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Article ; Online: Emulsifiers during gestation: The risks of ultra-processed food revealed in mice.

Franssen, Delphine / Parent, Anne-Simone

2023 Volume 21, Issue 8, Page(s) e3002265

Abstract: Several dietary components disrupt the control of energy balance. A new study in PLOS Biology shows that, in mice, maternal consumption of emulsifiers induces a rewiring of the hypothalamic feeding circuits and causes neuropsychological impairment in the ...

Abstract	Several dietary components disrupt the control of energy balance. A new study in PLOS Biology shows that, in mice, maternal consumption of emulsifiers induces a rewiring of the hypothalamic feeding circuits and causes neuropsychological impairment in the offspring.
MeSH term(s)	Animals ; Mice ; Pregnancy ; Female ; Food, Processed
Language	English
Publishing date	2023-08-25
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Comment
ZDB-ID	2126776-5
ISSN	1545-7885 ; 1544-9173
ISSN (online)	1545-7885
ISSN	1544-9173
DOI	10.1371/journal.pbio.3002265
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Article ; Online: The kisspeptin receptor: A key G-protein-coupled receptor in the control of the reproductive axis.

Franssen, Delphine / Tena-Sempere, Manuel

Best practice & research. Clinical endocrinology & metabolism

2018 Volume 32, Issue 2, Page(s) 107–123

Abstract: The kisspeptin receptor, Kiss1R, also known as Gpr54, is a G protein-coupled receptor (GPCR), deorphanized in 2001, when it was recognized as canonical receptor for the Kiss1-derived peptides, kisspeptins. In 2003, inactivating mutations of Kiss1R gene ... ...

Abstract	The kisspeptin receptor, Kiss1R, also known as Gpr54, is a G protein-coupled receptor (GPCR), deorphanized in 2001, when it was recognized as canonical receptor for the Kiss1-derived peptides, kisspeptins. In 2003, inactivating mutations of Kiss1R gene were first associated to lack of pubertal maturation and hypogonadotropic hypogonadism in humans and rodents. These seminal findings pointed out the previously unsuspected, essential role of Kiss1R and its ligands in control of reproductive maturation and function. This contention has been fully substantiated during the last decade by a wealth of clinical and experimental data, which has documented a fundamental function of the so-called Kiss1/Kiss1R system in the regulation of puberty onset, gonadotropin secretion and ovulation, as well as the metabolic and environmental modulation of fertility. In this review, we provide a succinct summary of some of the most salient facets of Kiss1R, as essential GPCR for the proper maturation and function of the reproductive axis.
MeSH term(s)	Animals ; Female ; Fertility/genetics ; Humans ; Kisspeptins/physiology ; Receptors, G-Protein-Coupled/physiology ; Receptors, Kisspeptin-1/physiology ; Reproduction/genetics ; Sexual Maturation/genetics ; Sexual Maturation/physiology ; Signal Transduction/genetics ; Signal Transduction/physiology
Chemical Substances	KISS1 protein, human ; KISS1R protein, human ; Kisspeptins ; Receptors, G-Protein-Coupled ; Receptors, Kisspeptin-1
Language	English
Publishing date	2018-02-03
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2052339-7
ISSN	1878-1594 ; 1532-1908 ; 1521-690X
ISSN (online)	1878-1594 ; 1532-1908
ISSN	1521-690X
DOI	10.1016/j.beem.2018.01.005
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Article ; Online: Endocrine-disrupting chemicals and their effects on puberty.

Lopez-Rodriguez, David / Franssen, Delphine / Heger, Sabine / Parent, Anne-Simone

Best practice & research. Clinical endocrinology & metabolism

2021 Volume 35, Issue 5, Page(s) 101579

Abstract: Sexual maturation in humans is characterized by a unique individual variability. Pubertal onset is a highly heritable polygenic trait but it is also affected by environmental factors such as obesity or endocrine disrupting chemicals. The last 30 years ... ...

Abstract	Sexual maturation in humans is characterized by a unique individual variability. Pubertal onset is a highly heritable polygenic trait but it is also affected by environmental factors such as obesity or endocrine disrupting chemicals. The last 30 years have been marked by a constant secular trend toward earlier age at onset of puberty in girls and boys around the world. More recent data, although more disputed, suggest an increased incidence in idiopathic central precocious puberty. Such trends point to a role for environmental factors in pubertal changes. Animal data suggest that the GnRH-neuronal network is highly sensitive to endocrine disruption during development. This review focuses on the most recent data regarding secular trend in pubertal timing as well as potential new epigenetic mechanisms explaining the developmental and transgenerational effects of endocrine disrupting chemicals on pubertal timing.
MeSH term(s)	Animals ; Endocrine Disruptors/toxicity ; Female ; Humans ; Male ; Obesity/chemically induced ; Obesity/epidemiology ; Obesity/genetics ; Puberty ; Puberty, Precocious/chemically induced ; Puberty, Precocious/epidemiology ; Puberty, Precocious/genetics ; Sexual Maturation
Chemical Substances	Endocrine Disruptors
Language	English
Publishing date	2021-09-17
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2052339-7
ISSN	1878-1594 ; 1532-1908 ; 1521-690X
ISSN (online)	1878-1594 ; 1532-1908
ISSN	1521-690X
DOI	10.1016/j.beem.2021.101579
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Article ; Online: Exposure to the pesticides linuron, dimethomorph and imazalil alters steroid hormone profiles and gene expression in developing rat ovaries.

Boberg, Julie / Johansson, Hanna K L / Franssen, Delphine / Draskau, Monica Kam / Christiansen, Sofie / Cramer, Johannah / Pedersen, Mikael / Parent, Anne-Simone / Svingen, Terje

Toxicology letters

2022 Volume 373, Page(s) 114–122

Abstract: Inhibition of androgen signaling during critical stages of ovary development can disrupt folliculogenesis with potential consequences for reproductive function later in life. Many environmental chemicals can inhibit the androgen signaling pathway, which ... ...

Abstract	Inhibition of androgen signaling during critical stages of ovary development can disrupt folliculogenesis with potential consequences for reproductive function later in life. Many environmental chemicals can inhibit the androgen signaling pathway, which raises the question if developmental exposure to anti-androgenic chemicals can negatively impact female fertility. Here, we report on altered reproductive hormone profiles in prepubertal female rats following developmental exposure to three pesticides with anti-androgenic potential: linuron (25 and 50 mg/kg bw/d), dimethomorph (60 and 180 mg/kg bw/d) and imazalil (8 and 24 mg/kg bw/d). Dams were orally exposed from gestational day 7 (dimethomorph and imazalil) or 13 (linuron) until birth, then until end of dosing at early postnatal life. Linuron and dimethomorph induced dose-related reductions to plasma corticosterone levels, whereas imazalil mainly suppressed gonadotropin levels. In the ovaries, expression levels of target genes were affected by linuron and dimethomorph, suggesting impaired follicle growth. Based on our results, we propose that anti-androgenic chemicals can negatively impact female reproductive development. This highlights a need to integrate data from all levels of the hypothalamic-pituitary-gonadal axis, as well as the hypothalamic-pituitary-adrenal axis, when investigating the potential impact of endocrine disruptors on female reproductive development and function.
Language	English
Publishing date	2022-11-21
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	433788-8
ISSN	1879-3169 ; 0378-4274
ISSN (online)	1879-3169
ISSN	0378-4274
DOI	10.1016/j.toxlet.2022.11.010
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Article ; Online: Male minipuberty involves the gonad-independent activation of preoptic nNOS neurons.

Delli, Virginia / Dehame, Julien / Franssen, Delphine / Rasika, S / Parent, Anne-Simone / Prevot, Vincent / Chachlaki, Konstantina

Free radical biology & medicine

2022

Abstract: Background: The maturation of the hypothalamic-pituitary-gonadal (HPG) axis is crucial for the establishment of reproductive function. In female mice, neuronal nitric oxide synthase (nNOS) activity appears to be key for the first postnatal activation of ...

Abstract	Background: The maturation of the hypothalamic-pituitary-gonadal (HPG) axis is crucial for the establishment of reproductive function. In female mice, neuronal nitric oxide synthase (nNOS) activity appears to be key for the first postnatal activation of the neural network promoting the release of gonadotropin-releasing hormone (GnRH), i.e. minipuberty. However, in males, the profile of minipuberty as well as the role of nNOS-expressing neurons remain unexplored. Methods: nNOS-deficient and wild-type mice were studied during postnatal development. The expression of androgen (AR) and estrogen receptor alpha (ERα) as well as nNOS phosphorylation were evaluated by immunohistochemistry in nNOS neurons in the median preoptic nucleus (MePO), where most GnRH neuronal cell bodies reside, and the hormonal profile of nNOS-deficient male mice was assessed using previously established radioimmunoassay and ELISA methods. Gonadectomy and pharmacological manipulation of ERα were used to elucidate the mechanism of minipubertal nNOS activation and the maturation of the HPG axis. Results: In male mice, minipubertal FSH release occurred at P23, preceding the LH surge at P30, when balanopreputial separation occurs. Progesterone and testosterone remained low during minipuberty, increasing around puberty, whereas estrogen levels were high throughout postnatal development. nNOS neurons showed a sharp increase in Ser Conclusions: Our results show that the timing of minipuberty differs in male mice when compared to females, but as in the latter, nNOS activity in the preoptic region plays a role in this process. Additionally, akin to male non-human primates, the profile of minipuberty in male mice is shaped by sex-independent mechanisms, and possibly involves extragonadal estrogen sources.
Language	English
Publishing date	2022-12-02
Publishing country	United States
Document type	Journal Article
ZDB-ID	807032-5
ISSN	1873-4596 ; 0891-5849
ISSN (online)	1873-4596
ISSN	0891-5849
DOI	10.1016/j.freeradbiomed.2022.11.040
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Article ; Online: Endocrine disrupters and possible contribution to pubertal changes.

Fudvoye, Julie / Lopez-Rodriguez, David / Franssen, Delphine / Parent, Anne-Simone

Best practice & research. Clinical endocrinology & metabolism

2019 Volume 33, Issue 3, Page(s) 101300

Abstract: The onset of puberty strongly depends on organizational processes taking place during the fetal and early postnatal life. Therefore, exposure to environmental pollutants such as Endocrine disrupting chemicals (EDCs) during critical periods of development ...

Abstract	The onset of puberty strongly depends on organizational processes taking place during the fetal and early postnatal life. Therefore, exposure to environmental pollutants such as Endocrine disrupting chemicals (EDCs) during critical periods of development can result in delayed/advanced puberty and long-term reproductive consequences. Human evidence of altered pubertal timing after exposure to endocrine disrupting chemicals is equivocal. However, the age distribution of pubertal signs points to a skewed distribution towards earliness for initial pubertal stages and towards lateness for final pubertal stages. Such distortion of distribution is a recent phenomenon and suggests environmental influences including the possible role of nutrition, stress and endocrine disruptors. Rodent and ovine studies indicate a role of fetal and neonatal exposure to EDCs, along the concept of early origin of health and disease. Such effects involve neuroendocrine mechanisms at the level of the hypothalamus where homeostasis of reproduction is programmed and regulated but also peripheral effects at the level of the gonads or the mammary gland.
MeSH term(s)	Animals ; Endocrine Disruptors/adverse effects ; Environmental Pollutants/adverse effects ; Female ; Homeostasis/drug effects ; Humans ; Hypothalamus/drug effects ; Male ; Puberty/drug effects ; Puberty, Precocious/epidemiology
Chemical Substances	Endocrine Disruptors ; Environmental Pollutants
Language	English
Publishing date	2019-07-27
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2052339-7
ISSN	1878-1594 ; 1532-1908 ; 1521-690X
ISSN (online)	1878-1594 ; 1532-1908
ISSN	1521-690X
DOI	10.1016/j.beem.2019.101300
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Article ; Online: Cellular and molecular features of EDC exposure: consequences for the GnRH network.

Lopez-Rodriguez, David / Franssen, Delphine / Bakker, Julie / Lomniczi, Alejandro / Parent, Anne-Simone

Nature reviews. Endocrinology

2020 Volume 17, Issue 2, Page(s) 83–96

Abstract: The onset of puberty and the female ovulatory cycle are important developmental milestones of the reproductive system. These processes are controlled by a tightly organized network of neurotransmitters and neuropeptides, as well as genetic, epigenetic ... ...

Abstract	The onset of puberty and the female ovulatory cycle are important developmental milestones of the reproductive system. These processes are controlled by a tightly organized network of neurotransmitters and neuropeptides, as well as genetic, epigenetic and hormonal factors, which ultimately drive the pulsatile secretion of gonadotropin-releasing hormone. They also strongly depend on organizational processes that take place during fetal and early postnatal life. Therefore, exposure to environmental pollutants such as endocrine-disrupting chemicals (EDCs) during critical periods of development can result in altered brain development, delayed or advanced puberty and long-term reproductive consequences, such as impaired fertility. The gonads and peripheral organs are targets of EDCs, and research from the past few years suggests that the organization of the neuroendocrine control of reproduction is also sensitive to environmental cues and disruption. Among other mechanisms, EDCs interfere with the action of steroidal and non-steroidal receptors, and alter enzymatic, metabolic and epigenetic pathways during development. In this Review, we discuss the cellular and molecular consequences of perinatal exposure (mostly in rodents) to representative EDCs with a focus on the neuroendocrine control of reproduction, pubertal timing and the female ovulatory cycle.
MeSH term(s)	Animals ; Cell Movement ; DNA Methylation/drug effects ; Endocrine Disruptors/pharmacology ; Environmental Exposure ; Epigenesis, Genetic/drug effects ; Estradiol/metabolism ; Feedback, Physiological/drug effects ; Female ; GABA Agents/metabolism ; Germ Cells/metabolism ; Glutamic Acid/metabolism ; Gonadotropin-Releasing Hormone/drug effects ; Gonadotropin-Releasing Hormone/metabolism ; Histone Code/drug effects ; Humans ; Hypothalamus/cytology ; Hypothalamus/drug effects ; Hypothalamus/growth & development ; Hypothalamus/metabolism ; Kisspeptins/metabolism ; Male ; Neurons/drug effects ; Neurons/metabolism ; Ovulation/drug effects ; Ovulation/metabolism ; Pregnancy ; Prenatal Exposure Delayed Effects
Chemical Substances	Endocrine Disruptors ; GABA Agents ; Kisspeptins ; Gonadotropin-Releasing Hormone (33515-09-2) ; Glutamic Acid (3KX376GY7L) ; Estradiol (4TI98Z838E)
Language	English
Publishing date	2020-12-07
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2489381-X
ISSN	1759-5037 ; 1759-5029
ISSN (online)	1759-5037
ISSN	1759-5029
DOI	10.1038/s41574-020-00436-3
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Article: Perinatal exposure to the fungicide ketoconazole alters hypothalamic control of puberty in female rats.

Franssen, Delphine / Johansson, Hanna K L / Lopez-Rodriguez, David / Lavergne, Arnaud / Terwagne, Quentin / Boberg, Julie / Christiansen, Sofie / Svingen, Terje / Parent, Anne-Simone

Frontiers in endocrinology

2023 Volume 14, Page(s) 1140886

Abstract: Introduction: Estrogenic endocrine disrupting chemicals (EDCs) such as diethylstilbestrol (DES) are known to alter the timing of puberty onset and reproductive function in females. Accumulating evidence suggests that steroid synthesis inhibitors such as ...

Abstract	Introduction: Estrogenic endocrine disrupting chemicals (EDCs) such as diethylstilbestrol (DES) are known to alter the timing of puberty onset and reproductive function in females. Accumulating evidence suggests that steroid synthesis inhibitors such as ketoconazole (KTZ) or phthalates may also affect female reproductive health, however their mode of action is poorly understood. Because hypothalamic activity is very sensitive to sex steroids, we aimed at determining whether and how EDCs with different mode of action can alter the hypothalamic transcriptome and GnRH release in female rats. Design: Female rats were exposed to KTZ or DES during perinatal (DES 3-6-12μg/kg.d; KTZ 3-6-12mg/kg.d), pubertal or adult periods (DES 3-12-48μg/kg.d; KTZ 3-12-48mg/kg.d). Results: Ex vivo study of GnRH pulsatility revealed that perinatal exposure to the highest doses of KTZ and DES delayed maturation of GnRH secretion before puberty, whereas pubertal or adult exposure had no effect on GnRH pulsatility. Hypothalamic transcriptome, studied by RNAsequencing in the preoptic area and in the mediobasal hypothalamus, was found to be very sensitive to perinatal exposure to all doses of KTZ before puberty with effects persisting until adulthood. Bioinformatic analysis with Ingenuity Pathway Analysis predicted "Creb signaling in Neurons" and "IGF-1 signaling" among the most downregulated pathways by all doses of KTZ and DES before puberty, and "PPARg" as a common upstream regulator driving gene expression changes. Deeper screening ofRNAseq datasets indicated that a high number of genes regulating the activity of the extrinsic GnRH pulse generator were consistently affected by all the doses of DES and KTZ before puberty. Several, including MKRN3, DNMT3 or Cbx7, showed similar alterations in expression at adulthood. Conclusion: nRH secretion and the hypothalamic transcriptome are highly sensitive to perinatal exposure to both DES and KTZ. The identified pathways should be exploredfurther to identify biomarkers for future testing strategies for EDC identification and when enhancing the current standard information requirements in regulation.
MeSH term(s)	Pregnancy ; Rats ; Animals ; Female ; Fungicides, Industrial/metabolism ; Fungicides, Industrial/pharmacology ; Ketoconazole/pharmacology ; Sexual Maturation/physiology ; Hypothalamus/metabolism ; Gonadotropin-Releasing Hormone/metabolism
Chemical Substances	Fungicides, Industrial ; Ketoconazole (R9400W927I) ; Gonadotropin-Releasing Hormone (33515-09-2)
Language	English
Publishing date	2023-04-03
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2592084-4
ISSN	1664-2392
ISSN	1664-2392
DOI	10.3389/fendo.2023.1140886
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Article ; Online: Perinatal exposure to known endocrine disrupters alters ovarian development and systemic steroid hormone profile in rats.

Boberg, Julie / Johansson, Hanna K L / Franssen, Delphine / Cramer, Johannah H / Usai, Diana / Pedersen, Mikael / Parent, Anne-Simone / Svingen, Terje

Toxicology

2021 Volume 458, Page(s) 152821

Abstract: Disrupted ovarian development induced by chemical exposure may impair fertility later in life. Since androgens are essential for early ovarian development, we speculated that perinatal exposure to a binary mixture of the known anti-androgens DEHP and ... ...

Abstract	Disrupted ovarian development induced by chemical exposure may impair fertility later in life. Since androgens are essential for early ovarian development, we speculated that perinatal exposure to a binary mixture of the known anti-androgens DEHP and procymidone could alter steroid synthesis, disrupt ovarian follicle recruitment and ultimately maturation in female rat offspring. Wistar rat dams were exposed by oral gavage from gestation day 7 to postnatatal day 22 to two mixture doses known to alter reproductive development in male offspring (low: 10 mg/kg bw/day of procymidone and 30 mg/kg bw/day of DEHP; high: 20 mg/kg bw/day of procymidone and 60 mg/kg bw/day of DEHP). The Effects on plasma steroid hormones, ovarian follicle distribution and expression of markers related to steroid synthesis were examined in female offspring. In prepubertal offspring, we observed an increased number of newly recruited (primary) follicles in exposed animals compared to controls, and the plasma steroid hormone profile was altered by exposure: levels of progesterone, corticosterone and estrone were dose dependently elevated, whereas androgen levels were unaffected. In adulthood, a trend towards a smaller number of early-stage follicles may point to accelerated loss of follicle reserves, which is disconcerting. The changes in follicle distribution in exposed ovaries may reflect the combined influence of androgen receptor antagonism and altered ovarian steroid synthesis. This study adds to a growing body of evidence showing altered ovarian development following exposure to human relevant chemicals with possible severe consequences for female fertility.
MeSH term(s)	Animals ; Animals, Newborn ; Dose-Response Relationship, Drug ; Endocrine Disruptors/toxicity ; Female ; Fertility/drug effects ; Gene Expression Regulation ; Gonadal Steroid Hormones/metabolism ; Male ; Ovarian Follicle ; Ovary/drug effects ; Ovary/growth & development ; Pregnancy ; Prenatal Exposure Delayed Effects/metabolism ; Rats ; Rats, Wistar ; Steroids/metabolism
Chemical Substances	Endocrine Disruptors ; Gonadal Steroid Hormones ; Steroids
Language	English
Publishing date	2021-05-27
Publishing country	Ireland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	184557-3
ISSN	1879-3185 ; 0300-483X
ISSN (online)	1879-3185
ISSN	0300-483X
DOI	10.1016/j.tox.2021.152821
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Article ; Online: A Putative Adverse Outcome Pathway Network for Disrupted Female Pubertal Onset to Improve Testing and Regulation of Endocrine Disrupting Chemicals.

Franssen, Delphine / Svingen, Terje / Lopez Rodriguez, David / Van Duursen, Majorie / Boberg, Julie / Parent, Anne-Simone

Neuroendocrinology

2021 Volume 112, Issue 2, Page(s) 101–114

Abstract: The average age for pubertal onset in girls has declined over recent decades. Epidemiological studies in humans and experimental studies in animals suggest a causal role for endocrine disrupting chemicals (EDCs) that are present in our environment. Of ... ...

Abstract	The average age for pubertal onset in girls has declined over recent decades. Epidemiological studies in humans and experimental studies in animals suggest a causal role for endocrine disrupting chemicals (EDCs) that are present in our environment. Of concern, current testing and screening regimens are inadequate in identifying EDCs that may affect pubertal maturation, not least because they do not consider early-life exposure. Also, the causal relationship between EDC exposure and pubertal timing is still a matter of debate. To address this issue, we have used current knowledge to elaborate a network of putative adverse outcome pathways (pAOPs) to identify how chemicals can affect pubertal onset. By using the AOP framework, we highlight current gaps in mechanistic understanding that need to be addressed and simultaneously point towards events causative of pubertal disturbance that could be exploited for alternative test methods. We propose 6 pAOPs that could explain the disruption of pubertal timing by interfering with the central hypothalamic trigger of puberty, GnRH neurons, and by so doing highlight specific modes of action that could be targeted for alternative test method development.
MeSH term(s)	Adverse Outcome Pathways ; Endocrine Disruptors/adverse effects ; Female ; Humans ; Puberty, Precocious/chemically induced ; Puberty, Precocious/metabolism
Chemical Substances	Endocrine Disruptors
Language	English
Publishing date	2021-02-26
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	123303-8
ISSN	1423-0194 ; 0028-3835
ISSN (online)	1423-0194
ISSN	0028-3835
DOI	10.1159/000515478
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