Impact of Neonatal Manipulation of Androgen Receptor Function on Endocrine-Metabolic Programming in the Juvenile Female Rat

Ongaro, Luisina; Giovambattista, Andrés; Spinedi, Eduardo

doi:10.1155/2013/181950

Cited by 6 publications

(6 citation statements)

References 30 publications

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“…There were long-term changes in metabolic parameters in response to neonatal androgenization, as previously reported [ 73 , 74 ]. Although body weight and glycemia were slightly increased at PND90 in androgenized females, the most drastic effects were observed on circulating leptin and IL1β levels, which rose above normal female values.…”

Section: Discussionsupporting

confidence: 78%

Age and sex dependent effects of early overnutrition on metabolic parameters and the role of neonatal androgens

et al. 2016

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BackgroundMales and females respond differently to diverse metabolic situations. Being raised in a small litter is reported to cause overnutrition that increases weight gain and predisposes an individual to metabolic disturbances in adulthood; however, existing data are inconsistent. Indeed, significant weight gain and/or metabolic disturbances, such as hyperinsulinemia and hyperleptinemia, are sometimes not encountered. We hypothesized that these inconsistencies could be due to the animal’s sex and/or age at which metabolic parameters are measured.MethodsTo analyze the effects of neonatal overnutrition, male and female Wistar rats were raised in litters of 4 or 12 pups/dam and killed at postnatal days (PND) 10, 21, 30, 50, 85, or 150. In a second study to determine if neonatal sex steroid levels influence sex differences in metabolic parameters, female rats were treated with testosterone on PND1. Effects on weight, length, fat pads, adipokine production, and serum levels of glucose, metabolic hormones, and cytokines were analyzed in both studies.ResultsBy PND10, both males and females raised in small litters had increased body weight, body length, adiposity, and serum glucose, insulin, leptin, and adiponectin levels. Females had a greater increase in inguinal fat, and males had higher expression of leptin messenger RNA (mRNA) and serum insulin, as well as increased testosterone levels. Most of the litter size effects diminished or disappeared after weaning and reappeared during adulthood in males, with sex differences in body size and adiposity being apparent postpubertally. Treatment of females with testosterone on PND1 tended to masculinize some metabolic parameters in adulthood such as increased body weight and serum leptin levels.ConclusionsOur results indicate that (1) both sex and age determine the response to neonatal overnutrition; (2) differences in neonatal sex steroid levels may participate in the development of sex differences in metabolic parameters in adulthood and possibly in the response to neonatal overnutrition; and (3) the comparison of circulating hormone and cytokine levels, even in normal control animals, should take into consideration the early neonatal nutritional environment.

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Section: Discussionsupporting

confidence: 78%

Age and sex dependent effects of early overnutrition on metabolic parameters and the role of neonatal androgens

et al. 2016

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“…Interestingly, PMAT mass was greater in TP than in CT rats, even after normalizing individual pad mass by the corresponding BW (Table 2). According to a previous finding [15], the latter difference correlated well with plasma leptin concentrations, being significantly higher in TP than in CT animals ( Table 2). Conversely, plasma concentrations of 17OHP4 were significantly lower in TP than in CT rats ( Table 2).…”

Section: The Juvenile Rat Phenotypesupporting

confidence: 78%

“…We have previously [15] found that TP rats grow faster than CT rats after being followed up between 21 (weaning) and 30 days of age. We now found that 30-day-old TP-treated rats were significantly heavier than CT rats ( Table 2).…”

Section: The Juvenile Rat Phenotypementioning

confidence: 97%

Neonatal androgenization-induced early endocrine–metabolic and ovary misprogramming in the female rat

et al. 2015

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Our results strongly suggest that transient neonatal hyperandrogenemia induced early misprogramming of metabolic-endocrine and ovarian (steroidogenesis/folliculogenesis) functions. Conversely, TP rats preserved their ovary GC endocrine function. Our results further support the high risk of developing ovarian hyperstimulation syndrome for infertile women with transient/chronic hyperandrogenemia (PCOS) subjected to assisted reproductive technologies.

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“…Collectively, these data indicate that early treatment with testosterone increases susceptibility to MS [ 36 ] development and, conversely, that flutamide treatment improves this condition. These observations strongly support that testosterone exerts specific receptor-mediated effects [ 37 ], the androgen receptor being expressed in both white adipocytes and APCs [ 38 ]. However, the level of androgen receptor expression differs among WAT depots.…”

Section: Cooperative Effect Of Androgens On White Adipose Tissue Dsupporting

confidence: 65%

The Polycystic Ovary Syndrome and the Metabolic Syndrome: A Possible Chronobiotic-Cytoprotective Adjuvant Therapy

Spinedi

Cardinali

2018

International Journal of Endocrinology

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Polycystic ovary syndrome is a highly frequent reproductive-endocrine disorder affecting up to 8–10% of women worldwide at reproductive age. Although its etiology is not fully understood, evidence suggests that insulin resistance, with or without compensatory hyperinsulinemia, and hyperandrogenism are very common features of the polycystic ovary syndrome phenotype. Dysfunctional white adipose tissue has been identified as a major contributing factor for insulin resistance in polycystic ovary syndrome. Environmental (e.g., chronodisruption) and genetic/epigenetic factors may also play relevant roles in syndrome development. Overweight and/or obesity are very common in women with polycystic ovary syndrome, thus suggesting that some polycystic ovary syndrome and metabolic syndrome female phenotypes share common characteristics. Sleep disturbances have been reported to double in women with PCOS and obstructive sleep apnea is a common feature in polycystic ovary syndrome patients. Maturation of the luteinizing hormone-releasing hormone secretion pattern in girls in puberty is closely related to changes in the sleep-wake cycle and could have relevance in the pathogenesis of polycystic ovary syndrome. This review article focuses on two main issues in the polycystic ovary syndrome-metabolic syndrome phenotype development: (a) the impact of androgen excess on white adipose tissue function and (b) the possible efficacy of adjuvant melatonin therapy to improve the chronobiologic profile in polycystic ovary syndrome-metabolic syndrome individuals. Genetic variants in melatonin receptor have been linked to increased risk of developing polycystic ovary syndrome, to impairments in insulin secretion, and to increased fasting glucose levels. Melatonin therapy may protect against several metabolic syndrome comorbidities in polycystic ovary syndrome and could be applied from the initial phases of patients' treatment.

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Impact of Neonatal Manipulation of Androgen Receptor Function on Endocrine-Metabolic Programming in the Juvenile Female Rat

Cited by 6 publications

References 30 publications

Age and sex dependent effects of early overnutrition on metabolic parameters and the role of neonatal androgens

Age and sex dependent effects of early overnutrition on metabolic parameters and the role of neonatal androgens

Neonatal androgenization-induced early endocrine–metabolic and ovary misprogramming in the female rat

The Polycystic Ovary Syndrome and the Metabolic Syndrome: A Possible Chronobiotic-Cytoprotective Adjuvant Therapy

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