Soybean diet alters the insulin-signaling pathway in the liver of rats recovering from early-life malnutrition

ObjectiveWe investigated if alterations in the insulin-signaling pathway could contribute to reduced hepatic glycogen levels in adult rats subjected to a protein deficiency during intrauterine life and lactation and reared through to recovery on a soybean diet.MethodsRats from mothers fed with 17% or 6% protein (casein) during pregnancy and lactation were maintained with a 17% casein diet (offspring born to and suckled by mothers fed a control diet and subsequently fed the same diet after weaning [CC group] and offspring born to and suckled by mothers fed a control diet and subsequently fed a soybean flour diet with 17% protein after weaning [CS group]), a soybean diet (offspring of mothers fed a low-protein diet and a control diet after weaning [LC group] and offspring of mothers fed a low-protein diet and fed a soybean flour diet containing 17% protein after weaning [LS group]), or a 6% casein diet (offspring of mothers fed a low-protein diet and subsequently fed the same diet after weaning [LL group]) from weaning until 90 d of life.ResultsA soybean diet did not modify basal serum glucose and glucagon concentrations, but raised basal serum insulin and consequently increased the serum insulin/glucose ratio. Insulin receptor and insulin receptor substrate-1 levels were lower in rats fed a soybean diet compared with those maintained with a casein diet. In the LS group, the p85 levels were higher than in the LC group, whereas in CS rats its expression was lower than in CC rats. The expression of p110 was lower in the CS group compared with the CC group and similar in the LS and LC groups. Insulin receptor substrate-1 phosphorylation was similar in the LS, LC, and CS groups and lower compared with the CC group. The insulin receptor substrate-1–p85/phosphatidylinositol 3-kinase association was lower in LS than in LC rats and in CS than in CC rats. Akt phosphorylation was lower in the CS and LS groups than in the CC and LC groups.ConclusionAdult rats maintained with a soybean diet exhibited insulin resistance due, at least in part, to alterations in the early steps of the insulin signal transduction pathway.     

A soyabean diet does not modify the activity of brown adipose tissue but alters the rate of lipolysis in the retroperitoneal white adipose tissue of male rats recovering from early-life malnutrition

Nutritional recovery with a soyabean diet decreases body and fat weights when compared with a casein diet. We investigated whether the reduced adiposity observed in rats recovering from early-life malnutrition with a soyabean diet results from alterations in lipid metabolism in white adipose tissue (WAT) and/or brown adipose tissue (BAT). Male rats from mothers fed either 17 or 6?% protein during pregnancy and lactation were maintained on 17?% casein (CC and LC groups), 17?% soyabean (CS and LS groups) or 6?% casein (LL group) diets over 60?d. The rats maintained on a soyabean diet had similar relative food intakes, but lower body and retroperitoneal WAT weights and a reduced lipid content in the retroperitoneal WAT. The insulin levels were lower in the recovered rats and were elevated in those fed a soyabean diet. Serum T3 concentration and uncoupling protein 1 content in the BAT were decreased in the recovered rats. The thermogenic capacity of the BAT was not affected by the soyabean diet. The lipogenesis rate in the retroperitoneal WAT was similar in all of the groups except for the LL group, which had exacerbated lipogenesis. The enhancement of the lipolysis rate by isoproterenol was decreased in white adipocytes from the soyabean-recovered rats and was elevated in adipocytes from the soyabean-control rats. Thus, in animals maintained on a soyabean diet, the proportions of fat deposits are determined by the lipolysis rate, which differs depending on the previous nutritional status.     

Growth in length of children recovering from severe malnutrition

The linear growth of 369 children treated for severe malnutrition at the Tropical Metabolism Research Unit, University Hospital of the West Indies, was examined retrospectively. Mean age was 12.6 months and 58 per cent of the children were oedematous on admission. Mean length for age was the same at admission and discharge (SD score - 3.4). Therefore when the sample is considered as a whole there was no catch-up in length for age. A sub-group of 108 children began to show catch-up growth in length. This sub-group did not differ in age or sex from the total sample but contained a greater proportion of non-oedematous children. Children in the sub-group were also more stunted initially (P less than 0.0001) than the group as a whole. The absolute rate of linear growth was similar in oedematous and non-oedematous children. Change in length for age during recovery was significantly less in children who were oedematous on admission. Two-thirds of the children attained at least 85 per cent weight for length before they began to increase in length. Thus in most cases linear growth followed replenishment of body weight. The data point to the need for further investigations to determine why some children were capable of early catch-up growth in length while others, with similar characteristics, showed minimal or no linear growth during recovery.     

Copper deficiency impairs growth of infants recovering from malnutrition

To evaluate the effect of copper deficiency on growth in humans we performed a prospective case-control study in 11 infants identified as Cu deficient based on low plasma Cu (less than 70 micrograms/dL [11.0 mumol/L]) and low ceruloplasmin (less than 200 mg/L). Growth was evaluated with anthropometric indices 1 mo before and 1 mo after onset of Cu supplementation of 80 micrograms.kg-1.d-1. Plasma Cu and ceruloplasmin rose significantly after 1 mo of supplementation. Weight-for-age and weight-for-length indices increased significantly after supplementation only in the Cu-deficient group. Daily energy intake was significantly higher in the Cu-deficient group after supplementation than it was in the control group. Daily weight gain after supplementation increased significantly in the Cu-deficient group and the value for daily weight gain after supplementation was significantly higher than that of the control group for the equivalent amount of time. Cu supplementation improves the growth of Cu-deficient infants recovering from malnutrition.     

Starvation impairs antioxidant defense in fatty livers of rats fed a choline-deficient diet

Although fatty liver (FL) is considered an innocuous condition, the frequent incidence of graft failure when FL are transplanted has renewed interest in the intracellular disorders causative of or consequent to fatty degeneration. Oxidative stress and nutritional status modulate the tolerance to reperfusion injury in control livers (CL), but very little is known in the case of FL. This study was designed to compare the oxidative balance in CL and FL from fed and food-deprived rats. Serum and liver samples were collected from fed and starved (18 h) rats with CL or FL induced by a choline-deficient diet. Hepatic injury was assessed by transaminase activities and histology. The hepatic concentrations of glutathione (GSH), vitamin C, alpha-tocopherol, thiobarbituric acid-reactive substances (TBARS) and protein carbonyls (PC) were measured. Fed rats with FL had significantly greater TBARS and lower alpha-tocopherol and vitamin C levels than those with CL, whereas GSH and PC concentrations were not affected. Starvation impaired the oxidative balance in both groups. However, compared with the other groups, FL from food-deprived rats generally had the lowest hepatic concentrations of alpha-tocopherol, vitamin C and GSH. Unlike in CL, protein oxidation occurred in FL. These data indicate that fatty liver induced by consumption of a choline-deficient diet is associated with a lower level of antioxidants, which results in lipid peroxidation. Starvation further affects these alterations and extends the damage to proteins. In conclusion, steatosis and starvation may act synergistically on the depletion of antioxidants, predisposing fatty livers to a reduced tolerance to oxidative injury.     

Body composition of children recovering from severe protein-energy malnutrition at two rates of catch-up growth

Twenty-two children with severe protein-energy malnutrition were randomly assigned to dietary treatments that permitted either moderate (4-6 g.kg-1.d-1) rates of weight gain (MG, n = 11) or rapid (12-16 g.kg-1.d-1) rates of weight gain (RG, n = 11) to test the hypothesis that restoration of weight deficits by the RG group restores reference body composition. Final total body water was 60 +/- 4% of body weight in the MG group and 62 +/- 3% in the RG group (NS) indicating reference body composition was attained by both groups. Composition of weight gained was measured by energy and nitrogen balance from doubly labeled water and metabolic collection data. In early recovery, the percent (+/- SEM) protein, fat, and water in weight gain was 20 +/- 1%, 40 +/- 8%, and 40 +/- 10% in the MG group and 14 +/- 1%, 43 +/- 4%, and 43 +/- 12% in the RG group. In late recovery these were 13 +/- 1%, 42 +/- 7%, and 47 +/- 14% in the MG group and 12 +/- 1%, 46 +/- 4%, and 42 +/- 6% in the RG group. We conclude that the nutritional therapy used to promote rapid weight gain restores reference body composition and significantly reduces time required for catch-up growth.     

三氯乙烯染毒SD大鼠肝脏的基因表达图谱

目的分析三氯乙烯(TCE)染毒多次后SD大鼠肝脏的基因表达图谱,为研究机体多次接触TCE其肝脏所产生的分子毒理学反应特性提供线索。方法SD大鼠背部皮内注射体积分数为15%的TCE,每7d1次。分别于第5和第7次染毒后24h收集大鼠的肝脏组织,提取总RNA,用Affymetrix的大鼠U34毒理基因芯片分析其基因表达谱。结果大鼠染毒TCE5次及7次24h肝脏中的Gadd45a、Myc和Mel基因及与固醇类、脂类代谢合成相关的基因或电子传递相关的P450家族基因显著性上调表达,而部分P450家族和热胁迫基因则下调表达。结论本文首次报道了SD大鼠多次接触TCE后肝脏组织的基因表达图谱。     

Creatine supplementation prevents the accumulation of fat in the livers of rats fed a high-fat diet

The aim of the present study was to examine the effects of creatine supplementation on liver fat accumulation induced by a high-fat diet in rats. Rats were fed 1 of 3 different diets for 3 wk: a control liquid diet (C), a high-fat liquid diet (HF), or a high-fat liquid diet supplemented with creatine (HFC). The C and HF diets contained, respectively, 35 and 71% of energy derived from fat. Creatine supplementation involved the addition of 1% (wt:v) of creatine monohydrate to the liquid diet. The HF diet increased total liver fat concentration, liver TG, and liver TBARS and decreased the hepatic S-adenosylmethionine (SAM) concentration. Creatine supplementation normalized all of these perturbations. Creatine supplementation significantly decreased the renal activity of l-arginine:glycine amidinotransferase and plasma guanidinoacetate and prevented the decrease in hepatic SAM concentration in rats fed the HF diet. However, there was no change in either the phosphatidylcholine:phosphatidylethanolamine (PE) ratio or PE N-methyltransferase activity. The HF diet decreased mRNA for PPARα as well as 2 of its targets, carnitine palmitoyltransferase and long-chain acylCoA dehydrogenase. Creatine supplementation normalized these mRNA levels. In conclusion, creatine supplementation prevented the fatty liver induced by feeding rats a HF diet, probably by normalization of the expression of key genes of β-oxidation.     

Yerba Mate (Ilex paraguariensis) modulates NF-kappaB pathway and AKT expression in the liver of rats fed on a high-fat diet

To investigate the effect of Yerba Mate (YM) aqueous extract intake on the NF-kB pathway and AKT expression in the liver, muscle, and adipose tissue of rats submitted to a high-fat diet (HFD). Male Wistar rats were fed a control (CON) (n?=?24) or a HFD (n?=?24) for 12 weeks. Afterwards, rats received YM daily (1?g/kg body weight) for 4 weeks. Intake of YM aqueous extract reduced body weight gain (p?p?相似文献   

Soybean protein hydrolysate improves plasma and liver lipid profiles in rats fed high-cholesterol diet

OBJECTIVE: This investigation attempted to clarify the hypolipidemic effects of non-dialyzed soybean protein hydrolysate (NSPH), which is hydrolyzed by pepsin from soybean acid-precipitated protein (APP), in rats fed a cholesterol-rich diet. METHODS: Forty Sprague-Dawley rats were divided into four groups as the control group (19.7% casein), the APP group (14.7% casein + 5% APP), the NSPH group (14.7% casein + 5% NSPH), and the ISO group (19.7% casein + 0.0013% soy isoflavone). RESULTS: After 12-week experimental period, the APP and NSPH groups had a significant lower plasma total cholesterol, triglycerides, and LDL-cholesterol concentrations compared with the control group. Additionally, the atherosclerosis index in APP and NSPH group had also markedly decreased. Liver cholesterol and triglyceride contents of the APP and NSPH group were significantly lower than those of the control group. There were no different in plasma LDL-C, liver cholesterol and triglycerides between the ISO group and control group. Fecal excretion of neutral steroids and nitrogen compounds was significantly higher in the APP and NSPH groups than that in the control group. An in vitro study also showed that NSPH, compared with casein, obviously decreased cholesterol micellar solubility. CONCLUSION: These results suggested that NSPH may decrease lipid accumulation in the liver and have a hypolipidemic effect by enhancing excretion and inhibiting absorption of lipids.     

Tissue-specific regulation of acetyl-CoA carboxylase gene expression by dietary soya protein isolate in rats

We have recently reported that intake of soya protein isolate (SPI) inhibited the DNA-binding activities of hepatic thyroid hormone receptor (TR). The genes for acetyl-CoA carboxylase (ACC), a rate-limiting enzyme in fatty acid synthesis, contain the thyroid hormone response element in their promoters and are regulated by TR. The present study has examined the effect of long-term feeding of SPI and soya isoflavones (ISF) on the gene expression and protein phosphorylation of different ACC isoforms in different tissues and plasma triacylglycerol (TAG) levels in rats. Sprague-Dawley female rats were fed diets containing 20 % casein or alcohol-washed SPI with or without supplemental ISF for 70, 190 and 310 d. SPI intake significantly reduced plasma TAG concentrations compared with casein, whereas supplemental ISF had no effect. Hepatic ACCalpha and ACCbeta mRNA abundance and protein content were markedly lower in the rats fed SPI than in those fed casein. The protein contents of ACCalpha in the kidney and ACCbeta, the predominant isoform in the heart and kidney, were unchanged by dietary SPI. The ratios of phospho-ACCalpha/ACCalpha and phospho-ACCbeta/ACCbeta were not different among dietary groups in all tissues measured. The present study demonstrates that ingestion of SPI decreases plasma TAG level and down-regulates ACCalpha and ACCbeta gene expression in the liver but not in the heart and kidney. The results indicate that the effect of SPI is tissue-specific and that alteration of ACC gene expression rather than phosphorylation status may play a major role in the regulation of ACC activities by soya proteins.     

Prenatal protein malnutrition in rats enhances serotonin release from hippocampus.

The effect of prenatal protein malnutrition on central serotonin metabolism was assessed in 220- to 240-d-old male rats. The malnourished rats (denoted 6,25 group) were males born to dams fed a 6% casein diet during pregnancy and fostered at birth to dams fed a control (25% casein) diet. They were compared with males born to dams fed 25% casein diet. Tissue concentrations of serotonin, 5-hydroxyindoleacetic acid, 5-hydroxytryptophan, L-tryptophan and catecholamines in the hippocampal formation in the 6,25 group were similar to those of well-fed controls (25,25 group). However, a twofold greater basal serotonin efflux from hippocampal slices of 6,25 rats compared with slices from 25,25 rats was observed during a 20-min incubation period. Hippocampal [3H]paroxetine binding indicated that there was no alteration of apparent maximal binding and affinity of the serotonin transporter in the 6,25 rats. In addition, there was no difference in serotonin receptor binding in hippocampal membranes from 6,25 and 25,25 rats. The results indicate that prenatal protein malnutrition causes selective changes in central serotonin metabolism.