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A research team from Emory University has developed a model for human premature ovarian falure (POF) with mice. The results from their mouse model could further research on what causes POF and poor ovarian reserve in women and potentially lead to treatment of such conditions. The researchers found that a quarter of the female mice who carried the fragile X premutation gene were infertile, and those that carried the gene but were fertile had fewer children than those without the premutation. The results concluding from the study are not only interesting, but the applications to POF in women could advance the science on the causes and treatment of this disease. Pregnancy and family planning are both linked to each other in the sense both are related with reproduction. Plasma insulin levels were measured with the Ultra-Sensitive Rat Insulin ELISA kit using the mouse standard, reference 90090 (Crystal Chem, Downers Grove, IL).
Cumulative food intake and FE were determined for females and males of the F1 and F2 generations after 24 wk on the CD or HFD (n = 20–158). As previously reported for diet-induced obesity in mice, triglyceride levels determined at 8, 16, and 24 wk were not significantly affected (data not shown). FPLC analysis revealed that the excess cholesterol was mostly associated with the HDL fraction, although a smaller increase in LDL cholesterol concentration was also observed, mostly in males (Fig.
Although they no longer ovulate, some women may continue to have menstrual cycles and around five percent may conceive on their own. There are several forms of POF, one of which is caused by a type of gene called the fragile X premutation gene. In addition, ovaries of mice with the premutation, independent of being fertile or infertile, had less active ovulation-related genes.
The resulting abnormal uterine environment may have deleterious effects on fetal metabolic programming and lead to MetS in adulthood. Like obesity and T2D, MetS is occurring earlier in childhood and worsening from generation to generation. After 1 wk of adaptation, the animals were housed in individual cages in a controlled-temperature room with a 12:12-h light-dark cycle.
For the CD, 10% of calories were in the form of fat, 20% were in the form of protein, and 70% were in the form of carbohydrates. The animals were fasted for 5–6 h, and blood samples were collected via retroorbital sinus puncture in unanesthetized animals.
Oral glucose tolerance tests (OGTTs) and intraperitoneal insulin tolerance tests (IPITTs) were performed after 4.5 mo on the HFD.
Data are expressed as means ± SE for quantitative variables, except for weight, which is expressed as means ± 2 SD. The majority of women with POF, however, have a very low chance of conceiving and many can only get pregnant with the help of egg donation. The mouse model study was developed based upon the previous data that women with the fragile X premutation gene have a higher chance of experiencing POF.

Food consumption was estimated by subtracting the amount of food left on the grid from initial food weight.
Plasma triglyceride, total cholesterol (tC), and high-density lipoprotein cholesterol (HDL-C) concentrations were determined using a Beckman CX7.
Mixed analyses of variance (SAS Proc Mixed) (21), modeling litter effect by a random component, were used to test differences between generations and diets.
FE was significantly higher in HFD-fed F1 and F2 females (F1-HFD and F2-HFD-S) showing diet-induced obesity.
However, in the F1 generation, LDL and HDL cholesterol levels were higher in obese males than in obese females. Poor ovarian reserve is associated with POF and is a condition that results in low fertility. An increasing number of women are overweight and consuming a calorific or fat-rich diet before and during pregnancy and lactation. Tail blood was collected at ?20, 20, 40, 60, 80, and 120 min for OGTT and at ?15, 15, 30, 45, 60, 90, and 120 min for IPITT.
At birth, litter size was adjusted to four to five pups of both sexes by random culling of the pups to prevent bias due to litter size. This difference was even more pronounced in the F2 generation, and the mild hypercholesterolemia in resistant females was due to an increase in HDL-C levels only. Human epidemiological studies and appropriate dietary interventions in animal models (3) have provided evidence to suggest that maternal nutritional imbalance and metabolic disturbances during critical developmental time windows may have a persistent effect on the health of the offspring and may even be transmitted to the next generation. For the HFD, 60% of calories were in the form of fat, 20% were in the form of protein, and 20% were in the form of carbohydrates. Food spilled on the floor of the cage was not weighed, but spillage was minimal because the diet was supplied as pellets. Blood glucose concentration was determined with a glucometer (Accu-Chek Active; Roche Diagnostics). A generalized estimating equations regression approach (SAS Proc Genmod) (15) defining the litter as a cluster variable was used for comparisons of qualitative data.
F1-HFD, F2-HFD-S, and F2-HFD-R weighed 38, 39, and 1% more, respectively, than F-CD females. However, the time course of this increase and final plasma tC and HDL-C concentrations differed between the groups of mice at 24 wk. Feed efficiency (FE) was calculated as (grams of body weight gain per kilocalorie of food consumed per animal) ? 1,000. Evidence has accumulated (11) to suggest that epigenetic regulation is responsible for this inheritance pattern.Most studies on developmental programming (1) have examined the consequences of protein restriction during gestation in rodents, which do not entirely match the features of the current epidemic of MetS. After being weaned, each mouse was transferred to an individual cage and randomly assigned to the control diet (CD) or HFD.

A few studies in rodents (2) have dealt with the consequences of a high-carbohydrate or fat-rich diet, which better correspond to the features of the current MetS epidemic in humans. Mice of both sexes were fed a CD ad libitum with 10% of calories from fat, the typical fat content of regular mouse chow, and the others were fed a HFD (60% of calories from fat) for 20 wk.
Thus there was no statistically significant difference in resistance to the HFD between F1 and F2 males.
3) Second generation (F2): at 6 mo of age, F1 female mice on the HFD were crossed with F1 male mice on the CD. In contrast, a significantly higher proportion of the female offspring (F2-HFD) of obese mothers than of F1-HFD females (43%, n = 47, vs. The pregnant F1 females were maintained on the CD from mating until the end of lactation, and all of the F2 male and female offspring were maintained on the HFD for 20 wk after being weaned (Fig. 17%, n = 87) showed resistance to the HFD and had a weight <2 SD above the mean at 6 mo (Fig. In F2-HFD females, HDL-C concentration increased between 8 and 16 wk and reached a plateau at 24 wk (Fig. These data, therefore, only partly reflect the features of MetS.Obesity during pregnancy is clearly a threat to the health and well being of the offspring, even into adulthood. In parallel F1 female mice on the CD were crossed with F1 male mice on the CD to generate F2 control mice fed the CD (Fig.
We defined this subpopulation of F2 females as “resistant” (F2-HFD-R) to the obesity-inducing effects of the HFD, with females above this cutoff defined as “sensitive” (F2-HFD-S). In F2-HFD-R and F2-HFD-S mice, HDL-C concentration was intermediate between those for F-CD females and obese F1-HFD females, but the latter did not reach significance (Fig.
As the weights and biological parameters of F1 and F2 mice on CD were not statistically different, we pooled the results into one control group, F-CD (F1 and F2 mice on CD), for each sex.
Total cholesterol (A and B) and HDL cholesterol (HDL-C; C and D) levels were determined for females and males of the F1 and F2 generations after 8, 16, or 24 wk on the CD or HFD (n = 8–47). Sera were also subjected to fast-protein liquid chromatography, and the cholesterol content of the eluted fractions was determined for females (E) and males (F) (n = 5–6). The percentages of obese and lean females are the percentage of animals weighing more or less than the cutoff value, mean weight of F1N + 2 standard deviations (SD). Weight and cumulative food intake were determined for females (C and E) and males (D and F) of the F1 and F2 generations after 24 wk on the CD or HFD (n = 20–158).

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