Neuroendocrine Pathways Mediating Nutritional Acceleration of Puberty: Insights from Ruminant Models

Amstalden, M.; Alves, Bruno Henrique; Liu, Songrui; Cardoso, Rodolfo C.; Williams, Gary L.

doi:10.3389/fendo.2011.00109

Cited by 38 publications

(27 citation statements)

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“…In primates and rodents, GnRH neurons (which ultimately regulate secretion of LH and control puberty) do not appear to express leptin receptors (Finn et al, 1998;Quennell et al, 2009), suggesting that leptin's effects on GnRH release are likely mediated by intermediate pathways (Schneider, 2004;. Information from other metabolic factors such as insulin, IGF-1, and ghrelin is also possibly integrated in a complex neural network that perceives and signals availability of metabolic fuels to the central reproductive system (Schneider, 2004;Amstalden et al, 2011). Hypothalamic neuropeptide Y (NPY) and proopiomelanocortin (POMC) neurons are considered key pathways for nutritional control of reproduction (Crown et al, 2007;Amstalden et al, 2011).…”

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confidence: 99%

“…Information from other metabolic factors such as insulin, IGF-1, and ghrelin is also possibly integrated in a complex neural network that perceives and signals availability of metabolic fuels to the central reproductive system (Schneider, 2004;Amstalden et al, 2011). Hypothalamic neuropeptide Y (NPY) and proopiomelanocortin (POMC) neurons are considered key pathways for nutritional control of reproduction (Crown et al, 2007;Amstalden et al, 2011). Neuropeptide Y has a predominant inhibitory action on the release of LH in ruminants (Gazal et al, 1998;Estrada et al, 2003;Morrison et al, 2003).…”

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confidence: 99%

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Use of a stair-step compensatory gain nutritional regimen to program the onset of puberty in beef heifers1

Cardoso

Alves

Prezotto

et al. 2014

Journal of Animal Science

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It was hypothesized that metabolic programming of processes underlying puberty can be shifted temporally through the use of a stair-step compensatory growth model such that puberty is optimally timed to occur at 11 to 12 mo of age. Forty crossbred beef heifers were weaned at approximately 3.5 mo of age and, after a 2-wk acclimation period, were assigned randomly to 1 of 4 nutritional groups: 1) low control (LC), restricted feed intake of a forage-based diet to promote BW gain of 0.5 kg/d until 14 mo of age, 2) high control (HC), controlled feed intake of a high-concentrate diet to promote BW gain of 1 kg/d until 14 mo of age, 3) stair-step 1 (SS-1), ad libitum feed intake of a high-concentrate diet until 6.5 mo of age followed by restricted access to a high-forage diet to promote BW gain of 0.35 kg/d until 9 mo of age, ad libitum feed intake of a high-concentrate diet until 11.5 mo of age, and restricted intake of a high-forage diet to promote BW gain of 0.35 kg/d until 14 mo of age, and 4) stair-step 2 (SS-2), reverse sequence of SS-1, beginning with restricted access to a high-forage diet. Body weight (every 2 wk) and circulating concentrations of leptin (monthly) were determined throughout the experiment. Concentrations of progesterone in blood samples collected twice weekly beginning at 8 mo of age were used to determine pubertal status. Body weight gain followed a pattern similar to that proposed in our experimental design. Circulating concentrations of leptin increased following distinct elevations in BW but decreased abruptly after feed intake restriction. Survival analysis indicated that the percentage of pubertal heifers in the LC group was lower (P < 0.05) than all other groups throughout the experiment. Although heifers in SS-1 were nutritionally restricted between 6.5 and 9 mo of age, the proportion pubertal by 12 mo of age did not differ (P = 0.36) from that of the HC group, with 80% and 70% pubertal in SS-1 and HC, respectively. In contrast, the proportion of heifers pubertal by 12 mo of age in the SS-2 group (40%) was lower (P < 0.05) than both HC and SS-1. However, by 14 mo of age, 90% of heifers in the SS-2 group had also attained puberty compared to only 40% of the LC group. In summary, these data provide evidence that changes in the nutritional and metabolic status during the early juvenile period can program the onset of puberty that occurs months later, allowing optimal timing of sexual maturation in replacement beef heifers.

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confidence: 99%

Section: Itemmentioning

confidence: 99%

Use of a stair-step compensatory gain nutritional regimen to program the onset of puberty in beef heifers1

Cardoso

Alves

Prezotto

et al. 2014

Journal of Animal Science

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“…Klingerman et al (2011) highlight the metabolic influence on sexual behavior, and food intake or food hoarding in hamsters, and suggest a role for neuropeptide Y (NPY) and gonadotropin inhibiting hormone (GnIH) expressing cells in these processes. Amstalden et al (2011) emphasize observations made in ruminant species in a very welcome comparative perspective. Clearly, research examining the metabolic control of reproduction is advancing at a rapid pace.…”

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confidence: 94%

From precocious puberty to infertility: metabolic control of the reproductive function

2013

Frontiers Research Topics

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insulin or leptin resistance, the repercussions may include both imbalanced metabolic homeostasis and reproductive dysfunction. Indeed, leptin-deficient patients become hyperphagic, massively obese, and infertile. This eBook has assembled multidisciplinary specialists to provide up-to-date information on recent advances in understanding the complex physiologic interaction between metabolism and reproduction.In the initial article, True et al. (2011) discuss the role of the adipocyte hormone leptin as a key metabolic signal and predominant focus of interest in the field. In their review, it is emphasized that although leptin may be an important permissive signal for reproductive function as indicated by many years of research, factors other than leptin must critically contribute to negative energy balance-induced reproductive inhibition. Schneider et al. (2012) call attention to the "metabolic hypothesis," which predicts that sensory systems monitor the availability of oxidizable metabolic fuels and allow behavioral responses to optimize reproductive success. Following these provocative introductory articles, three reviews discuss the role of specific groups of neurons in this physiologic regulation. Bianco (2012) highlights the Kisspeptin system as the converging target of environmental, metabolic, and hormonal signals, and proposes a potential correlation between the existence of a sexual dimorphism of pubertal disorders in children of different ethnicities and the sexually dimorphic expression of kisspeptin neurons. Supported by recent genetic studies, Xu et al. (2012) focused their review on two sets of hypothalamic neurons: the pro-opiomelanocortin (POMC) neurons in the arcuate nucleus and the steroidogenic factor-1 (SF1) neurons in the ventromedial hypothalamic nucleus. Their discussion calls attention to exciting new findings showing that disruption of metabolic signals (e.g., leptin and insulin) or reproductive signals (e.g., estradiol) in these neurons leads to impaired regulation of both energy homeostasis and fertility. Donato and Elias (2011) discuss the role of the ventral premammillary nucleus as integrator of environmental, metabolic, and reproductive cues, and its emergence as a critical previously unrecognized hypothalamic site linking metabolism and reproduction. Acosta-Martínez (2012) proposes a role for phosphatidylinositol-3-kinase (PI3K) signaling pathway as potential integrator of a number of peripheral metabolic cues, including insulin and leptin, in the metabolic control of the reproductive function. Tolson and Chappell (2012) offer an Reproduction is calorically expensive. The energy demands of mate seeking, gamete production, pregnancy, and lactation require increased food consumption and appropriate regulation of energy expenditure. Therefore, control of the reproductive function by the brain must be responsive to the metabolic state of the animal. Conversely, when survival is threatened by insufficient fuels or increased energy demands, males and females of most species divert e...

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From Precocious Puberty to Infertility: Metabolic Control of the Reproductive Function

2013

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Neuroendocrine Pathways Mediating Nutritional Acceleration of Puberty: Insights from Ruminant Models

Cited by 38 publications

References 84 publications

Use of a stair-step compensatory gain nutritional regimen to program the onset of puberty in beef heifers1

Use of a stair-step compensatory gain nutritional regimen to program the onset of puberty in beef heifers1

From precocious puberty to infertility: metabolic control of the reproductive function

From Precocious Puberty to Infertility: Metabolic Control of the Reproductive Function

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