESULTS: We found an increase in the expression of autophagy-related BECN1 and ATG7 genes after the long-term consumption of the HMUFA diet (p = 0.001 and p = 0.004, respectively) and an increase in the expression of the apoptosis-related CASP3 gene after the long-term consumption of the LFHCC and LFHCC n-3 diets (p = 0.001 and p = 0.029, respectively). CASP3 and CASP7 gene expression changes correlated with HOMA index. CONCLUSION: Our results suggest that the processes of autophagy and apoptosis in adipose tissue may be modified by diet and that the consumption of a diet rich in monounsaturated fat may contribute to adipose tissue homeostasis by increasing autophagy. They also reinforce the notion that apoptosis in adipose tissue is linked to insulin resistance. CLINICAL TRIAL REGISTRATION NUMBER: ClinicalTrials.gov NCT00429195. PMID: 27029919 [PubMed - indexed for MEDLINE]