Effect Of Low Protein Diet Research Articles

Nutritional Programming of Blood Pressure and Renal Morphology

A range of epidemiological evidence from several diverse populations, supports the hypothesis that risk of essential hypertension, coronary heart disease and non-insulin dependent diabetes is, in part, programmed by intrauterine nutritional status. Animal models developed to investigate the mechanisms that are responsible for such programming are becoming more important as challenges to the epidemiological data become more robust. With strong evidence from animal studies it is now widely accepted that maternal nutritional status in pregnancy is a major programming influence upon the fetus. This paper considers the hypothesis that renal structure and function are determined by prenatal nutrition and that this is a key mechanism in the programming of hypertension. The feeding of low protein diets or other insults in pregnancy that have an impact upon the development of cardiovascular functions, also appears to impact upon nephron number. In the sheep nephron number is related to weight at birth following nutrient restriction, and in the rat low protein diets reduce nephron number by approximately 30%. However, it is possible that hypertension and reduced renal reserve merely coincide and are not causally associated. A study of rats fed low protein diets supplemented with additional nitrogen sources found that whilst only glycine could reverse the hypertensive effects of low protein diets, all supplements could normalise nephron number. The evidence thus suggests that prenatal undernutrition may programme renal structure in later life, but that renal programming is not one of the primary mechanisms leading to hypertension.

Progressive renal and cardiovascular disease: Optimal treatment strategies

Progressive renal and cardiovascular disease: Optimal treatment strategies

Effect of low-protein diets on growth performance and body composition of broiler chicks

Three experiments were conducted to investigate effects of dietary manipulations to improve growth performance and whole-body composition of broiler chicks fed low-protein diets supplemented with crystalline amino acids. In all experiments, male chicks (1 d old) were fed a common corn-soybean meal diet (23% CP) for 7 d and subsequently allotted to treatment diets in a completely randomized design (10 chicks per floor pen, six replications). Chicks had free access to the isoenergetic diets (3,200 kcal MEn/kg) for 2 wk, after which chicks were weighed and then fasted for 24 h, and the whole-body DM, N, and ether extract contents of two chicks per pen (and six baseline chicks) were determined. In Experiment 1, Gln or Asn replaced 1% triammonium citrate in the low-protein diet (19% CP). In Experiments 2 and 3, dietary concentrations of crystalline essential and nonessential amino acids, respectively, were increased incrementally in the low-protein diets (19 to 20% CP). In all experiments, chicks fed low-protein diets grew slower, used feed less efficiently, and retained less N and more ether extract than chicks fed the control diets (P < or = 0.05), despite additions of crystalline Gln or Asn and despite increased dietary concentrations of crystalline essential and nonessential amino acids. Chicks fed low-protein diets excreted less N (P < 0.001) than did chicks fed the high-protein diets, and N excretion increased linearly (P < 0.001) with N intake. In summary, low-protein diets failed to support equal growth performance to that of high-protein control diets.

Effects of Low-Protein Diet on Pancreatic Endocrine Function of Fetal and Adult Rats

Effects of Low-Protein Diet on Pancreatic Endocrine Function of Fetal and Adult Rats

Effect of Low Protein Diets with Amino Acid Supplementation on Broiler Growth

Reduction of litter N and ammonia production can be accomplished by decreasing dietary CP to levels below the requirements listed by the National Research Council. However, amino acids must be added to low CP diets to obtain satisfactory growth performance. It is important to know what levels of amino acid supplementation are required in low CP diets to avoid decreased growth performance and feeding excess amounts of expensive ingredients. Two studies were conducted to determine if further supplementation with essential amino acids (EAA) or nonessential amino acids (NEAA) or energy to corn-soybean meal diets low in CP (17.3 or 17.7% CP and already supplemented with multiple essential amino acids) could improve growth of broilers during Weeks 2 and 3. Ten cages of six males were assigned to each of eight treatments per study. In both trials, a high CP diet (22.6 or 23.0%) resulted in higher BW gain and gain to feed ratio (GFR), compared with all other treatments. In Experiment 1, adding Arg, Thr or Trp, but not Ile nor Glu, increased BW gain and feed intake. Supplemental Thr improved GFR. In Experiment 2, supplemental Thr + Trp + Arg was beneficial in the presence of extra energy or NEAA. The results of Experiment 1, but not of Experiment 2, suggest that the low CP diet was not limiting in NEAA but had insufficient Thr.

DOMINANT EFFECT OF SUPPLEMENTED-SUCROSE ON THE LOW PROTEIN DIET-INDUCED INCREASE IN BLOOD PRESSURE OF SPRAGUE-DAWLEY RATS

A low-protein diet (LPD) is known to affect the regulation of hemodynamics, and could contribute to the genesis of hypertension. We investigated the mechanism for the LPD-induced elevation of blood pressure in 52 Sprague-Dawley rats. Rats fed the LPD for 8 weeks showed a significantly higher blood pressure than those fed on a normal-protein diet (NPD) when the LPD included sucrose as a predominant component of carbohydrate (LPD with a high sucrose content, 135 ±2 mmHg; NPD, 124 ±2 mmHg; p<0.05). However, LPD with a low sucrose content, in which corn starch was the main component of carbohydrate, did not have a hypertensive effect (125 ±2 mmHg). Urinary epinephrine and norepinephrine excretion was significantly higher in the LPD high-sucrose group than in the NPD and LPD low-sucrose groups, and there was a significant positive correlation between urinary norepinephrine excretion and systolic blood pressure. Urinary nitric oxide excretion was no different between these groups, and 2 % L-arginine administration exerted no antihypertensive effect on the LPD-induced elevation of blood pressure. Sodium restriction also did not attenuate the LPD-induced elevation of blood pressure. These results suggest that the effect of LPD on blood pressure could be interpreted as the effect of the high sucrose content supplemented to the LPD rather than the direct effect of protein restriction, and that the stimulation of sympathetic nervous activity was associated with this elevation of blood pressure.

INTERACTION OF NITRIC OXIDE AND TRANSFORMING GROWTH FACTOR-β1 INDUCED BY ANGIOTENSIN II AND MECHANICAL STRETCH IN RAT RENAL TUBULAR EPITHELIAL CELLS

Changes in intrarenal pressure accompanying unilateral ureteral obstruction can result in tubular mechanical stretch and mediator release from renal tubules. Therefore, we examined the synthesis of nitric oxide and transforming growth factor-beta (TGF-beta), and their interaction in rat renal epithelial cells (NRK-52E) exposed to either angiotensin II or mechanical stretch. NRK-52E were exposed to either angiotensin II or mechanical stretch. Nitrite and TGF-beta in the supernatant were assessed by the Greiss reaction and bioassay, respectively. The level of cell hypertrophy and intracellular TGF-beta protein was determined by flow cytometry. TGF-beta messenger RNA and inducible nitric oxide synthase protein were detected by reverse transcriptase polymerase chain reaction and Western blot, respectively. Angiotensin II stimulated TGF-beta1 and nitric oxide. The nitric oxide synthase inhibitor, N-nitro-L-arginine (L-NAME) or angiotensin II type I receptor blocker, losartan, inhibited nitric oxide and TGF-beta1 induced by angiotensin II. Flow cytometry showed that either L-NAME or losartan inhibited angiotensin II induced cell hypertrophy. TGF-beta1 inhibited iNOS protein and nitric oxide, whereas an anti-TGF-beta antibody enhanced iNOS. Mechanical stretch induced TGF-beta, inducible NOS protein and nitric oxide. However, TGF-beta expression was not affected by L-arginine or L-NAME when cells were exposed to mechanical stretch. These results demonstrate that nitric oxide is an intermediate in angiotensin II stimulated TGF-beta1 expression but not in stretch induced TGF-beta expression, and that TGF-beta1 is a negative regulator of nitric oxide in rat renal epithelial cells. The complex interaction of these cytokines may be a target for intervention in the fibrotic and apoptotic processes in the obstructed kidney.

Effects of low-protein diet on the pancreatic endocrine function of newborn and adult rats

Effects of low-protein diet on the pancreatic endocrine function of newborn and adult rats

From rats to man: a perspective on dietary L-arginine supplementation in human renal disease.

Experimental studies have shown both therapeutic and detrimental consequences of modifying dietary L-arginine intake in renal diseases which likely reflect the complexity of L-arginine metabolism. L-Arginine intake is semi-essential and provides substrate for a number of L-arginine metabolites involved in renal pathology. Dietary L-arginine restriction has been identified as a key mediator of the beneficial effects of low protein diets on human renal fibrosis. Supplementing dietary L-arginine in renal diseases with increased iNOS expression appears to be detrimental and thus, may be harmful in immune-mediated human kidney disorders. Increasing L-arginine intake is beneficial in experimental models of hypertensive renal disease. Based upon available data, we believe additional questions must be answered experimentally, not only to prevent an adverse outcome in humans, but to enhance our chances of human trials which will result in substantially better amelioration of disease than currently available.

Low protein diet exacerbates NO synthase inhibitor-induced hypertension in rats

Background. A low-protein diet (LPD) may suppress nitric oxide (NO) production through the reduction of L-arginine intake, and possibly exacerbates hypertension under certain conditions. We examined the effect of LPD on blood pressure in rats that received a low dose of an inhibitor of nitric oxide synthesis.

Dietary treatment of diabetic nephropathy with chronic renal failure.

Thirty-two patients with diabetes mellitus (22 IDDM and 10 NIDDM, 21 males and 11 females, age 44+/-11.8 years) were followed for 5.2+/-3.8 years after the onset of chronic renal failure, with the aim of evaluating the effect of low protein diets on the rate of decline of the residual renal function. During the 1.8+/-1.6 year follow-up period on free or uncontrolled low protein diet the mean rate of decline of creatinine clearance was 0.9+/-0.6 ml/min/month, significantly greater than that observed during 3.7+/-3.1 years on low or very low protein diets. The reduction of protein intake was followed by a significant decrease in daily urinary protein loss. A better glycaemic control was obtained on the low protein diet, and the daily insulin requirement decreased. The anthropometry, as well as the serum concentrations of rapid turnover proteins, did not change, in spite of the low or very low protein dietary supply for a long duration. The values of mean arterial pressure were quite similar during the follow-up period on free or uncontrolled low protein diet and during the study period on the low protein diet. A good compliance with reduced dietary intake (as demonstrated by the measurement of the daily urea excretion) was obtained in a large number of patients. In conclusion, our study confirms the protective effect on the residual renal function of low protein diets in IDDM and NIDDM patients with chronic renal failure due to diabetic nephropathy, in the absence of any sign of protein malnutrition.

Maternal carbenoxolone treatment lowers birthweight and induces hypertension in the offspring of rats fed a protein-replete diet.

1. In the rat low birthweight and raised systolic blood pressure are the consequence of fetal exposure to maternal low protein diets. Nutritional down-regulation of the placental isoform of 11 beta-hydroxysteroid dehydrogenase, which may increase exposure of the fetus to maternal glucocorticoids, has been suggested to underlie effects of low protein diets on fetal growth and blood pressure. 2. Pregnant rats were fed control (18% casein) or low protein (9% casein) diets throughout gestation. Animals fed the control diet were injected with carbenoxolone, an inhibitor of 11 beta-hydroxysteroid dehydrogenase. Injections were administered either throughout pregnancy (day 0-22), or targeted to specific periods in early (days 0-7), mid- (days 8-14) or late (days 15-22) gestation. 3. Exposure to a low protein diet reduced birthweight and at 4 weeks of age systolic blood pressure was significantly elevated in the rats exposed to low protein. These hypertensive animals had small kidneys in proportion to body weight. 4. Fetal exposure to carbenoxolone at any period in gestation resulted in lower weight at birth. In rats exposed to the inhibitor over days 8-14, 15-22 or 0-22 systolic blood pressure at 4 weeks was significantly higher than in control animals. The greatest elevation of pressure was associated with carbenoxolone treatment in late (days 15-22) gestation. Animals with carbenoxolone-induced hypertension did not exhibit evidence of retarded renal growth. 5. Increased fetal exposure to maternal glucocorticoids impairs fetal growth and programmes elevated blood pressure in later life.

EFFECTS OF PROTEIN MALNUTRITION ON METABOLIC AND HORMONAL ADAPTATIONS IN YOUNG TRAINED RATS 1144

The present study was designed to examine the effect of protein malnutrition and nutritional recuperation on metabolic and hormonal adaptations in young trained rats. In two separate experiments, six groups of young male rats were differently fed. During the first month, a normal-protein diet (NP) and a low-protein diet (LP) groups received 17% and 6% of casein, respectively. Following this period half of rats were sacrificed and other half were assigned to four groups: sedentary (SG); trained (TG), sedentary recuperate (SRG) and trained recuperate (TRG). During this second month all rats received a normal-protein diet. TG and TRG performed a swimming exercise protocol (overload of 5% body weight). LP rats presented reduced serum total protein levels (7.21±0.32 g/dL; n=11); glucose (116±11 mg/dL; n=11) and insulin (1.39±0.35 ng/mL n=11) when compared to NP(7.61±0.22 g/dL, n=10; 129±11 mg/dL n=10; 2.60±1.11 ng/mL, n=10, respectively; p<0.05). SRG and TRG rats showed no significant decrease in the serum total protein levels but the SG and TRG presented a higher concentration of serum glucose (142±10 mg/dL, n=6; 140±7 mg/dL, n=5, respectively) when compared to TG (130±8 mg/dL, n=7, p<0.05). The SRG showed a higher concentration of serum insulin when compared to SG (3.28±0.55 ng/mL, n=6; 2.38±0.71 ng/mL, n=8, respectively; p<0.05). In conclusion, the effect of low-protein diet followed by nutritional recuperation led to augmented levels of glucose and insulin but exercise did not affect this response. When a low-protein diet was not present, exercise decreased the level of glucose.

Renal angiotensin-converting enzyme localization in diabetic rats and the effect of low protein diet.

Recent evidence suggests a role of angiotensin-converting enzyme (ACE) in diabetic nephropathy. The effect of diabetes and low protein diet on renal immunohistochemical ACE localization was studied in streptozotocin-induced DM rats. Immunohistochemical ACE localization was reduced in DM rats, and a low protein diet partially resolved this abnormality while inhibiting the progression of diabetic nephropathy.

Role of tumor necrosis factor-alpha in insulin sensitivity and effect of low protein diet on the TNF-alpha response in patients with diabetic renal failure

In patients with diabetic renal failure, attention must be paid to the prevention of atherosclerosis as well as the preservation of renal function. Insulin resistance is one of the important risk-factors of atherosclerosis and the involvement of tumor necrosis factor-alpha (TNF-alpha) has been shown in the pathogenesis of insulin resistance in some diseases. A low-protein diet (LPD) is recommended for patients with advanced renal disease, but a large proportion of the total caloric intake is supplied from carbohydrates and fat in LPD. Therefore, we designed a study to determine: (1) the effect of TNF-alpha on insulin sensitivity, and (2) the effect of LPD on the TNF-alpha response and the risk factors of atherosclerosis, such as insulin sensitivity and lipid metabolism, in patients with diabetic renal failure. Insulin sensitivity was measured by an euglycemic hyperinsulinemic clamp technique and serum TNF-alpha level and in vitro release of TNF-alpha from peripheral blood mononuclear cells (PBMCs) was measured in patients with diabetic renal failure. A significant negative correlation was observed between lipopolysaccharide-stimulated TNF-alpha release from PBMCs and insulin sensitivity (r = -0.58, p < 0.05). Secondly, risk factors of atherosclerosis were measured before and two weeks after the introduction of LPD in patients with diabetic renal failure. LPD did not have any significant effect on insulin sensitivity, the production of TNF-alpha by PBMCs, lipid metabolism and glucose metabolism. These results indicate that: (1) TNF-alpha derived from PBMCs might affect insulin sensitivity in patients with diabetic renal failure, and (2) LPD does not have any significant effect on the risk factors of atherosclerosis.

No effect of low-protein diet on the progression of chronic renal failure in children

No effect of low-protein diet on the progression of chronic renal failure in children

Effect of Low-Protein Diet on Glomerular Changes in ddY Mice; A Spontaneous Animal Model of IgA Nephropathy

Effect of Low-Protein Diet on Glomerular Changes in ddY Mice; A Spontaneous Animal Model of IgA Nephropathy

Effect of low-protein diets on renal disease: are non-haemodynamic factors involved?

Effect of low-protein diets on renal disease: are non-haemodynamic factors involved?

L-arginine may mediate the therapeutic effects of low protein diets.

We have previously shown beneficial effects of dietary protein restriction on transforming growth factor beta (TGF-beta) expression and glomerular matrix accumulation in experimental glomerulonephritis. We hypothesized that these effects result from restriction of dietary L-arginine intake. Arginine is a precursor for three pathways, the products of which are involved in tissue injury and repair: nitric oxide, an effector molecule in inflammatory and immunological tissue injury; polyamines, which are required for DNA synthesis and cell growth; and proline, which is required for collagen production. Rats were fed six isocaloric diets differing in L-arginine and/or total protein content, starting immediately after induction of glomerulonephritis by injection of an antibody reactive to glomerular mesangial cells. Mesangial cell lysis and monocyte/macrophage infiltration did not differ with diet. However, restriction of dietary L-arginine intake, even when total protein intake was normal, resulted in decreased proteinuria, decreased expression of TGF-beta 1 mRNA and TGF-beta 1 protein, and decreased production and deposition of matrix components. L-Arginine, but not D-arginine, supplementation to low protein diets reversed these effects. These results implicate arginine as a key component in the beneficial effects of low protein diet.

Effect of Low Protein Diet on Progression of the Nephrotic Syndrome in Seven Consecutive Patients with Non-Insulin-Dependent Diabetes Mellitus

Effect of Low Protein Diet on Progression of the Nephrotic Syndrome in Seven Consecutive Patients with Non-Insulin-Dependent Diabetes Mellitus