scholarly journals Comprehensive miRNA and DNA Microarray Analyses Reveal the Response of Hepatic miR-203 and Its Target Gene to Protein Malnutrition in Rats

Genes ◽  
2021 ◽  
Vol 13 (1) ◽  
pp. 75
Author(s):  
Kaoru Takahashi ◽  
Huijuan Jia ◽  
Shoko Takahashi ◽  
Hisanori Kato

Adequate protein nutrition is essential for good health. Effects of protein malnutrition in animals have been widely studied at the mRNA level with the development of DNA microarray technology. Although microRNAs (miRNAs) have attracted attention for their function in regulating gene expression and have been studied in several disciplines, fewer studies have clarified the effects of protein malnutrition on miRNA alterations. The present study aimed to elucidate the relationship between protein malnutrition and miRNAs. Six-week old Wistar male rats were fed a control diet (20% casein) or a low-protein diet (5% casein) for two weeks, and their livers were subjected to both DNA microarray and miRNA array analysis. miR-203 was downregulated and its putative target Hadhb (hydroxyacyl-CoA dehydrogenase β subunit), known to regulate β-oxidation of fatty acids, was upregulated by the low-protein diet. In an in vitro experiment, miR-203 or its inhibitor were transfected in HepG2 cells, and the pattern of Hadhb expression was opposite to that of miR-203 expression. In addition, to clarifying the hepatic miRNA profile in response to protein malnutrition, these results showed that a low-protein diet increased Hadhb expression through downregulation of miR-203 and induced β-oxidation of fatty acids.

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.


1989 ◽  
Vol 61 (2) ◽  
pp. 223-233 ◽  
Author(s):  
R. W. Rosebrough ◽  
J. P. McMurtry ◽  
N. C. Steele

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.


2002 ◽  
Vol 87 (2) ◽  
pp. 147-155 ◽  
Author(s):  
Francisco B. Barbosa ◽  
Kirsten Capito ◽  
Hans Kofod ◽  
Peter Thams

Pancreatic islets were isolated from rats that had been nursed by dams fed with a control or an 8·7 % protein diet during the first 12 d of the lactation period. Glucose-induced insulin secretion from islets in the 8·7 % protein group was reduced 50 %. The islet insulin and DNA content were similar, whereas the pancreatic insulin content was reduced by 30 % in the rats fed 8·7 % protein. In order to elucidate the mechanism responsible for the attenuation of insulin secretion, measurements were performed of the activity of several islet enzymes that had previously been supposed to be involved in the coupling of glucose stimulation to insulin secretion. Islet glucose oxidation was unaffected, but glucose-stimulated hydrolysis of phosphatidylinositol was reduced by one-third in the islets of rats fed 8·7 % protein. The activity of mitochondrial glycerophosphate dehydrogenase was similar in islets of rats fed the 8·7 % protein diet and those fed the control diet. The activity of Ca-independent phospholipase A2was increased fourfold in the islets of rats fed 8·7 % protein. It is concluded that impairment of glucose-induced insulin secretion in rats fed a low-protein diet may be caused by attenuation of islet phosphatidylinositol hydrolysis, and it is tentatively suggested that the increased activity of Ca-independent phospholipase A2in islets of rats fed a low-protein diet may participate in the stimulation of apoptosis.


2016 ◽  
Vol 8 (2) ◽  
pp. 178-187 ◽  
Author(s):  
E. Matsumoto ◽  
S. Kataoka ◽  
Y. Mukai ◽  
M. Sato ◽  
S. Sato

Maternal dietary restriction is often associated with cardiovascular disease in offspring. The aim of this study was to investigate the effect of green tea extract (GTE) intake during lactation on macrophage infiltration, and activation of adenosine monophosphate (AMP)-activated protein kinase (AMPK) and serine-threonine kinase Akt (Akt) in the hearts of weanlings exposed to maternal dietary protein restriction. Pregnant Wistar rats were fed control (C) or low-protein diets (LP) throughout gestation. Following delivery, the dams received a control or a GTE-containing control diet during lactation: control diet during gestation and lactation (CC), low-protein diet during gestation and lactation (LPC), low-protein diet during gestation and 0.12% GTE-containing low-protein diet during lactation (LPL), and low-protein diet during gestation and 0.24% GTE-containing low-protein diet during lactation (LPH). The female offspring were sacrificed at day 22. Biochemical parameters in the plasma, macrophage infiltration, degree of fibrosis and expression levels of AMPK and Akt were examined. The plasma insulin level increased in LPH compared with LPC. Percentage of the fibrotic areas and the number of macrophages in LPC were higher than those in CC. Conversely, the fibrotic areas and the macrophage number in LPH were smaller (21 and 56%, respectively) than those in LPC. The levels of phosphorylated AMPK in LPL and LPH, and Akt in LPH were greater than those in LPC. In conclusion, maternal protein restriction may induce macrophage infiltration and the decrease of insulin levels. However, GTE intake during lactation may suppress macrophage infiltration and restore insulin secretion function via upregulation of AMPK and insulin signaling in weanlings.


AMB Express ◽  
2018 ◽  
Vol 8 (1) ◽  
Author(s):  
Imtiaz Hussain Raja Abbasi ◽  
Farzana Abbasi ◽  
Mohamed E. Abd El-Hack ◽  
Ayman A. Swelum ◽  
Junhu Yao ◽  
...  

1996 ◽  
Vol 270 (6) ◽  
pp. R1189-R1196 ◽  
Author(s):  
A. Okiyama ◽  
K. Torii ◽  
M. G. Tordoff

Four studies were conducted to assess the effect of a low-protein diet on NaCl intake. Young rats fed either control (20% casein) or low-protein (5% casein) high-carbohydrate (CHO) diet were allowed to drink either water alone or water and 300 mM NaCl. Relative to rats fed control diet, rats fed the low-protein diet progressively increased NaCl intake so that, despite lower food and water intakes, they drank 180% more NaCl during the last 3 days of the 21-day test. Additional studies found that rats fed low-protein diet always maintained positive sodium balance, were neither sodium depleted nor hypovolemic, and had normal plasma renin activity and aldosterone concentrations. The elevated NaCl intake was not secondary to calcium deficiency and was unaffected by mineral supplementation of the protein-deficient diet. Increases in the diet's CH and/or fat content incidental to decreases in its protein content influenced, but could not completely account for, the effect of protein deficiency on NaCl intake. We conclude that protein deficiency is the primary cause of the elevated NaCl preference produced by being fed a low-protein diet and that a novel physiological mechanism underlies this behavior.


2002 ◽  
Vol 283 (3) ◽  
pp. R623-R630 ◽  
Author(s):  
Eric Bertin ◽  
Marie-Noëlle Gangnerau ◽  
Georges Bellon ◽  
Danièle Bailbé ◽  
Annick Arbelot De Vacqueur ◽  
...  

Fetal malnutrition is now proposed as a risk factor of later obesity and type II diabetes. We previously analyzed the long-term impact of reduced protein and/or energy intake strictly limited to the last week of pregnancy in Wistar rats. Three protocols of gestational malnutrition were used: 1) low-protein isocaloric diet (5 instead of 15%) with pair feeding to the mothers receiving the control diet, 2) restricted diet (50% of control diet), and 3) low protein-restricted diet (50% of low-protein diet). Only isolated protein restriction induced a long-term β-cell mass decrease. In the present study, we used the same protocols of food restriction to analyze their short-term impact (on day 21.5 of pregnancy) on β-cell mass development. A 50% β-cell mass decrease was present in the three restricted groups, but low-protein diet, either associated or not to energy restriction, increased fetal β-cell insulin content. Among all the parameters analyzed to further explain our results, we found that the fetal plasma level of taurine was lowered by low-protein diet and was the main predictor of the fetal plasma insulin level ( r = 0.63, P < 0.01). In conclusion, rat fetuses exposed to protein and/or energy restriction during the third part of pregnancy have a similar dramatic decrease in β-cell mass, and their ability to recover β-cell mass development retardation depends on the type of malnutrition used. Moreover, our results support the hypothesis that taurine might play an important role in fetal β-cell mass function.


Reproduction ◽  
2006 ◽  
Vol 132 (2) ◽  
pp. 265-277 ◽  
Author(s):  
Wing Yee Kwong ◽  
Daniel J Miller ◽  
Elizabeth Ursell ◽  
Arthur E Wild ◽  
Adrian P Wilkins ◽  
...  

In our previous study, we have shown that maternal low protein diet (LPD, 9% casein vs 18% casein control) fed exclusively during the rat preimplantation period (0–4.25 day postcoitum) induced low birth weight, altered postnatal growth and hypertension in a gender-specific manner. In this study, we investigated the effect of maternal LPD restricted only to the preimplantation period (switched diet) or provided throughout gestation on fetal growth and imprinted gene expression in blastocyst and fetal stages of development. Male, but not female, blastocysts collected from LPD dams displayed a significant reduction (30%) inH19mRNA level. A significant reduction inH19(9.4%) andIgf2(10.9%) mRNA was also observed in male, but not in female, fetal liver at day 20 postcoitum in response to maternal LPD restricted to the preimplantation period. No effect on the blastocyst expression ofIgf2Rwas observed in relation to maternal diet. The reduction inH19mRNA expression did not correlate with an observed alteration in DNA methylation at theH19differentially methylated region in fetal liver. In contrast, maternal LPD throughout 20 days of gestation did not affect male or femaleH19andIgf2imprinted gene expression in fetal liver. Neither LPD nor switched diet treatments affectedH19andIgf2imprinted gene expression in day 20 placenta. Our findings demonstrate that one contributor to the alteration in postnatal growth induced by periconceptional maternal LPD may derive from a gender-specific programming of imprinted gene expression originating within the preimplantation embryo itself.


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