The high-fructose intake of dams during pregnancy and lactation exerts sex-specific effects on adult rat offspring metabolism

Author(s):  
Francisca A. Tobar-Bernal ◽  
Sergio R. Zamudio ◽  
Lucía Quevedo-Corona

Abstract Experimental studies have demonstrated the effects of maternal fructose consumption during pregnancy and lactation on metabolic alterations in their offspring, especially male offspring. However, few studies have focused on female offspring after providing fructose in food to dam rats. Here, we studied whether offspring of both sexes were differentially affected by a maternal high-fructose diet (HFD). For this purpose, Sprague-Dawley rats were fed during pregnancy and lactation with a standard diet (SD) or a HFD (50% w/w). After weaning, offspring were fed an SD; 3 days later, dams were sacrificed, and their offspring were sacrificed on postnatal day 90. Body weight (BW), food and water intake (only for dams), and various biomarkers of metabolic syndrome were measured. When compared to the SD-fed dams, HFD-fed dams had a reduction in BW and food and water intake. Conversely, adiposity, liver weight, liver lipids, and plasma levels of glucose, insulin, cholesterol, triglycerides, and uric acid were increased in HFD-fed dams. Moreover, the BW, food consumption, weight of retroperitoneal fat pads, and liver lipids increased in female and male offspring of HFD-fed dams. Interestingly, the pups of HFD-fed mothers showed increased levels of leptin and insulin resistance and decreased levels of adiponectin which were more pronounced in male offspring than in female offspring. In contrast, a higher increase in BW was shown earlier in female offspring. Thus, high-fructose consumption by dams during pregnancy and lactation led to sex-specific developmental programming of the metabolic syndrome phenotype in adult offspring.

2021 ◽  
Vol 22 (5) ◽  
pp. 2674
Author(s):  
Chien-Ning Hsu ◽  
Julie Y. H. Chan ◽  
Kay L. H. Wu ◽  
Hong-Ren Yu ◽  
Wei-Chia Lee ◽  
...  

Gut microbiota-derived metabolites, in particular short chain fatty acids (SCFAs) and their receptors, are linked to hypertension. Fructose and antibiotics are commonly used worldwide, and they have a negative impact on the gut microbiota. Our previous study revealed that maternal high-fructose (HF) diet-induced hypertension in adult offspring is relevant to altered gut microbiome and its metabolites. We, therefore, intended to examine whether minocycline administration during pregnancy and lactation may further affect blood pressure (BP) programmed by maternal HF intake via mediating gut microbiota and SCFAs. Pregnant Sprague-Dawley rats received a normal diet or diet containing 60% fructose throughout pregnancy and lactation periods. Additionally, pregnant dams received minocycline (50 mg/kg/day) via oral gavage or a vehicle during pregnancy and lactation periods. Four groups of male offspring were studied (n = 8 per group): normal diet (ND), high-fructose diet (HF), normal diet + minocycline (NDM), and HF + minocycline (HFM). Male offspring were killed at 12 weeks of age. We observed that the HF diet and minocycline administration, both individually and together, causes the elevation of BP in adult male offspring, while there is no synergistic effect between them. Four groups displayed distinct enterotypes. Minocycline treatment leads to an increase in the F/B ratio, but decreased abundance of genera Lactobacillus, Ruminococcus, and Odoribacter. Additionally, minocycline treatment decreases plasma acetic acid and butyric acid levels. Hypertension programmed by maternal HF diet plus minocycline exposure is related to the increased expression of several SCFA receptors. Moreover, minocycline- and HF-induced hypertension, individually or together, is associated with the aberrant activation of the renin–angiotensin system (RAS). Conclusively, our results provide a new insight into the support of gut microbiota and its metabolite SCAFs in the developmental programming of hypertension and cast new light on the role of RAS in this process, which will help prevent hypertension programmed by maternal high-fructose and antibiotic exposure.


2018 ◽  
Vol 96 (1) ◽  
pp. 97-102 ◽  
Author(s):  
Hanin Aburasayn ◽  
Rami Al Batran ◽  
Keshav Gopal ◽  
Malak Almutairi ◽  
Amina Eshreif ◽  
...  

The percentage of women who are obese at the time of conception or during pregnancy is increasing, with animal and human studies demonstrating that offspring born to obese dams or mothers are at increased risk for obesity and the metabolic syndrome. Our goal was to confirm in an experimental model of metabolic syndrome in the dam, whether the offspring would be at increased risk of obesity. Conversely, we observed that male offspring born to dams with metabolic syndrome had no alterations in their body mass profiles, whereas female offspring born to dams with metabolic syndrome were heavier at weaning, but exhibited no perturbations in energy metabolism. Moreover, they gained weight at a reduced rate versus female offspring born to healthy dams, and thus weighed less at study completion. Hence, our findings suggest that factors other than increased adiposity and insulin resistance during pregnancy are responsible for the increased risk of obesity in children born to obese mothers.


2007 ◽  
Vol 292 (5) ◽  
pp. E1318-E1324 ◽  
Author(s):  
Lucie Šedová ◽  
Ondřej Šeda ◽  
Ludmila Kazdová ◽  
Blanka Chylíková ◽  
Pavel Hamet ◽  
...  

The importance of early environment, including maternal diet during pregnancy, is suspected to play a major role in pathogenesis of metabolic syndrome and related conditions. One of the proposed mechanisms is a mismatch between the prenatal and postnatal environments, leading to misprogramming of the metabolic and signaling pathways of the developing fetus. We assessed whether the exposure to high-sucrose diet (HSD) alleviates the detrimental effects of sucrose feeding in later life (predictive adaptive hypothesis) in a highly inbred model of metabolic syndrome, the PD/Cub rat. Rat dams were continuously fed either standard or HSD (70% calories as sucrose) starting 1 wk before breeding, throughout pregnancy, at birth, and until weaning of the offspring. After weaning, all male offspring were fed HSD until the age of 20 wk, when detailed metabolic and morphometric profiles were ascertained. The early life exposure to a sucrose-rich diet resulted in distinct responses to longtime postnatal HSD feeding. Offspring of the sucrose-fed mothers displayed higher adiposity and substantial increases in triglyceride liver content together with unfavorable distribution of cholesterol into lipoprotein subfractions. On the other hand, their adiponectin concentrations were significantly higher, and insulin sensitivity of skeletal muscle was enhanced compared with the offspring of standard diet-fed mothers. Triglycerides, free fatty acids, overall glucose tolerance, and the insulin sensitivity of adipose tissue were comparable in both groups. In the genetically identical animals, maternal HSD feeding elicited a variety of subtle effects but did not lead to predictive adaptive protection from most HSD-induced metabolic derangements.


2020 ◽  
Vol 11 (5) ◽  
pp. 473-483 ◽  
Author(s):  
Graciela Pedrana ◽  
Helen Viotti ◽  
Paula Lombide ◽  
Daniel Cavestany ◽  
Graeme B. Martin ◽  
...  

AbstractMaternal undernutrition decreases sperm production in male offspring, possibly through insulin-like growth factor (IGF-I). To test this hypothesis, we fed pregnant Wistar rats ad libitum with a standard diet (CONTROL) or fed 50% of CONTROL intake, either throughout pregnancy (UNP), lactation (UNL, or both (UNPL). After weaning, male offspring (n = 10 per treatment) were fed a standard diet until postnatal day 160, when testes process for histological and molecular analyses. IGF-I immunostaining area and intensity in the testis were greater (P = 0.003) in the UNPL group compared to CONTROL, but lower in the UNP group (P < 0.0001). Levels of IGF-I receptor transcript were lower in the UNPL and UNL groups, compared to CONTROL. There were more Ki-67-positive germ and Sertoli cells, in all underfed groups than in CONTROL. Compared to CONTROL, frequency of spermatogenic cycle stage VII was lower in all underfed groups, and seminiferous tubule diameter was smaller in UNP and UNPL. Plasma FSH concentrations were greater in UNP male offspring compared to all groups (P = 0.05), whereas inhibin B concentrations were greater in UNP (P = 0.01) and UNL (P = 0.003) than in CONTROL or UNPL. Thus, prenatal undernutrition leads to a decrease in testicular IGF-I levels, whereas of pre- and postnatal undernutrition increased testicular IGF-I levels and decreased amounts of IGF-I receptor mRNA in adult offspring. We conclude that maternal undernutrition during pregnancy and lactation leads to long-lasting effects on adult male offspring testicular morphology, spermatogenesis, and IGF-I testicular system.


2011 ◽  
Vol 107 (10) ◽  
pp. 1429-1434 ◽  
Author(s):  
Jinjin Chen ◽  
Ren Wang ◽  
Xiao-Fang Li ◽  
Rui-Liang Wang

The aim of the present study was to investigate the effects of Bifidobacterium adolescentis (Bif) supplementation on visceral fat accumulation and insulin sensitivity of the metabolic syndrome in HF-diet-fed rats. Adult male Wistar rats (n 10 per group) were fed four different experimental diets for 12 weeks as follows: standard diet; high-fat (HF) diet; a mix of HF diet and Bif; a mix of standard diet and Bif. Liver, mesenteric fat, epididymal fat, retroperitoneal fat, and inguinal fat, pancreas and triceps surae in all four groups of the rats were weighed, while liver steatosis and insulin sensitivity were evaluated at the end point of the study. As the number of intestinal Bifidobacterium species decreased obviously, fat pad weight and body weight increased significantly in the HF group compared with in the other three groups (P <0·05). Addition of Bif led to a reduction in body weight and fat pad weight (P <0·05). With an increase in liver weight, more severe steatosis of hepatocytes was observed in the HF group compared with in the other three groups. A significant decrease of the glucose infusion rate and pancreas weight was found in the HF group (P <0·05). This deleterious effect was alleviated when Bif was added to the diets. Bifidobacterium supplementation ameliorated visceral fat accumulation and insulin sensitivity of the metabolic syndrome in HF-diet-fed rats.


2020 ◽  
Vol 3 (2) ◽  
pp. 76-86
Author(s):  
Mahmoud M. Farag ◽  
Ehab H. Ashour ◽  
Wessam F. El-Hadidy

Background: The use of high-fructose (Fr) corn sweeteners and sucrose in manufactured food has markedly increased recently. This excessive Fr intake has been proposed in the etiology of the metabolic syndrome, which shows an increasing prevalence throughout the world. Objective: In this study, we questioned whether fenofibrate (FF), a peroxisome proliferator-activated receptor (PPAR)-α agonist, and pioglitazone (PG), a PPAR-γ agonist, might be effective in ameliorating the metabolic syndrome in a rat model. Materials and Methods: The metabolic syndrome was induced by feeding rats a high-Fr (60%) diet for 10 weeks. The rats were divided into 5 groups: control group, fed a normal rat chow; Fr + vehicle group; Fr + FF group; Fr + PG group; and Fr + (FF + PG) group (treated with both drugs). Drug or vehicle treatment was given daily for 6 weeks (from weeks 5 to 10). Thereafter, blood and liver samples were obtained for biochemical studies. Results: Rats fed a high-Fr diet developed hyperglycemia, hyperinsulinemia, hyperuricemia, hypertriglyceri­demia, and hypercholesterolemia, and had increased serum alanine aminotransferase, hepatic tumor necrosis factor-α, and malondialdehyde levels but decreases in both glutathione content and superoxide dismutase activity. Rat treatment with FF and/or PG attenuated these alterations. The improvement was greater with the combined treatment than with either drug alone, and normalization of insulin sensitivity was observed only in rats treated with the combination therapy. Conclusion: Acting on the 2 main PPAR subfamilies, the combination of FF and PG provides a more efficacious therapy for modulating the changes in serum insulin, uric acid, and lipids, as well as the accompanying hepatic inflammation and oxidative stress that characterize the Fr-induced metabolic syndrome.


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