Interactive effects of food deprivation and exercise on reproductive function in female hamsters

1994 ◽  
Vol 267 (1) ◽  
pp. R185-R190 ◽  
Author(s):  
J. B. Powers ◽  
A. E. Jetton ◽  
G. N. Wade

Two experiments evaluated the combined effects of food deprivation and runningwheel access on estrous cycles and estrous behavior of female hamsters. In experiment 1, food deprivation on days 1 and 2 of the estrous cycle disrupted the next expected ovulation, and this effect was more, rather than less, robust in females allowed to exercise in running wheels while they were deprived. In experiment 2, a similar protocol was used except the females were ovariectomized and received sequential injections of estradiol benzoate (EB; 5 micrograms) and progesterone (P; 200 micrograms) separated by 48 h to induce lordosis, which was tested 4-5 after P. Food deprivation concomitant with hormonal treatment diminished lordosis durations, but this effect was significant only among the females that were permitted to run in activity wheels. Previous findings demonstrated that access to running wheels attenuated the inhibitory effects of short photoperiod exposure on hamster estrous cycles. In contrast, the present results indicate that this same manipulation exaggerates rather than diminishes the inhibitory effects of food deprivation on estrous cycles and hormone-induced behavioral estrus.

1993 ◽  
Vol 264 (3) ◽  
pp. R568-R572 ◽  
Author(s):  
R. W. Dickerman ◽  
H. Y. Li ◽  
G. N. Wade

The availability of oxidizable metabolic fuels affects reproductive physiology and behaviors in female mammals. In Syrian hamsters, 48 h of food deprivation is sufficient to suppress secretion of gonadotropins and ovarian steroids and to prevent the occurrence of ovulation and estrous behavior. These experiments attempted to determine whether the deprivation-induced suppression of lordosis is entirely due to the disruption of ovarian steroid secretion or whether there are also changes in behavioral responsiveness to estradiol and/or progesterone (P). Estrous behavior was induced in ovariectomized hamsters with sequential injections of 5 micrograms of estradiol benzoate (EB) and 200 micrograms P. Food deprivation for 48 h, either before or just after EB treatment, significantly suppressed the amount of time females spent in lordosis during a 5-min test with a sexually experienced male. Treatment with an inhibitor of glycolysis (2-deoxy-D-glucose) in combination with an inhibitor of fatty acid oxidation (methyl palmoxirate) for 48 h mimicked the effects of food deprivation and suppressed the amount of time spent in lordosis after treatment with EB+P. Given alone, neither metabolic inhibitor had an effect on lordosis. These findings indicate that suppression of hamster estrous behavior by metabolic fuel deprivation is at least in part due to a reduced responsiveness to estradiol and/or progesterone. Furthermore, estrous behavior is responsive to metabolic fuels in general. This is unlike hamster ovulatory cycles, which are primarily responsive to glucose availability.


1990 ◽  
Vol 258 (3) ◽  
pp. R750-R755 ◽  
Author(s):  
J. E. Schneider ◽  
G. N. Wade

Food deprivation inhibits ovulation and estrous behavior in golden hamsters. In experiment 1, the effects of phasic starvation (food deprivation on days 1 and 2 of the 4-day estrous cycle) depended on prior body weight and fat content. Starvation-induced anestrus, which occurs after only one cycle of phasic starvation in lean hamsters, did not occur until after three or more cycles in fat hamsters. None of the fat hamsters became anestrous until their body weights had declined to the level of lean hamsters. However, in experiment 2, we found evidence that changes in reproductive status were not signaled by any dimension of body size per se but instead by the general availability of metabolic fuels. Estrous cycles of thin hamsters were not significantly affected by food deprivation and weight loss when the hamsters were provided with either a 25% glucose solution or with vegetable shortening. In experiment 3, simultaneous pharmacological reduction of both fatty acid oxidation and glycolysis inhibited estrous cycles in hamsters fed ad libitum. Estradiol treatment restored estrous behavior, but not ovulation, in food-deprived, lean hamsters and in hamsters in which both fatty acid oxidation and glycolysis were reduced. Decreased availability of utilizable metabolic fuels may inhibit follicular development, which may in turn lead to circulating estradiol levels that are insufficient to stimulate estrous behavior.


1986 ◽  
Vol 251 (4) ◽  
pp. R663-R669 ◽  
Author(s):  
L. P. Morin

Reproductive capacity of female hamsters, as estimated by the ovulatory response, is particularly susceptible to interference by food deprivation. Previous studies showed that hamsters generally fail to ovulate if deprived of food for one or two estrous cycles. The present work demonstrates that starvation which is specific to the 2 days immediately after ovulation will block the next expected ovulation in approximately 80% of the animals. Such phasic starvation also resulted in significantly smaller ovarian follicle sizes. When placed with vigorous males, anovulatory animals failed to show lordosis behavior unless exogenous estradiol benzoate (EB) was supplied. With EB provided, all animals showed short-latency lordosis. These bioassay data suggested that poorly developed follicles were secreting insufficient estradiol for the facilitation of lordosis. Exogenous luteinizing hormone (LH) given 6 h before lights off on cycle day 4 failed to elicit ovulation, further suggesting that the follicles were not mature. Radioimmunoassay of LH and follicle-stimulating hormone (FSH) levels during the ovulatory gonadotropin surge showed that LH was vastly reduced, whereas FSH was in the low-to-normal range. Estradiol levels, assayed immediately before the gonadotropin surge, were low compared with controls, whereas progesterone levels were higher than normal. The results suggest that ovulatory failure in response to phasic food deprivation is a joint function of absence of an ovulatory LH surge and a set of immature follicles.


2021 ◽  
Vol 8 ◽  
Author(s):  
Yuanyuan Feng ◽  
Fei Chai ◽  
Mark L. Wells ◽  
Yan Liao ◽  
Pengfei Li ◽  
...  

In addition to ocean acidification, a significant recent warming trend in Chinese coastal waters has received much attention. However, studies of the combined effects of warming and acidification on natural coastal phytoplankton assemblages here are scarce. We conducted a continuous incubation experiment with a natural spring phytoplankton assemblage collected from the Bohai Sea near Tianjin. Experimental treatments used a full factorial combination of temperature (7 and 11°C) and pCO2 (400 and 800 ppm) treatments. Results suggest that changes in pCO2 and temperature had both individual and interactive effects on phytoplankton species composition and elemental stoichiometry. Warming mainly favored the accumulation of picoplankton and dinoflagellate biomass. Increased pCO2 significantly increased particulate organic carbon to particulate organic phosphorus (C:P) and particulate organic carbon to biogenic silica (C:BSi) ratios, and decreased total diatom abundance; in the meanwhile, higher pCO2 significantly increased the ratio of centric to pennate diatom abundance. Warming and increased pCO2 both greatly decreased the proportion of diatoms to dinoflagellates. The highest chlorophyll a biomass was observed in the high pCO2, high temperature phytoplankton assemblage, which also had the slowest sinking rate of all treatments. Overall, there were significant interactive effects of increased pCO2 and warming on dinoflagellate abundance, pennate diatom abundance, diatom vs. dinoflagellates ratio and the centric vs. pennate ratio. These findings suggest that future ocean acidification and warming trends may individually and cumulatively affect coastal biogeochemistry and carbon fluxes through shifts in phytoplankton species composition and sinking rates.


Author(s):  
Jorge Alonso Peralta-Torres ◽  
Jesús Ricardo Aké-López ◽  
Carlos Luna-Palomera ◽  
José Candelario Segura-Correa ◽  
Oswaldo Margarito Torres-Chablé ◽  
...  

Evaluation of the reproductive tract development (RTD) is a criterion rarely used when heifers are included in estrous synchronization programs. The objective of the present study was to determine the effect of RTD (mature and immature) and hormonal treatment (EC and EB) on estrous expression rate and pregnancy rate in Bos indicus heifers under tropical conditions. RTD was evaluated with an ultrasound and classified as mature (n=99) or immature (n=101). Heifers received an intravaginal device (DIB®; day 0), 2 mg of estradiol benzoate (EB) and 250 µg of cloprostenol (PGF2α). The DIB was removed on day 7 post insertion, and 250 µg of PGF2α was applied and heifers were divided into two groups: One group of heifers received 0.5 mg of estradiol cypionate (EC group), and on day 8, a second group of heifers received 1 mg of estradiol benzoate (EB group). Estrus was detected by visual observation, and all heifers were inseminated at a fixed-time (FTAI). Fifteen days after insemination, bulls were introduced to the treatment groups. Data were analyzed using general modeling and binary logistic regression procedures. The percentage of estrus was similar for both mature and immature heifers (P>0.05), however, the heifers treated with EB had 17% animals in estrus, than the heifers that received EC (P <0.05). The pregnancy rate after FTAI (74.8%) and total pregnancy (FTAI + natural mating = 91.9%) was greater for the group of heifers with a mature reproductive tract (P<0.05). The hormone treatment had not effect (P>0.05) on the pregnancy rate. In conclusion, the heifers with mature reproductive tracts had the highest pregnancy rate after artificial insemination and total pregnancy. Hormonal treatment did not influence the pregnancy rate.


1997 ◽  
Vol 272 (1) ◽  
pp. R400-R405 ◽  
Author(s):  
J. E. Schneider ◽  
A. J. Hall ◽  
G. N. Wade

Metabolic energy availability has profound effects on reproduction in a wide variety of species. We have been studying the effects of fasting on estrous cycles in Syrian hamsters as a model system for metabolic control of reproduction. In previous experiments, a 48-h period of fasting inhibited estrous cycles in lean, but not fat, hamsters. In fat hamsters the effects of fasting may have been offset by the presence of high circulating levels of free fatty acids mobilized from lipids in adipose tissue. Consistent with this idea fat hamsters treated with the inhibitor of fatty acid oxidation methyl palmoxirate (MP) showed fasting-induced anestrus. Experiment 1 was designed to examine whether vagally transmitted signals are critical for the inhibitory effects of fasting and MP treatment. Lean or fat hamsters that had received bilateral subdiaphragmatic vagotomy or sham surgery were fasted and treated with MP or vehicle. In vagotomized and sham-operated hamsters, estrous cycles were inhibited in lean fasted hamsters and in fat fasted hamsters treated with MP, but not in fat fasted hamsters treated with vehicle. Thus the results of experiment 1 indicated that vagally transmitted signals about peripheral fatty acid availability are not critical for the effects of these particular metabolic challenges on estrous cycles in Syrian hamsters. In experiment 2, hamsters without food were allowed to ingest pure glucose or fructose solutions or vegetable shortening. One-half of each group was treated with an inhibitor of glucose utilization, 2-deoxy-D-glucose (2-DG), or vehicle. If ingestion of fructose or shortening, but not glucose, had protected hamsters from 2-DG-induced anestrus, this might have indicated that peripheral fuel availability is critical for anestrus. On the contrary, 2-DG treatment induced anestrus regardless of the type of fuel ingested. Neither experiment yielded results that implicated changes in peripheral fuel availability as a critical signal in metabolic control of estrous cycles.


2016 ◽  
Vol 6 (12) ◽  
pp. 1018-1020
Author(s):  
S Subedi ◽  
B Banerjee ◽  
C Manisha

Background: Thyroid hormones play a key role in the menstrual and reproductive function of women .It is recognized universally that menstrual disturbances may accompany clinical alteration in thyroid function and every clinician has encountered altered menstrual pattern among women suffering from thyroid disorders. The aim of this study was to find the incidence of thyroid disorders in Dysfunctional uterine bleeding and its correlation with menstrual patterns.Materials and Methods: A hospital based cross-sectional study including 75 cases with dysfunctional uterine bleeding attending the OPD of Nobel Medical College, where incidence of thyroid disorder was evaluated along with its correlation with menstrual patterns and histopathology.Results: The incidence of Gynecological OPD attendance due to abnormal uterine bleeding was 3%.and the incidence of thyroid dysfunction was 10.6% with hypothyroidism being the commonest. (9.3%). The commonest menstrual pattern found was menorrhagia/polymenorrhoea in 8 percent.Conclusion: Prevalence of hypothyroidism was more common in DUB. Thus every woman with menstrual irregularities should undergo thyroid assessment and this will ultimately avoid unnecessary intervention like misuse of hormonal treatment and hysterectomy.


Endocrinology ◽  
2003 ◽  
Vol 144 (5) ◽  
pp. 1780-1786 ◽  
Author(s):  
Jennifer W. Hill ◽  
Jon E. Levine

Neuropeptide Y (NPY) plays a key role in both food intake and GnRH secretion. Food deprivation elevates hypothalamic NPY activity and suppresses LH and gonadal steroid secretion. Similarly, lactation up-regulates NPY expression as food consumption increases and estrous cycles cease. These observations suggest that NPY coordinates reproductive suppression in response to energy deficiency; if so, the reproductive axis of NPY knockout (KO) mice should be impervious to lactation and food deprivation. We monitored food consumption, body weight, and estrous cyclicity during lactation in NPY KO mice with large and small litters. NPY KO mice with either litter size resembled wild types (WTs) in weight regulation and food consumption. Large-litter mothers had longer anestrous periods and smaller pups at weaning, but NPY KOs and WTs did not differ in either respect. We also examined the LH response of NPY KO mice to 48 h without food. Basal levels of LH in ovariectomized NPY KO animals decreased in response to fasting, but LH levels in intact and estrogen-treated ovariectomized NPY KO animals did not. In contrast, WTs consistently showed fasting-induced suppression of LH. Our findings suggest that other systems can sustain the hyperphagia of lactation and NPY alone is not responsible for suppressing cyclicity during lactation. Nevertheless, the suppression of basal LH release that accompanies food deprivation in normal female mice appears to require the steroid-dependent actions of NPY.


Endocrinology ◽  
2018 ◽  
Vol 159 (3) ◽  
pp. 1496-1510 ◽  
Author(s):  
Carrie R Jonak ◽  
Nancy M Lainez ◽  
Ulrich Boehm ◽  
Djurdjica Coss

Abstract Gonadotropin-releasing hormone (GnRH) from the hypothalamus regulates synthesis and secretion of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) from the anterior pituitary gonadotropes. LH and FSH are heterodimers composed of a common α-subunit and unique β-subunits, which provide biological specificity and are limiting components of mature hormone synthesis. Gonadotrope cells respond to GnRH via specific expression of the GnRH receptor (Gnrhr). GnRH induces the expression of gonadotropin genes and of the Gnrhr by activation of specific transcription factors. The JUN (c-Jun) transcription factor binds to AP-1 sites in the promoters of target genes and mediates induction of the FSHβ gene and of the Gnrhr in gonadotrope-derived cell lines. To analyze the role of JUN in reproductive function in vivo, we generated a mouse model that lacks JUN specifically in GnRH receptor‒expressing cells (conditional JUN knockout; JUN-cKO). JUN-cKO mice displayed profound reproductive anomalies such as reduced LH levels resulting in lower gonadal steroid levels, longer estrous cycles in females, and diminished sperm numbers in males. Unexpectedly, FSH levels were unchanged in these animals, whereas Gnrhr expression in the pituitary was reduced. Steroidogenic enzyme expression was reduced in the gonads of JUN-cKO mice, likely as a consequence of reduced LH levels. GnRH receptor‒driven Cre activity was detected in the hypothalamus but not in the GnRH neuron. Female, but not male, JUN-cKO mice exhibited reduced GnRH expression. Taken together, our results demonstrate that GnRH receptor‒expression levels depend on JUN and are critical for reproductive function.


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