Influences On The Reproductive Hormones In Animals Biology Essay


Nutritional factor is the main controlling factor for reproduction. The essay focuses on whether the role of nutrition has any influence on various phases of reproduction hormone secretion and control mechanisms of reproduction or not. Decreased nutrient intake or poor diet quality or quantity delays puberty; increases the postpartum delivery and disturbance in estrous cycles. In contrast, some studies have found no relevance of nutrient intake on hormones. Energy intake impacts greatly on the endocrine system and also on neural mechanisms, which influence the release of reproductive hormones. Influence of nutrition on changes in gonadotropic hormone secretion from the pituitary gland, progesterone secretion during the estrous cycle and during pregnancy, follicular development, ovulation, ovarian activity changes measured by hormone secretion, and sensitivity to the pituitary-hypothalamus releasing gonadotropin hormones are discussed. In addition, effects of dietary elements individually are described and found that fat and protein in low concentration decrease release and formation of reproductive hormones.


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The reproductive function becomes impaired with inadequate nutrition. Insufficient nutrition impacts in many ways on the reproductive system like, delay in puberty onset, an estrous induction in female cycles, and lengthened postpartum an estrous (Randel 1990). The detrimental effects of inadequate nutrition can be exerted at the ovary level, at anterior pituitary gland, and hypothalamus. High frequency mode of pulsatile LH secretion is vital for the final phase of ovarian follicles maturation and hence induces ovulation and estrous (Randel 1990). Neuroendocrine control of LH release gets affected by nutrition which further influences reproductive activity.

Primary effector of reproduction efficiency in animals is nutrition. In limited nutrient availability, body of animal adapts a mechanism to avoid reproduction to prevent energy loss in this process. It has been noticed by the producers that undernourished animals show decreased reproductive rates. It was known that nutrition has profound influence on reproductive hormones, but the underlying mechanism is not yet understood. Researchers have found the nutrition play a significant role in the initiation of estrous cycles. Due to nutritional deficiencies, female animals fail to become pregnant. Recent investigations done with ultrasound, growth factor assays, and molecular techniques have shown that nutrient availability not only affects estrous cyclicity but also affects the oocyte quality, follicular development, and gene expression (Schillo 1992). The issue of whether the role of nutrition has any influence on various phases of reproduction hormone secretion and control mechanisms of reproduction or not has sparked much debate some argue for and other are against. This paper will consider both sides of the argument and show that nutrition has a direct effecton animal's reproductive activity.



Animals that feed on low-plane showed the delay in puberty and reduced growth rates. Effects of low-plane feeding are more pronounced in early post-natal than in immediate pre-pubertal phase. Ferrell (1982) experimented on beefs and Petitclerc et al. (1983) experimented on dairy cattle by giving reduced feed and found that the animals showed a delay in puberty by more than few weeks and Topps found that heifers showed nine months delay in puberty when reared on low planes of nutrition. Why low plane feeding affects the puberty status can be explained with the researches' observation that proteins, and vitamins and minerals play specific roles in reproductive tissue functioning. For example, vitamin A determines the mode of action of ovarian and pituitary cells producing hormones, and similarly in the study by Phillippo et al. (1987) it was found that luteinizing hormone (LH) secretion is influenced by the molybdenum and thus delays puberty by causing disruption in ovarian steroid secretion.

2. In MALE:

The relationship between nutrition and puberty is similar to that in females. Therefore, males who fed on high planes of nutrition showed early puberty and influences are more pronounced in early life. Males who fed on low nutrition planes have found with reduction in sperm production (Alkass et al. 1982).Low concentrations of protein in ruminant's feed delay puberty in male animals.


Attainment of puberty delays with low plane-of nutrition because of inhibition in the gonadotropin releasing hormone (GnRH) pulsatile release from the hypothalamus and release of LH from the pituitary gland. In a study done by Foster et al. (1988), it was found that high plane feeding reversed the suppression of LH secretion and follicle stimulating hormone in a lamb who was earlier undernourished. Similarly, in an experimented model, it was observed that on infusion of a dextrose-amino acid mixture (compared to high-plane nutrition) was effective in maintaining normal LH pulse frequency. This illustrated that GnRH neuron controlling mechanisms of release of hormones are very sensitive to the alterations in the nutritional state of the animal. The proper mechanism how hormonal releases get affected by the nutrition was not known. To find the correlation between the two several studies were performed, but none gave the justified explanation. It was further explained by the Foster and Steiner that in response to energy yielding nutrients, body might release insulin, which might bind to the receptors in the brain regions (median eminence and arcuate nucleus) that are involved in GnRH secretion control.

1. Onset of Puberty:

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Normally, the puberty onset in the animals is due to LH pulse frequency pre-pubertal increase due to decline in hypothalamic-pituitary axis responsiveness to negative feedback of estrogen. This pulsatile LH secretion increase provokes the ovarian follicles development to the pre-ovulatory stage. Various experiments' results formulated a hypothesis that onset of puberty in animals is prevented by the inadequate nutrition by blocking the increase in pre-pubertal LH pulse frequency. Foster and Olster conducted many experiments in 1985 and concluded that insufficient nutrition in ovariectomized lambs declined the pulsatile LH secretion in both conditions of presence and absence of the estradiol negative feedback. This showed that estradiol-induced surges do not get influenced by inadequate nutrition. Based on the observations of experiments done by McShane and Keisler (1990), it was inferred that primary mechanism by which insufficient nutrition delays puberty onset is due to disruption of pulsatile LH secretion. Foster et al. (1989) observed depression in LH pulse frequencies due to restricted nutrition with no effect on prolactin hormone. It seemed that anterior pituitary hormones do not get affected by the low nutrition. However, nutritional effects on pre-pubertal LH frequency were only theoretical, absolute scientific evidence were not established.


Conflicting results were found on the effects of nutrition on estrous cycles. The disturbance in estrous cycles is also attributed to LH secretion reduction. In an experiment (Imakawa et al. 1986), change in body weight influence the follicular phase of the estrous cycle due to changes in the frequency of LH pulses. Decrease in LH frequency pulses induces anestrous due to poor nutrition. This effect was produced because of enhanced responsiveness to estrogen negative feedback and steroid-independent direct effect on LHRH release. In an experiment, where adult ewes were fed on low planes of nutrition showed decreased ovulation rates, which were thought to be an attributed response to reduced development of ovarian follicles but the reason given for this influence was only hypothesized and not proved. Disruption in pulsatile release of LH generates effects on follicular development. Low nutrition produces few LH pulses and decrease LH serum concentrations but increases the LHRH concentrations in the hypothalamus (Tatman et al. 1990). Similar results were demonstrated by Thomas et al. (1990) in experiment on ovariectomized ewes. Collectively, these results supported a hypothesis that pulsatile administration of LHRH recovered the LH concentrations in the serum and anterior pituitary gland in undernourished animals during breeding season (Kile et al. 1991).According to Tatman et al. (1990), restricted dietary energy produced no influence on the number of LHRH pituitary receptors. Furthermore, LHRH different dose effects on release of LH have not been yet confirmed associated with nutritional status; therefore, established conclusions cannot be made on pituitary gland sensitivity to LHRH in respect to subtle effects of nutrition.
Feed restriction for prolonged time reduces LH pulse frequency and increase in GH concentrations but no influence found on prolactin concentrations (Thomas et al., 1990). Long-term feed restriction in adult, ovariectomized ewes reduced frequency of LH pulses and increased GH concentrations but did not influence anterior pituitary hormones. In summary, decreased ovulation rate and anestrous nutritional cycles involved with pulsatile LH release disruption and some effects on ovary are also seen. Inadequate nutrition negative effects on LH release seem to occur at the central nervous system level and reduced LHRH release may be the probable reason. Though the given reason was not established scientifically and only thought as it might be the cause of nutrition effects.

Mechanisms Linking Luteinizing Hormone:

Secretion to Nutritional Status: previous studies and discussions emphasized on the involvement of the central mechanism of controlling LHRH secretion by the hypothalamus due to inhibitory effects on LH secretion by low nutrition. However, the mechanism how the information of low nutritional status transfers to the central nervous system and secretion of hormone was ambiguous.
According to researchers (Richards et al. 1989; Tatman et al. 1990), one more theory was suggested that long term dietary restrictions cause the reduction in LH pulse frequencies, which is due to body fatness reduction. Nevertheless, it was felt doubtful later as theunknown pathway of neuroendocrine was linked to the body fat relation with LHRH release. Furthermore, from other studies and experiments, the complexity of the endocrine and biochemical control of metabolism and absorption of nutrients suggested that various mechanisms may be responsible for LH frequency pulse reduction. It was seemed that most likely metabolic changes from nutrition changes along with body fatness changes might be controlling release of pulsatile LH. This influence on LH release may be due to transfer of metabolites (due to metabolic changes) specific blood-borne signals. In other words, nutritional changes might cause alteration in the availability of metabolic fuels that are important for functioning of neurons controlling release of LHRH. Steiner et al. (1983) were the first researchers to suggest that metabolic signals that influence LH secretion via blood could be insulin concentrations in response to fodder taken by animals, non-esterified fatty acids (NEFAI), and certain amino acids (metabolic products of proteins). Low nutrition periods are generally associated with decreased insulin secretion, increased concentrations of NEFA (lipolysis occurs and lipogenesis reduces at low nutritional status), and serum amino acid concentration changes the quantity and the quality of feed taken by the animals influence the plasma concentrations of insulin directly, which acts as a metabolic signal and influences the release of LH. Moreover, insulin on passing the blood-brain barrier influence the activity of neurons in the central nervous system which further influence the release of gonadotropin hormones.


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In animals, it was found that ovulation rates were higher in good nutritional condition as compared to poor nutrition status that may be due to development of high numbers of ovarian follicles in late luteal phase during the estrous cycle It was thought by Rhind & McNeilly (1986) that high ovulation rate occurred due to high serum FSH concentrations during the follicular phases and late luteal of the estrous cycle that was due to improved body condition. However, in other studies, this was not the conclusion rather LH pulse frequency enhancement during follicular phase mediated the increase in ovulation rate. Incontrast,other studiesfounddid notshowanyeffect ofLHorFSHon theovulation rate.

In several experiments, it was found that a significant increase in ovulation rate was observed with insulin hormone.Then it was suggested that insulin effects is due to the fact that it supplies nutrients, which are used in GnRH neurotransmitters' synthesis because insulin attaches to those receptors which control GnRH secretion in brain. Insulin also has action on ovary directly as it increases the production of progesterone by luteal cells and granulosa and androstenedione release by thecal cells. This explained that dietary protein is associated with enhanced serum concentrations of androstenedione and insulin both which as response increase ovulation rate. In one hand, it was observed in an experiment done on ewes who ovulation rate increased as nutrition mediated the increase in concentrations of hepatic microsomal protein of enzymes that are involved in steroids oxidative metabolism.On the other hand,some studies found no effect of nutrition on ovulation rate in ewes (Thomas et al. 1987).


1. Energy intake:

The reproduction process is regulated by the energy derived from the nutrients. Availability of energy influences the reproduction, mainly via the pathways that block or allow the GnRH release from the hypothalamus, and LH and FSH from the pituitary. Metabolic response or energy substrates affect the follicular growth, production of estrogen, and circulating progesterone levels by acting upon the ovary. Reduced energy intake during late gestation time prolongs the postpartum anestrus period and thus declines the pregnancy rate subsequently. And this effect of inadequate energy received during late gestation is not reversed by increasing intake of energy at the postpartum period (Randel 1990). Studies showed that late gestation is a critical period were insufficient nutrition impacts the reproductive process strongly.
Low energy diets were associated with low pregnancy rates and delay in onset of puberty. This delay in puberty was until the animals gain 65% of their mature weight, after that nutrition does not have any impact on attainment of puberty. Recent study from Nebraska found that heiferswhich gain 50-55% of mature weight did not have any effect on pregnancy rates as compared to heifers that developed 60-65% of mature weight. Studies done later doubted the role of energy availability on pregnancy rates or on ovary (Funston and Deutscher 2004; Martin et al. 2008; Larsen et al. 2009).


Various studies have investigated that source of energy (calories) has fewer concern aspects than the varying levels of dietary energy. Animals get energy from starch, fibers, and fats (in ruminants) and animal proteins (in carnivores) and each source produce different effects in animals physiologically. Diets which are isoenergetic in which calories are derived from different energy sources have been varying effects on reproduction. A two year study was conducted to examine the effects of energy source on reproductive development in animals. Heifers were fed on isoenergetic supplements made of from corn/soy (high starch), soy hulls (high fiber), and whole cottonseed (high fat). The observation showed that there is no effect on the pregnancy rates or puberty onset by the supplements. A similar experiment was conducted by the Howlett and co-workers, (2003) with whole soybeans or whole cottonseed in place of soyhulls or a corn/soy, and they also found opposite results. Therefore, the role of energy in the field of research to determine the effect of energy on the animal'sreproductive system, still need more investigation.

3. Influence of Fats:

Fat impact has been seen on the reproduction process and is a common focus of research (Funston 2004; Hess et al. 2008). Fatty acids and cholesterol constitute the substrates for hormone synthesis. Increased fat component in the diet may either directly influence the reproductive axis, or it may elevate the reproductive hormones (like, progesterone, prostaglandins) levels. Thus, fats may produce an independent effect or additive effect in addition to energy availability.
Fats are usually supplemented in the diet of animals to increase the energy density. For instance, in cattle, 5-8% fat is required in the diet and exceeding this level will produce an impaired effect on the rumen function. Previous studies (Talavera et al. 1985; Williams 1989) done explained the increased progesterone production and long lifespan of the corpus luteum on feeding the animals on high fat diets during cycling period and postpartum period. Improved fertility was observed during luteal phase due to high progesterone levels. High fat diet also showed increased follicular growth which in turn further increased estrogen and progesterone production but experiments done recently on animals did not confirm the direct influence of fats on reproductive hormones. As a result, reproduction process enhanced due to follicular growth and production of hormones. Improved pregnancy rates were observed by the Montana researchers when cows were given fat supplements during the last trimester. Missouri group of researchers also confirmed this fact of improvement in pregnancy rates on feeding high-fat diets to cows. From all above, it is clearly that the fats have a positive influence on animals,anditsroleisincreasinganimal'senergyand there is no contrary statement to this fact.

4. Influence of Protein Intake:

Deficiency of proteins in the diet delays the estrus return. Theresearcher is not confirmed the effects of protein on the reproduction. They are still confounded whether the effect is due to general poor nutrition or due to solely protein deficiency. Some earlier studies had indicated that postpartum interval decreases and pregnancy rate increases by providing protein supplements to cows (Vanzant and Cochran 1994). Cows grazed on medium to low quality of forages and digestibility and energy intake both enhanced by increasing the amount of digestible intake protein. Consequently, it was unclear that whether improvements observed in reproductive efficiency are resulting of protein/amino acids direct effect or result of availability of improved energy.
Giving excess protein was also associated with reduced pregnancy rates as observed by researchers in cattle (Blanchard et al. 1990; Sinclair et al. 2000). Excess protein diet produces excess of ammonia or urea in the animal body which subsequently may disrupt the oocyte's maturation, and thus impairs the fertilization of developing embryos. Notwithstanding, the exact mechanism by which reproduction in animals gets affected by levels of protein is still unknown.


In spite the fact that, conflicting data were found no research and experiment completely agreed with the statement that nutrition has influence on reproductive hormones. Moreover, some theories behind the nutritional influence onthem have been hypothesized until the exact fact is revealed. Nevertheless,itisclearlyfrommostconductingstudiesthat nutrition enhancement has a direct effect on improvementof animal's reproductivity. Dietary energy restrictions from a long time delays puberty onset, causes disruption in cyclicity in sexually mature female animals, and postpartum anestrous period gets lengthened in animals. After several experiments done by the researchers, the topic of whether dietary energy restrictions have inhibitory effects on reproductive activity in animals or, just a perception of researchersisstill argumentative issue. The investigators in animal nutrition and hormones field have been assumed many theories such as: firstly, important mechanism by which reproductive activity thought to be impaired by the restriction of energy nutrients is the inhibition of the increase in LH pulse frequency, which is vital for the ovarian follicles growth to the pre-ovulatory stage. Secondly, inadequate nutrition suppresses the pulsatile LH secretion by causing the reduction in the LHRH (luteinizing hormone-releasing hormone) secretion by the hypothalamus. Thirdly, changes in fat or proteins or other mineral components of nutrient impact the reproductive activity, the reason may be due to affect on central mechanisms (neurons activity) that control LHRH release. These neurons are sensitive to the availability of metabolic fuels. These suggested theories were given to findoutsome satisfactory answers to the conflict that, whether nutrition really has got any influence on reproduction in animals or not.