scholarly journals Hyperlipidic diet affects body composition and induces anxiety‐like behaviour in intrauterine growth‐restricted adult mice

2020 ◽  
Vol 105 (12) ◽  
pp. 2061-2072
Author(s):  
Luana Cristina Almeida Silva ◽  
Allan Chiaratti Oliveira ◽  
Vanessa Cavalcante‐Silva ◽  
Maria do Carmo Franco ◽  
Vânia D'Almeida
2019 ◽  
Vol 10 ◽  
Author(s):  
Peter B. Noble ◽  
Darshinee Kowlessur ◽  
Alexander N. Larcombe ◽  
Graham M. Donovan ◽  
Kimberley C. W. Wang

2016 ◽  
Vol 7 (5) ◽  
pp. 548-562 ◽  
Author(s):  
D. M. Horton ◽  
D. A. Saint ◽  
J. A. Owens ◽  
K. L. Kind ◽  
K. L. Gatford

Intrauterine growth restriction (IUGR) and subsequent neonatal catch-up growth are implicated in the programming of increased appetite, adiposity and cardiometabolic diseases. Guinea pigs provide an alternate small animal model to rodents to investigate mechanisms underlying prenatal programming, being relatively precocial at birth, with smaller litter sizes and undergoing neonatal catch-up growth after IUGR. The current study, therefore, investigated postnatal consequences of spontaneous IUGR due to varying litter size in this species. Size at birth, neonatal, juvenile (post-weaning, 30–60 days) and adolescent (60–90 days) growth, juvenile and adolescent food intake, and body composition of young adults (120 days) were measured in 158 male and female guinea pigs from litter sizes of one to five pups. Compared with singleton pups, birth weight of pups from litters of five was reduced by 38%. Other birth size measures were reduced to lesser degrees with head dimensions being relatively conserved. Pups from larger litters had faster fractional neonatal growth and faster absolute and fractional juvenile growth rates (P<0.005 for all). Relationships of post-weaning growth, feed intakes and adult body composition with size at birth and neonatal growth rate were sex specific, with neonatal growth rates strongly and positively correlated with adiposity in males only. In conclusion, spontaneous IUGR due to large litter sizes in the guinea pig causes many of the programmed sequelae of IUGR reported in other species, including human. This may therefore be a useful model to investigate the mechanisms underpinning perinatal programming of hyperphagia, obesity and longer-term metabolic consequences.


2020 ◽  
Vol 12 (1) ◽  
Author(s):  
Dana Binyamin ◽  
Nir Werbner ◽  
Meital Nuriel-Ohayon ◽  
Atara Uzan ◽  
Hadar Mor ◽  
...  

Abstract Background During aging, there is a physiological decline, an increase of morbidity and mortality, and a natural change in the gut microbiome. In this study, we investigated the influence of the gut microbiome on different metabolic parameters in adult and aged mice. Methods Fecal and blood samples from adult (n = 42, 100–300 days) and aging (n = 32, 550–750 days) mice were collected. Microbiome analysis was done using QIIME2. Mouse weight and body composition were measured using NMR, and insulin and leptin levels in the blood were measured with Mouse Adipokine Magnetic Bead Panel kit. Fecal microbiota transplantation experiments from adult and aged mice into young germ-free mice were carried out in order to examine the effect of the gut microbiome of adult and aging mice on weight, body composition, insulin, and leptin. Results We demonstrate that the microbiomes from adult and aged mice are distinguishable. We also report changes in metabolic parameters as we observed significantly higher weight and fat mass and low lean mass in aged compared to adult mice along with high insulin and leptin levels in the blood. The transplanted gut microbiome from aged mice transferred part of the phenotypes seen in aged mice. Fat body mass and insulin levels were higher in the mice who received feces from aged mice than mice receiving feces from adult mice. In addition, they consumed more food and had a higher respiratory quotient compared to mice receiving adult feces. Conclusions We conclude that aged mice have a gut microbiota with obesogenic characteristics. In addition, the gut bacterial population itself is sufficient to induce some of the manifestations of obesity.


2007 ◽  
Vol 157 (5) ◽  
pp. 605-612 ◽  
Author(s):  
R Verkauskiene ◽  
J Beltrand ◽  
O Claris ◽  
D Chevenne ◽  
S Deghmoun ◽  
...  

AbstractBackgroundFetal growth restriction (FGR) has been related to several health risks, which have been generally identified in small-for-gestational age (SGA) individuals.ObjectiveTo evaluate the impact of FGR on body composition and hormonal status in infants born either small- or appropriate-for-gestational age (AGA).MethodsFetal growth was assessed by ultrasound every 4 weeks from mid-gestation to birth in 248 high-risk pregnancies for SGA. Fetal growth velocity was calculated as change in the estimated fetal weight percentiles and FGR defined as its reduction by more than 20 percentiles from 22 gestational weeks to birth. Impact of FGR on body composition, cord insulin, IGF-I, IGF binding protein-3 (IGFBP-3), and cortisol concentrations was assessed in SGA and AGA newborns.ResultsGrowth-retarded AGA infants showed significantly reduced birth weight, ponderal index, percentage of fat mass, and bone mineral density when compared with AGA newborns with stable intrauterine growth. Cord IGF-I and IGFBP-3 concentrations were significantly decreased in growth-retarded infants in both SGA and AGA groups. Cord insulin concentration was significantly lower and cord cortisol significantly higher in AGA infants with FGR versus AGA newborns with stable intrauterine growth.After adjustment for gestational age and gender, birth weight was directly related to fetal growth velocity and cord IGF-I concentration. The variation in infant's adiposity was best explained by fetal growth velocity and cord insulin concentration.ConclusionsFGR affects body composition and hormonal parameters in newborns with birth weight within the normal range, suggesting these individuals could be at similar metabolic risks as SGA.


2005 ◽  
Vol 26 (3) ◽  
pp. 258-262 ◽  
Author(s):  
G. Larciprete ◽  
H. Valensise ◽  
G. Di Pierro ◽  
B. Vasapollo ◽  
B. Casalino ◽  
...  

1993 ◽  
Vol 13 (6) ◽  
pp. 325-331 ◽  
Author(s):  
Anders Hyltander ◽  
Gösta Svaninger ◽  
Kent Lundholm

The aim of this study was to investigate the effect of a selective β2-adrenoceptor agonist, clenbuterol, on body composition in tumour-bearing adult and growing mice. Therefore, adult female C57/BL6 mice (n = 20) were inoculated subcutaneously with a 3-methylcholanthrene-induced sarcoma and divided into two identical groups. One group received injections twice a day of clenbuterol corresponding to 1 mg/kg body weight, the other group received sham injections. Growing mice (n = 20) were similarly divided after tumour inoculation into one study group with clenbuterol injections and one control group. The growing animals were sacrificed on day 11 after commencement of treatment, the adult mice on day 16. Clenbuterol treatment had no statistically significant effect on accumulated food intake or body composition in the adult mice. However, fooe intake in these animals increased numerically compared to control animals after day 12 of the study. Tumour growth was also unaffected. The growing animals displayed an increased carcass dry weight with borderline significance (p = 0.06) and an increased quadriceps muscle fat free dry weight after clenbuterol treatment. Tumour growth was not affected. Food intake measured on a daily basis was significantly increased in the growing clenbuterol treated animals and accumulated food intake was increased with a trend towards statistical significance (p = 0.06). The results support the suggestion that treatment with a selective β2-adrenoceptor agonist does not improve body composition in tumour-bearing adult mice relying on spontaneous food intake while growing animals may benefit from such treatment.


2005 ◽  
Vol 26 (4) ◽  
pp. 443-444
Author(s):  
G. Di Pierro ◽  
G. Larciprete ◽  
B. Vasapollo ◽  
G. Novelli ◽  
B. Casalino ◽  
...  

1998 ◽  
Vol 274 (4) ◽  
pp. R985-R990 ◽  
Author(s):  
Wendy K. Chung ◽  
Kristen Belfi ◽  
Melvin Chua ◽  
Jennifer Wiley ◽  
Ronald Mackintosh ◽  
...  

In an effort to understand the genetics of human obesity, we have studied the physiology and molecular genetics of rodent models with monogenetic forms of obesity including the leptin gene-defective ( Lepob / Lepob ) and leptin receptor gene-defective ( Leprdb / Leprdb ) mouse. In the experiments reported here, we investigated the effects of heterozygosity at Lepob and Leprdb on body composition and circulating leptin concentration in +/+, Leprdb /+, and Lepob /+ adult mice to identify possible gene dosage effects of these mutations that might elucidate their physiology. Adult mice heterozygous for the Lepob or Leprdb allele had equivalent fat mass and percentage body fat, which was increased 27–47% and 23–35%, respectively, relative to +/+ littermates. Plasma leptin concentrations adjusted for fat mass were 6.5 ng/ml in the Lepob /+, 9.6 ng/ml in the +/+, and 11.5 ng/ml in the Leprdb /+ mice. Sex had no effect on plasma leptin after controlling for fat mass. These data, and data from a small number of mice heterozygous at both Lepob and Leprdb (compound heterozygotes), suggest that leptin protein produced per mass of body fat is reduced in Lepob /+ mice and that body fat is increased in Lepob /+ mice until plasma leptin concentrations reach that of a normal +/+ mouse. The elevated plasma leptin concentration in the Leprdb /+ mice suggests that LEPR may mediate autocrine suppression of Lep expression. These results raise the possibility that human mutations that have even subtle effects on the leptin/leptin receptor system in either the homozygous or heterozygous state may have significant effects on adiposity.


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