A Low Protein Diet Alters Bone Material Level Properties and the Response toIn VitroRepeated Mechanical Loading

Low protein intake is associated with an alteration of bone microstructure and material level properties. However, it remains unknown whether these alterations of bone tissue could influence the response to repeated mechanical loading. The authors investigated thein vitroeffect of repeated loading on bone strength in humeri collected from 20 6-month-old female rats pair-fed with a control (15% casein) or an isocaloric low protein (2.5% casein) diet for 10 weeks. Bone specimens were cyclically loaded in three-point bending under load control for 2000 cycles. Humeri were then monotonically loaded to failure. The load-displacement curve of thein vitrocyclically loaded humerus was compared to the contralateral noncyclically loaded humerus and the influence of both protein diets. Material level properties were also evaluated through a nanoindentation test. Cyclic loading decreased postyield load and plastic deflection in rats fed a low protein diet, but not in those on a regular diet. Bone material level properties were altered in rats fed a low protein diet. This suggests that bone biomechanical alterations consequent to cyclic loading are more likely to occur in rats fed a low protein diet than in control animals subjected to the samein vitrocyclic loading regimen.

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Low-protein diet impairs vascular relaxation in virgin and pregnant rats

Clinical Science ◽

10.1042/cs1020553 ◽

2002 ◽

Vol 102 (5) ◽

pp. 553-560 ◽

Cited By ~ 11

Author(s):

Angeliki KOUMENTAKI ◽

Frederick ANTHONY ◽

Lucilla POSTON ◽

Timothy WHEELER

Keyword(s):

Cardiac Output ◽

Plasma Volume ◽

Vascular Function ◽

Mesenteric Arteries ◽

Protein Diet ◽

Female Rats ◽

Low Protein Diet ◽

Pregnant Rats ◽

No Donor ◽

Low Protein

Pregnancy is associated with increases in maternal cardiac output and plasma volume and a reduction in peripheral vascular resistance. Cardiac output and plasma volume are substantially reduced in pregnant rats fed a low-protein diet, but it is not known whether vascular function is also compromised. We have investigated vascular function in virgin and pregnant Wistar rats subjected to dietary protein restriction [9% (w/v) casein, compared with 18% (w/v) casein for controls]. The diets were fed to the groups for 18 days; in the pregnant rats, the diets were given from day 1 of pregnancy. Branches of the mesenteric arteries were studied on day 18 of the dietary period using myography. Significant reductions in sensitivity to acetylcholine occurred in vessels from virgin (P = 0.04) and pregnant (P = 0.01) rats that had consumed the 9% casein diet. In arteries from the virgin rats on the restricted diet there was also a significant reduction in sensitivity (P = 0.0003) and maximum relaxation (P = 0.009) to the NO donor spermine NONOate. Mean placental and fetal weights were significantly lower in the rats fed on 9% casein (P<0.0001 and P = 0.005 respectively). Thus low-protein diets impair vasodilator responses in female rats. These effects may contribute to the poor cardiovascular adaptation to pregnancy and lower fetal weights associated with restricted protein intake.

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High fat-low protein diet induces metabolic alterations and cognitive dysfunction in female rats

Metabolic Brain Disease ◽

10.1007/s11011-019-00459-4 ◽

2019 ◽

Vol 34 (6) ◽

pp. 1531-1546 ◽

Cited By ~ 5

Author(s):

Ravinder Naik Dharavath ◽

Shiyana Arora ◽

Mahendra Bishnoi ◽

Kanthi Kiran Kondepudi ◽

Kanwaljit Chopra

Keyword(s):

Cognitive Dysfunction ◽

Protein Diet ◽

Female Rats ◽

Low Protein Diet ◽

High Fat ◽

Metabolic Alterations ◽

Low Protein

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Post-ruminal effects of rumen-protected methionine supplementation with low protein diet using long-term simulation and in vitro digestibility technique

AMB Express ◽

10.1186/s13568-018-0566-7 ◽

2018 ◽

Vol 8 (1) ◽

Cited By ~ 5

Author(s):

Imtiaz Hussain Raja Abbasi ◽

Farzana Abbasi ◽

Mohamed E. Abd El-Hack ◽

Ayman A. Swelum ◽

Junhu Yao ◽

...

Keyword(s):

Protein Diet ◽

Low Protein Diet ◽

In Vitro Digestibility ◽

Low Protein ◽

Methionine Supplementation

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Healing of Gingival Wounds in Female Rats Fed a Low-Protein Diet

Journal of Dental Research ◽

10.1177/00220345630420062901 ◽

1963 ◽

Vol 42 (6) ◽

pp. 1511-1516 ◽

Cited By ~ 13

Author(s):

S.S. Stahl

Keyword(s):

Protein Diet ◽

Female Rats ◽

Low Protein Diet ◽

Low Protein

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THE EFFECT OF PARATHION ON THE LIVER AND KIDNEY CARBOXYLESTERASES AND THE PLASMA ACETYLCHOLINESTERASES OF RATS FED NUTRITIONALLY DEFICIENT DIETS

Canadian Journal of Biochemistry ◽

10.1139/o66-099 ◽

1966 ◽

Vol 44 (6) ◽

pp. 809-817 ◽

Cited By ~ 6

Author(s):

Sheila I. Read ◽

E. J. Middleton ◽

W. P. Mckinley

Keyword(s):

Control Diet ◽

Acetylcholinesterase Activity ◽

Protein Diet ◽

Female Rats ◽

Male Rats ◽

Low Protein Diet ◽

Male And Female ◽

Low Protein ◽

Male And Female Rats ◽

Liver And Kidney

Female rats were fed diets low in minerals, vitamins, or protein, or a control diet, both alone and supplemented with 10 parts per million (p.p.m.) parathion for 3 weeks. Male and female rats were fed control and tow-vitamin diets both with and without parathion supplementation (0–10 p.p.m.) for 3 weeks. The liver and kidney carboxylesterases (EC 3.1.1.1.), and the plasma acetylcholinesterases (EC 3.1.1.7.) of the male rats, were measured.In the female rats, a low-mineral diet resulted in an increase of carboxylesterases in the liver and kidney; a low-vitamin diet caused a marked increase in liver carboxylesterases but had no effect on the carboxylesterases of the kidney. Parathion at 10 p.p.m. in all diets greatly reduced the liver carboxylesterases but had less effect on kidney carboxylesterases, except in the case of the low-protein diet, for which the reduction was similar to that in the liver. Varying amounts of parathion added to the low-vitamin diet reduced the liver and kidney carboxylesterases, but to a less extent than when added to the control diet.The liver carboxylesterases of male rats were inhibited approximately 50% by 2 p.p.m. parathion in the control diet and by 4 p.p.m. parathion in the low-vitamin diet. However, inhibition of plasma acetylcholinesterase and kidney carboxylesterases was not marked until the 10 p.p.m. parathion level was fed. The acetylcholinesterase activity of the plasma of male rats did not decrease until the level of liver carboxylesterases was very low.

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Isocaloric maternal low-protein diet alters IGF-I, IGFBPs, and hepatocyte proliferation in the fetal rat

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.00037.2003 ◽

2003 ◽

Vol 285 (5) ◽

pp. E991-E1000 ◽

Cited By ~ 44

Author(s):

Ilham El Khattabi ◽

Francine Grégoire ◽

Claude Remacle ◽

Brigitte Reusens

Keyword(s):

Cell Proliferation ◽

Fetal Liver ◽

Protein Diet ◽

Low Protein Diet ◽

Hepatocyte Proliferation ◽

Liver Growth ◽

Fetal Plasma ◽

Low Protein ◽

Igf I

We investigated the effect of an isocaloric maternal low-protein diet during pregnancy in rats on the proliferative capacity of cultured fetal hepatocytes. The potential roles of these changes on the IGF-IGF-binding protein (IGFBP) axis, and the role of insulin and glucocorticoids in liver growth retardation, were also evaluated. Pregnant Wistar rats were fed a control (C) diet (20% protein) or a low-protein (LP) diet (8%) throughout gestation. In primary culture, the DNA synthesis of hepatocytes derived from LP fetuses was decreased by ∼30% compared with control hepatocytes ( P < 0.05). In parallel, in vivo moderate protein restriction in the dam reduced the fetal liver weight and IGF-I level in fetal plasma ( P < 0.01) and augmented the abundance of 29- to 32-kDa IGFBPs in fetal plasma ( P < 0.01) and fetal liver ( P < 0.01). By contrast, the abundance of IGF-II mRNA in liver of LP fetuses was unaffected by the LP diet. In vitro, the LP-derived hepatocytes produced less IGF-I ( P < 0.01) and more 29- to 32-kDa IGFBPs ( P < 0.01) than hepatocytes derived from control fetuses. These alterations still appeared after 3–4 days of culture, indicating some persistence in programming. Dexamethasone treatment of control-derived hepatocytes decreased cell proliferation (54 ± 2.3%, P < 0.01) and stimulated 29- to 32-kDa IGFBPs, whereas insulin promoted fetal hepatocyte growth (127 ± 5.5%, P < 0.01) and inhibited 29- to 32-kDa IGFBPs. These results show that liver growth and cell proliferation in association with IGF-I and IGFBP levels are affected in utero by fetal undernutrition. It also suggests that glucocorticoids and insulin may modulate these effects.

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Gestational and Postnatal Low Protein Diet Alters Insulin Sensitivity in Female Rats

Experimental Biology and Medicine ◽

10.3181/0903-rm-111 ◽

2009 ◽

Vol 234 (12) ◽

pp. 1437-1444 ◽

Cited By ~ 11

Author(s):

Kally J. Berleze ◽

Alexandre P. Müller ◽

Ingrid D. Schweigert ◽

Aline Longoni ◽

Fernanda Sordi ◽

...

Keyword(s):

Insulin Sensitivity ◽

Protein Diet ◽

Female Rats ◽

Low Protein Diet ◽

Low Protein

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Protein and energy relations in the broiler chicken

British Journal Of Nutrition ◽

10.1079/bjn19890111 ◽

1989 ◽

Vol 61 (2) ◽

pp. 223-233 ◽

Cited By ~ 16

Author(s):

R. W. Rosebrough ◽

J. P. McMurtry ◽

N. C. Steele

Keyword(s):

G Protein ◽

Broiler Chickens ◽

Control Diet ◽

Glucose Production ◽

Protein Diet ◽

Low Protein Diet ◽

Intermittent Feeding ◽

Low Protein ◽

Feeding Regimen

1. Broiler chickens growing from 7 to 28 d of age were given: (1) a 210 g protein/kg control diet for the entire experimental period, (2) an intermittent feeding regimen (210 g protein/kg diet for either 1 or 2 d followed by a 1 d fast), or (3) a daily change in the dietary protein level from 120 to 300 g/kg diet. Treatment variables examined were lipogenesis and glucose production in vitro, and circulating concentrations of insulin, triiodothyronine (T3) and thyroxine (T4) to determine the effects of chronic or acute dietary treatments.2. Giving the 300 g protein/kg diet or withholding feed for 1 d decreased (P < 0.05) lipogenesis in vitro compared with controls.3. Giving the 120 g protein/kg diet or refeeding with a 210 g protein/kg diet for 1 or 2 d increased (P < 0.05) lipogenesis in vitro compared with controls. Glucose production was affected in the same manner.4. Fasting decreased (P < 0.05) plasma insulin and T3 and increased T4. Both refeeding and a low-protein diet increased T3. Refeeding increased and a low-protein diet decreased insulin.5. Chronic use (7-28 d of age) of either an alternating protein or intermittent feeding regimen caused greater responses compared with acute bouts (single cycle) of either of the regimens.

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Decreased serum insulin-like growth factor I response to growth hormone in hypophysectomized rats fed a low protein diet: evidence for a postreceptor defect

Acta Endocrinologica ◽

10.1530/acta.0.1170320 ◽

1988 ◽

Vol 117 (3) ◽

pp. 320-326 ◽

Cited By ~ 39

Author(s):

M. Maes ◽

Y. Amand ◽

L. E. Underwood ◽

D. Maiter ◽

J.-M. Ketelslegers

Keyword(s):

Binding Sites ◽

Protein Diet ◽

Female Rats ◽

Low Protein Diet ◽

Affinity Constant ◽

Protein Calorie Malnutrition ◽

Low Protein ◽

Igf I ◽

Hypophysectomized Rats ◽

Gh Resistance

Abstract. In protein-calorie malnutrition, serum IGF-I concentrations are low despite high GH. This GH resistance might be due to a reduced number of liver GH binding sites as suggested by studies performed in fasted rats that were refed a low protein diet. To determine whether a postreceptor defect in GH action might also contribute to the GH resistance, we measured the number and the affinity constant of the liver GH binding sites and the serum IGF-I responses to injections of recombinant bGH in hypophysectomized female rats, fed a standard (15% protein) diet (N = 25) or a low (5%) protein diet (N = 25) for 8 days. There were no significant differences in the liver GH binding capacities between the 15% and the 5% protein-fed rats, whether expressed as pmol per liver (20.6 ± 3.5 vs 14.4 ± 1.3; mean ± sem; P < 0.2; N = 5, respectively), pmol per mg DNA (1.08 ± 0.16 vs 0.84 ± 0.07; P <0.4) or fmol per mg of protein (28.98 ± 5.04 vs 30.26 ± 2.00; P > 0.5). Likewise, the affinity constants of the GH binding sites of the 15% and the 5% protein-fed rats were not significantly different (0.78 ± 0.05 vs 0.78 ± 0.07 × 109 l/mol; P > 0.5). Despite these non-significant reductions in liver GH binding sites, the IGF-I responses 24 h after sc injections of increasing doses of bovine GH were blunted in the rats fed the 5% protein diet. The maximal IGF-I response in the rats with the normal protein intake was 360 ± 30 U/I, but only 130 ± 40 U/l in the 5% protein-fed animals (P < 0.001). The blunted serum IGF-I responses to GH, together with decreased maximal stimulation in the 5% protein-fed hypophysectomized rats, support the possibility that a postreceptor defect in GH action contributes to the GH resistance in protein-calorie malnutrition.

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