scholarly journals Pamidronate Prevents Bone Loss and Decreased Bone Strength in Adult Female and Male Rats Fed an Isocaloric Low-Protein Diet

2005 ◽  
Vol 20 (8) ◽  
pp. 1365-1371 ◽  
Author(s):  
Samia Mekraldi ◽  
Anne Toromanoff ◽  
René Rizzoli ◽  
Patrick Ammann
1966 ◽  
Vol 44 (6) ◽  
pp. 809-817 ◽  
Author(s):  
Sheila I. Read ◽  
E. J. Middleton ◽  
W. P. Mckinley

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.


1996 ◽  
Vol 91 (5) ◽  
pp. 607-615 ◽  
Author(s):  
Simon C. Langley-Evans ◽  
Simon J. M. Welham ◽  
Rachel C. Sherman ◽  
Alan A. Jackson

1. In the rat, hypertension is induced by fetal exposure to maternal low-protein diets. The effect on blood pressure of undernutrition before conception and during discrete periods in early, mid or late pregnancy was assessed using an 18% casein (control) diet and a 9% casein diet to apply mild protein restriction. 2. The offspring of rats fed 9% casein developed raised blood pressure by weaning age. Feeding a low-protein diet before conception was not a prerequisite for programming of hypertension. 3. Hypertension was observed in rats exposed to low protein during the following gestational periods: days 0–7, days 8–14 and days 15–22. Blood pressure increases elicited by these discrete periods of undernutrition were lower than those induced by feeding a low-protein diet throughout pregnancy. The effect in early gestation was significant only in male animals. Post-natal growth of male rats exposed to low-protein diets was accelerated, but kidneys were small in relation to body weight. 4. Biochemical indices of glucocorticoid action in liver, hippocampus, hypothalamus and lung were elevated in rats exposed to low-protein diets in utero. The apparent hypersensitivity to glucocorticoids was primarily associated with undernutrition in mid to late gestation. 5. Plasma renin activity was elevated in rats exposed to 9% casein over days 15–22 of gestation. Animals undernourished over days 0–7 and 8–14 produced pups with lower plasma angiotensin II concentrations at weaning. 6. Fetal exposure to maternal low-protein diets for any period in gestation may programme hypertension in the rat. Alterations to renal structure, renal hormone action or the hypothalamic—pituitary-adrenal axis may all play a role in the programming phenomenon, either independently or in concert.


2008 ◽  
Vol 78 (Suppl_1) ◽  
pp. 200-200
Author(s):  
Chandrasekhar Yallampalli ◽  
Rebakah Elkins ◽  
Uma Yallampalli ◽  
Kunjureddiar Sathishkumar

2016 ◽  
Vol 49 (1) ◽  
pp. 50-59 ◽  
Author(s):  
Amanda Alves Marcelino Silva ◽  
Mayara Matias Oliveira ◽  
Taisy Cinthia Ferro Cavalcante ◽  
Larissa Cavalcanti Amaral Almeida ◽  
Julliet Araújo Souza ◽  
...  

2019 ◽  
Vol 9 (1) ◽  
pp. 02-06 ◽  
Author(s):  
Roshankhah Shiva ◽  
Arash Ziapoor ◽  
Cyrus Jalili ◽  
Mohammad Reza Salahshoor

1968 ◽  
Vol 46 (1) ◽  
pp. 19-23 ◽  
Author(s):  
J. R. Beaton ◽  
V. Feleki ◽  
J. A. F. Stevenson

Male rats of the Wistar strain were fed either a control (20% casein) or a low-protein (5% casein) diet. Following the intraperitoneal injection of glucose solution it was observed from the blood glucose curve that low-protein fed rats had a delayed or impaired utilization of this carbohydrate. Resting oxygen consumption was not significantly different, and after glucose injection the slight increase in both groups was not significant. On refeeding after fasting, the colonic temperature of low-protein fed rats rose to a greater extent than did that of controls. Administration of protamine zinc insulin (PZI) decreased colonic temperature during fasting particularly in low-protein fed animals, and also during refeeding following a brief fasting period. From the results of these several experiments, it would appear that low-protein fed rats may have (a) an impairment in utilization of carbohydrate, and (b) a defect in immediate energy dissipation or an increased rate of energy production from ingested food. These two abnormalities may contribute to the reduced food intake of such animals. The association of a greater increase in colonic temperature on feeding and the hypophagia of rats fed a low-protein diet, as well as the hypothermic effect of PZI associated with an increase in food intake are suggestive of a thermostatic control of food intake in addition to a glucostatic control.


Bone Reports ◽  
2020 ◽  
Vol 13 ◽  
pp. 100685
Author(s):  
Ioannis Kanakis ◽  
Moussira Alameddine ◽  
Mattia Scalabrin ◽  
Rob van ’tHof ◽  
Susan Ozanne ◽  
...  

2018 ◽  
Vol 237 (3) ◽  
pp. 243-254 ◽  
Author(s):  
Júlio Cezar de Oliveira ◽  
Egberto Gaspar de Moura ◽  
Rosiane Aparecida Miranda ◽  
Ana Maria Praxedes de Moraes ◽  
Luiz Felipe Barella ◽  
...  

We examined the long-term effects of protein restriction during puberty on the function of hypothalamic–pituitary–adrenal (HPA) and hypothalamic–pituitary–gonadal (HPG) axes in male rats. Male Wistar rats from the age of 30 to 60 days were fed a low-protein diet (4%, LP). A normal-protein diet (20.5%) was reintroduced to rats from the age of 60 to 120 days. Control rats were fed a normal-protein diet throughout life (NP). Rats of 60 or 120 days old were killed. Food consumption, body weight, visceral fat deposits, lipid profile, glycemia, insulinemia, corticosteronemia, adrenocorticotropic hormone (ACTH), testosteronemia and leptinemia were evaluated. Glucose-insulin homeostasis, pancreatic-islet insulinotropic response, testosterone production and hypothalamic protein expression of the androgen receptor (AR), glucocorticoid receptor (GR) and leptin signaling pathway were also determined. LP rats were hypophagic, leaner, hypoglycemic, hypoinsulinemic and hypoleptinemic at the age of 60 days (P < 0.05). These rats exhibited hyperactivity of the HPA axis, hypoactivity of the HPG axis and a weak insulinotropic response (P < 0.01). LP rats at the age of 120 days were hyperphagic and exhibited higher visceral fat accumulation, hyperleptinemia and dyslipidemia; lower blood ACTH, testosterone and testosterone release; and reduced hypothalamic expression of AR, GR and SOCS3, with a higher pSTAT3/STAT3 ratio (P < 0.05). Glucose-insulin homeostasis was disrupted and associated with hyperglycemia, hyperinsulinemia and increased insulinotropic response of the pancreatic islets. The cholinergic and glucose pancreatic-islet responses were small in 60-day-old LP rats but increased in 120-day-old LP rats. The hyperactivity of the HPA axis and the suppression of the HPG axis caused by protein restriction at puberty contributed to energy and metabolic disorders as long-term consequences.


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