Effect of obesity on rat reproduction and on the development of their adult offspring (original) (raw)
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Female reproductive profile in a fertile, genetically obese line of rats
Journal of Experimental Zoology, 1994
The female reproductive profile of a fertile genetically obese line of rats, named β, is characterized. Hypophysis, ovaries, oviducts, and uteri weights do not differ from those of nonobese controls. Histological features in ovary, uterus, and vagina in β line and α controls are similar, in agreement with classical descriptions in the subject.Vaginal opening, number of estrus, number of corpora lutea at ovulation time, and pregnancy patterns (i.e., ovary weight, number of corpora lutea, sites of implantation, and living fetuses, as well as productivity, fertility, litter size, and preweaning mortality) show no significant differences between obese and nonobese animals.From a reproductive standpoint, obese β line would behave as nonobese. Up to now β would represent the only fertile genetically obese line of rats, appearing as a profitable biological model to widen and deepen reproductive analysis on obesity. © Wiley-Liss, Inc.
The effects of high fat diet on reproduction in female rats
Behavioral and Neural Biology, 1979
Female rats who had been made obese on a protein-supplemented high fat diet were mated. Impaired estrous cycling prevented conception in nearly half the experimental females. The young who were born to the remaining experimental mothers were lighter in birth weight. Most were cannibalized within the first week postpartum. Observation of mother-young interactions revealed a high level ofpup licking. The disruptions in reproductive behaviors are similar to those reported in females whose obesity is a consequence of hypothalamic lesion. 1We wish to thank Jan Berger and Jessie Namidas for their help in collecting the observations of maternal behavior.
Diabetologia, 2009
Aims/hypothesis Accumulating evidence suggests that maternal obesity may increase the risk of metabolic disease in the offspring. We investigated the effects of established maternal diet-induced obesity on male and female offspring appetite, glucose homeostasis and body composition in rats. Methods Female Wistar rats were fed either a standard chow (3% fat, 7% sugar [wt/wt]) or a palatable obesogenic diet (11% fat, 43% sugar [wt/wt]) for 8 weeks before mating and throughout pregnancy and lactation. Male and female offspring of control and obese dams were weaned on to standard chow and assessed until 12 months of age. Results At mating, obese dams were heavier than control with associated hyperglycaemia and hyperinsulinaemia. Male and female offspring of obese dams were hyperphagic (p<0.0001) and heavier than control (p<0.0001) until 12 months of age. NEFA were raised at 2 months but not at 12 months. At 3 months, OGTT showed more pronounced alteration of glucose homeostasis in male than in female offspring of obese animals. Euglycaemic-hyperinsulinaemic clamps performed at 8 to 9 months in female and 10 to 11 months in male offspring revealed insulin resistance in male offspring of obese dams (p<0.05 compared with control). Body compositional analysis at 12 months also showed increased fat pad weights in male and female offspring of obese animals. Conclusions/interpretation Diet-induced obesity in female rats leads to a state of insulin resistance in male offspring, associated with development of obesity and increased adiposity. An increase in food intake may play a role.
Introduction: Globally, the prevalence of overweight and obesity is increasing, predisposing females to health hazards including compromised reproductive capacity. Our objective was to investigate the effect of ad libitum, isocalorically and hypocalorically restricted high-fat diet (HFD) feeding on reproductive function in diet-induced obese female rats. Material and methods: Twenty female albino Sprague Dawley rats were used; 5 rats were kept on a standard pellet animal diet to serve as a control group (A) and 15 rats were fed a HFD for 9 weeks to induce obesity. The HFD fed animals were equally divided into three groups: an ad libitum HFD group (B), an isocalorically restricted HFD group (C), and a hypocalorically restricted HFD group (D). Estrous cyclicity, hormonal levels, ovarian histopathology and caspase-3 immunoreactivity were evaluated. Results: The HFD-fed rats in groups B, C and D had significant irregularity in estrous cyclicity Vs group A (p = 0.001, 0.003 and 0.034 respectively). Groups C and D had significant reduction in serum progesterone level (p = 0.006 and 0.018 Vs A). Isocaloric restriction of HFD feeding significantly increased serum LH. Groups B and C had a significant increase in caspase-3 expression in the ovary (p < 0.001). Conclusions: Ad libitum HFD interfered with the normal estrous cycle and enhanced apoptosis of luteal cells in obese female rats. The HFD restriction interfered with the normal estrous cycle and caused functional insufficiency of the corpus luteum in obese female rats. These results suggest that HFD feeding determinately affects female reproductive function independently of caloric intake.
Overweight and Fertility: What We Can Learn from an Intergenerational Mouse Obesity Model
International Journal of Environmental Research and Public Health
The aim of this study was to evaluate the effects of being overweight on the ability to conceive, fertilization rate, and in vivo development of embryos in regularly cycling, spontaneously ovulating, and naturally mated female mice. The study was based on statistical analysis of data collected during 14 experiments with identical design, performed on 319 control and 327 obese mice, developed in an intergenerational model of obesity induction which eliminates the impact of aging and high-fat feeding. Six-week-old mice with a vaginal sperm plug were slaughtered on embryonic days 2, 3, or 4, and the flushed contents of the oviducts and uteri were assessed by stereomicroscopy. The results showed no association between being overweight and the proportion of ovulating or fertilized females. On the other hand, a strong association was found between being overweight and ovulation yield. On embryonic day 2, significantly higher numbers of eggs were recovered from the oviducts of fertilized o...
Effect of the induction of transgenerational obesity on maternal-fetal parameters
Systems biology in reproductive medicine, 2018
Maternal obesity can cause complications for both women and their offspring for generations. Therefore, we intended to verify the repercussions of induction of transgenerational obesity on biochemical parameters, reproductive performance, and congenital anomaly frequency in Wistar rats. Female rats were used from successive generations. The female rats of parental generation (F0, n=10) were mated to obtain their offspring (F1 generation). F1 female rats received a monosodium glutamate (MSG) solution to induce obesity (n=07) or vehicle (control, n=06) during the neonatal period. These adult female rats were classified as normal or obese using the Lee Index, mated, and delivered offspring (F2 generation), which were also evaluated for obesity using the Lee Index in adult life (F2MSG, n=13, born from obese dams) or non-obesity status (F2Control, n=12, born from control dams), and were mated in adulthood. During pregnancy, glycemia and an oral glucose tolerance test (OGTT) were analyzed...
Diet-induced obesity in gravid rats engenders early hyperadiposity in the offspring
Metabolism-clinical and Experimental, 2007
Exposure to a dysmetabolic in utero environment may be one of the mechanisms to explain why individuals with high birth weight are more likely to remain overweight. We explored this hypothesis in an animal model of diet-induced obesity (DIO). We studied adipose tissue development and glucose tolerance in the offspring of rat dams fed a diet rich in milk and sugar from early adulthood until day (d) 2 postpartum. This diet promoted body weight (BW) gain and was previously shown to produce insulin resistance and gestational glucose intolerance. The DIO offspring showed a higher BW in early life (between d7 and d35), with a maximum of 1 SD above the mean BW of controls; however, BW in DIO offspring after d35 was comparable with that of controls. Neonatal DIO offspring also showed larger fat depots, adipocyte hypertrophy (P ≤ .001), and more than 2-fold increased tumor necrosis factor α messenger RNA levels in subcutaneous adipose tissue (P b .05). In addition, they displayed a higher peak glucose response to a glucose challenge (P b .05). In postpubertal (d56) and adult (d98) offspring, we found differences in fat mass and distribution and glucose tolerance relating to the offspring's sex but not the maternal diet. In conclusion, DIO during pregnancy results in hyperadiposity and reduced glucose tolerance only in their neonatal/weanling but not postpubertal offspring. Future research should disclose whether these early-life effects are reactivated in conditions of heightened insulin resistance.
Life Sciences, 2013
Aims: To investigate whether the effects of diet-induced obesity in mothers are passed on to their offspring fed a control diet in a gender-specific manner. Main methods: Mother mice received either standard chow (SC; 17% energy from fat) or high-fat (HF; 49% energy from fat) diet for eight weeks pre-pregnancy until lactation. After weaning (at 21 days of age), offspring received SC diet and were divided into four groups according to the mother's diet (Mo): male Mo-SC, female Mo-SC, male Mo-HF, and female Mo-HF. Stereology, Elisa and western blotting were performed. Key findings: HF diet-fed mothers were overweight, and had metabolic abnormalities, all of which were found in their adult offspring. Male Mo-HF offspring had higher cholesterol, triglycerides, leptin and insulin levels and lower circulating adiponectin than female Mo-HF offspring. Mo-HF offspring of both genders had higher expression of tumor necrosis factor-alpha, interleukin-6 and leptin and lower expression of adiponectin than Mo-SC offspring; however, male Mo-HF were more affected than female Mo-HF offspring for these variables, demonstrating sexual dimorphism. Significance: Exposure to HF diet is effective in inducing obesity and metabolic alterations in mothers, and this phenotype can be passed on to their offspring. An adverse pattern in the body fat distribution in males probably has favored the intensification of a pro-inflammatory profile compared with females. In adulthood, the male offspring responds to the maternal obesity more than the female offspring, indicating a relevant sexual dimorphism that is a novel finding in this animal study.
Maternal Overweight Disrupts the Sexual Maturation of the Offspring
Reproductive Sciences, 2016
The aims of the present work were to study the effect of maternal overweight and obesity on the ovarian reserve, follicular development, and ovulation of the offspring and to assess whether this maternal condition alters oocyte integrity. To this end, female offspring from rats fed standard (OSD) or cafeteria (OCD) diet were used. Body weight, vaginal opening, and estrous cycle were recorded and ovaries were obtained on the day of the second estrus. In addition, ovarian weight, ovulation rate (measured by the number of oocytes within oviducts), follicular development (determined by histology), and oocyte integrity were examined. The OCD were divided into 2 groups: offspring from rats with 17% and 28% of overweight (OCD17 and OCD28, respectively). Both OCD groups showed higher body weight, but OCD28 also exhibited early vaginal opening and higher ovarian weight and glycemia at euthanasia compared with OSD. Both OCD17 and OCD28 had lower number of primordial and primary follicles, and only OCD28 exhibited lower number of antral follicles, all compared with OSD rats. In addition, both OCD17 and OCD28 had higher ovulation rate than controls, and OCD28 had lower number of healthy oocytes, which, in turn, exhibited morphological alterations such as larger perivitelline space and zona pellucida than those of control animals. These results suggest that maternal overweight may severely affect the reproductive ability of the offspring, likely as a result of altering the organogenesis.