Role of hormonal and inflammatory alterations in obesity-related reproductive dysfunction at the level of the hypothalamic-pituitary-ovarian axis

Goldsammler, Michelle; Merhi, Zaher; Büyük, Erkan

doi:10.1186/s12958-018-0366-6

Cited by 71 publications

(65 citation statements)

References 179 publications

(186 reference statements)

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“…The energy homeostasis related to the leptin was proven to altering ovulation. The normal leptin homeostasis is required for normal physiologic functions at the level of the hypothalamus and the ovaries . These functions include the regulation of sex steroids which is critical in female reproduction.…”

Section: Discussionmentioning

confidence: 99%

“…The normal leptin homeostasis is required for normal physiologic functions at the level of the hypothalamus and the ovaries. 34 These functions include the regulation of sex steroids which is critical in female reproduction. For example, E2 which is secreted by granulosa cells plays an important role in maintaining the menstrual cycle.…”

Section: F I G U R E 4 Effects Of Melatoninmentioning

confidence: 99%

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Leptin mediates the effects of melatonin on female reproduction in mammals

Tan

Zhu

et al. 2019

Journal of Pineal Research

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Melatonin is a natural molecule produced in the pineal gland and other tissues. It participates in numerous biological activities including the regulation of reproduction. However, the mechanism by which melatonin affects mammalian female reproductive performance is not fully investigated. In the present study, it was observed that melatonin positively regulated the level of leptin in female mouse and pig. To understand the potential association between melatonin and leptin on the female reproductive activities, the melatonin receptor 1 MT1 knockout (MT1−/−) mouse and Leptin knockout (Leptin−/−) pig were created. It was found that the deficiency of M T1 caused low leptin secretion and litter size in mouse. Meanwhile, the deletion of leptin in pig did not affect melatonin production, but significantly reduced follicle‐stimulating hormone, estradiol‐17β (E2), and Luteinizing hormone and increased progesterone (P) at estrum stage, which also led to smaller litter size than that in control. Melatonin treatment increased the production of leptin in pigs, while the supplementary of leptin was also able to improve the ovulation number, polar body rates, and expression of StAR in MT1−/− females. Therefore, it is first time, we described that leptin is the downstream target of melatonin in regulating female reproduction. These findings provide the novel information on the physiology of melatonin in animal reproduction.

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Section: Discussionmentioning

confidence: 99%

Section: F I G U R E 4 Effects Of Melatoninmentioning

confidence: 99%

Leptin mediates the effects of melatonin on female reproduction in mammals

Tan

Zhu

et al. 2019

Journal of Pineal Research

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“…As a matter of fact, the GnRH secretion (and therefore the reproductive function) is influenced by various substances involved in the energy homeostasis regulation and/or in the adaptive response to stress. The main known substances and neuroendocrine networks involved in functional hypothalamic amenorrhea are the following: activation of the hypothalamic-pituitary-adrenal axis with production of CRH and cortisol, which reduces the pulsatile GnRH secretion in stressful conditions; reduced levels of leptin, a hormone normally produced by adipose tissue in the case of energy abundance, able to reduce appetite and food intake, to stimulate energy expenditure, and indirectly (through central GABA and kisspeptin neurons) to increase the GnRH pulsatility, this effect being lacking in case of caloric deprivation with little leptin produced; increased levels of ghrelin, a orexigenic enterokine produced by the stomach, which can decrease both GnRH secretion and pulsatility in the hypothalamus, possibly through NPY neurons (Goldsammler et al 2018).…”

Section: Hypothalamic Amenorrheamentioning

confidence: 99%

“…Then, also a low quality of the oocytes produced is described. Moreover, chronic inflammation typical of obese patients has been hypothesized to directly affect ovarian function by increased macrophage infiltration in the ovaries through pro-inflammatory molecules like advanced glycation end products (AGEs) and monocyte chemotactic protein-1 (MCP-1) (Goldsammler et al 2018;Talmor and Dunphy 2014).…”

Section: Obesitymentioning

confidence: 99%

Infertility

Marca¹,

Mastellari²

2020

Endocrinology

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cause that impairs reproductive organs anatomy, ovarian reserve, or hypothalamic-pituitary-ovarian axis can cause infertility. However, in 15-30% of patients, infertility remains unexplained. 2-3% of couples are able to conceive but experience a recurrent pregnancy loss, a condition that impair fecundity as well as chances of childbearing, although this condition is not properly included in the infertility definition.

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“…Mutations causing infertility through obesity tend to be related to insufficient hypothalamo-pituitary-gonadal drive during the development of reproductive organs. The involvement of hypothalamic-pituitary dysfunction in obesity-related reproductive failure has been well described [ 14 ].…”

mentioning

confidence: 99%

Overaccumulation of Fat Caused Rapid Reproductive Senescence but not Loss of Ovarian Reserve in ob/ob Mice

Mollah

Yang

Jeon

et al. 2020

Journal of the Endocrine Society

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Ovarian reserve and fertility are reduced by aging and a poor energy balance. To date, the relationships of high energy accumulation and aging with the ovarian reserve have not been elucidated. Here, the effects of obesity on the aging ovarian reserve were evaluated in a leptin-deficient (ob/ob) mouse model. Abnormal estrous cyclicity appeared as early as 6 wks and worsened with aging. The blood level patterns of 17β-estradiol (E2), testosterone (T), and progesterone (P4) with aging were similar between lean and ob/ob mice. The blood level of E2 but not P4 or T was similar at 24 wks. Many more atretic follicles but fewer corpora lutea were observed in ob/ob mice than in lean mice within all age groups. Anti-Müllerian hormone (Amh) mRNA levels were similar between genotypes. Dazl, Stra8, and ZP3 mRNAs were highly expressed in ob/ob mice after 12 wks. Sohlh1 and Ybx2 mRNAs were highly expressed at 24 wks in ob/ob compared with lean mice. In addition, SOHLH1-positive primordial follicle counts were significantly increased in ob/ob mice at 24 wks. The proportions of AMH-positive secondary and small antral follicles were similar between genotypes. Together, these results show that the ovarian reserve lasts longer in ob/ob mice than in lean mice, suggesting that the loss of normal physiological or physical status causes decreased fertility at a young age in ob/ob mice and that an increase in adipocytes without leptin as in ob/ob mice, can improve the ovarian reserve. Such knowledge can be applied to understanding reproductive dysfunction.

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Role of hormonal and inflammatory alterations in obesity-related reproductive dysfunction at the level of the hypothalamic-pituitary-ovarian axis

Cited by 71 publications

References 179 publications

Leptin mediates the effects of melatonin on female reproduction in mammals

Leptin mediates the effects of melatonin on female reproduction in mammals

Infertility

Overaccumulation of Fat Caused Rapid Reproductive Senescence but not Loss of Ovarian Reserve in ob/ob Mice

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