Adipokines: A gear shift in puberty

Nieuwenhuis, Desirée; Pujol‐Gualdo, Natàlia; Arnoldussen, Ilse A.C.; Kiliaan, Amanda J.

doi:10.1111/obr.13005

Cited by 66 publications

(45 citation statements)

References 80 publications

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“…Some epidemiological studies have found sex related differences but do not show a consistent pattern since some of the studies find associations in boys whereas others do in girls [37,38]. It is also possible that boys have a different response to a proinflammatory diet at a similar age since boys start sexual development later than girls and that adiposity distribution is different, being the third adipose rebound first in girls (10 years) than in boys (11-12 years) [39,40]. Other factors such as the effects of hormones and fetal and early-life exposures could determine later gender dependent responses as suggested by animal models and some epidemiological studies [3,[41][42][43].…”

Section: Discussionmentioning

confidence: 99%

Pro-Inflammatory Diet Is Associated with Adiposity during Childhood and with Adipokines and Inflammatory Markers at 11 Years in Mexican Children

et al. 2020

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There is limited evidence about the inflammatory potential of diet in children. The aim of this study was to evaluate the association between the Children’s Dietary Inflammatory Index (C-DII) from 5 to 11 years with adiposity and inflammatory biomarkers in Mexican children. We analyzed 726 children from a birth cohort study with complete dietary information and measurements to evaluate adiposity at 5, 7 and 11 y and 286 children with IL-6, hsCRP, leptin and adiponectin information at 11 y. C-DII trajectories were estimated using latent class linear mixed models. We used linear mixed models for adiposity and logistic and multinomial regression for biomarkers. In girls, each one-point increase in C-DII score was associated with greater adiposity (abdominal-circumference 0.41%, p = 0.03; skinfold-sum 1.76%, p = 0.01; and BMI Z-score 0.05, p = 0.01). At 11 y the C-DII was associated with greater leptin (34% ≥ 13.0 ng/mL, p = 0.03) and hsCRP concentrations (29% ≥ 3.00 mg/L, p = 0.06) and lower adiponectin/leptin ratio (75% < 2.45, p = 0.02). C-DII trajectory 3 in boys was associated with a 75.2% (p < 0.01) increase in leptin concentrations and a 37.9% decrease (p = 0.02) in the adiponectin/leptin ratio. This study suggests that the inflammatory potential of diet may influence adiposity in girls and the homeostasis of adipose tissue and chronic subclinical inflammation in 11-year-old children.

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Section: Discussionmentioning

confidence: 99%

Pro-Inflammatory Diet Is Associated with Adiposity during Childhood and with Adipokines and Inflammatory Markers at 11 Years in Mexican Children

et al. 2020

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“…Leptin is implicated with the onset of puberty and related disorders in human females [ 139 ]. Leptin also directly or indirectly regulates GnRH secretion through Kisspeptin neurons [ 140 , 141 , 142 , 143 ]. It is not difficult to propose that estrogen signaling genes might impact heifer fertility and therefore could be proposed as both positional and functional candidate genes.…”

Section: Discussionmentioning

confidence: 99%

Meta-Analysis of Heifer Traits Identified Reproductive Pathways in Bos indicus Cattle

Tahir

Porto-Neto

Gondro

et al. 2021

Genes

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Fertility traits measured early in life define the reproductive potential of heifers. Knowledge of genetics and biology can help devise genomic selection methods to improve heifer fertility. In this study, we used ~2400 Brahman cattle to perform GWAS and multi-trait meta-analysis to determine genomic regions associated with heifer fertility. Heifer traits measured were pregnancy at first mating opportunity (PREG1, a binary trait), first conception score (FCS, score 1 to 3) and rebreeding score (REB, score 1 to 3.5). The heritability estimates were 0.17 (0.03) for PREG1, 0.11 (0.05) for FCS and 0.28 (0.05) for REB. The three traits were highly genetically correlated (0.75–0.83) as expected. Meta-analysis was performed using SNP effects estimated for each of the three traits, adjusted for standard error. We identified 1359 significant SNPs (p-value < 9.9 × 10−6 at FDR < 0.0001) in the multi-trait meta-analysis. Genomic regions of 0.5 Mb around each significant SNP from the meta-analysis were annotated to create a list of 2560 positional candidate genes. The most significant SNP was in the vicinity of a genomic region on chromosome 8, encompassing the genes SLC44A1, FSD1L, FKTN, TAL2 and TMEM38B. The genomic region in humans that contains homologs of these genes is associated with age at puberty in girls. Top significant SNPs pointed to additional fertility-related genes, again within a 0.5 Mb region, including ESR2, ITPR1, GNG2, RGS9BP, ANKRD27, TDRD12, GRM1, MTHFD1, PTGDR and NTNG1. Functional pathway enrichment analysis resulted in many positional candidate genes relating to known fertility pathways, including GnRH signaling, estrogen signaling, progesterone mediated oocyte maturation, cAMP signaling, calcium signaling, glutamatergic signaling, focal adhesion, PI3K-AKT signaling and ovarian steroidogenesis pathway. The comparison of results from this study with previous transcriptomics and proteomics studies on puberty of the same cattle breed (Brahman) but in a different population identified 392 genes in common from which some genes—BRAF, GABRA2, GABR1B, GAD1, FSHR, CNGA3, PDE10A, SNAP25, ESR2, GRIA2, ORAI1, EGFR, CHRNA5, VDAC2, ACVR2B, ORAI3, CYP11A1, GRIN2A, ATP2B3, CAMK2A, PLA2G, CAMK2D and MAPK3—are also part of the above-mentioned pathways. The biological functions of the positional candidate genes and their annotation to known pathways allowed integrating the results into a bigger picture of molecular mechanisms related to puberty in the hypothalamus–pituitary–ovarian axis. A reasonable number of genes, common between previous puberty studies and this study on early reproductive traits, corroborates the proposed molecular mechanisms. This study identified the polymorphism associated with early reproductive traits, and candidate genes that provided a visualization of the proposed mechanisms, coordinating the hypothalamic, pituitary, and ovarian functions for reproductive performance in Brahman cattle.

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“…It is noteworthy that girls with obesity enter puberty at younger ages than girls with normal weight [ 98 ]. The adipokines leptin and adiponectin may play a role in the inverse association between menarche onset and weight status by modulating the hypothalamic–pituitary–gonadal axis [ 99 ]. Briefly, leptin activates the hypothalamus through secretion of the hormone kisspeptin to secrete gonadotropin releasing hormone.…”

Section: Adipose Tissue Developmentmentioning

confidence: 99%

“…This hormone then activates the pituitary gland to produce follicle stimulating hormone and luteinizing hormone, resulting in the secretion of estrogen by the ovaries and, consequently, menarche onset. On the other hand, adiponectin inhibits the secretion of gonadotropin releasing hormone and delays puberty onset [ 99 ].…”

Section: Adipose Tissue Developmentmentioning

confidence: 99%

Adipose Tissue Development and Expansion from the Womb to Adolescence: An Overview

et al. 2020

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Prevalence rates of pediatric obesity continue to rise worldwide. Adipose tissue (AT) development and expansion initiate in the fetus and extend throughout the lifespan. This paper presents an overview of the AT developmental trajectories from the intrauterine period to adolescence; factors determining adiposity expansion are also discussed. The greatest fetal increases in AT were observed in the third pregnancy trimester, with growing evidence suggesting that maternal health and nutrition, toxin exposure, and genetic defects impact AT development. From birth up to six months, healthy term newborns experience steep increases in AT; but a subsequent reduction in AT is observed during infancy. Important determinants of AT in infancy identified in this review included feeding practices and factors shaping the gut microbiome. Low AT accrual rates are maintained up to puberty onset, at which time, the pattern of adiposity expansion becomes sex dependent. As girls experience rapid increases and boys experience decreases in AT, sexual dimorphism in hormone secretion can be considered the main contributor for changes. Eating patterns/behaviors and interactions between dietary components, gut microbiome, and immune cells also influence AT expansion. Despite the plasticity of this tissue, substantial evidence supports that adiposity at birth and infancy highly influences its levels across subsequent life stages. Thus, a unique window of opportunity for the prevention and/or slowing down of the predisposition toward obesity, exists from pregnancy through childhood.

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Adipokines: A gear shift in puberty

Cited by 66 publications

References 80 publications

Pro-Inflammatory Diet Is Associated with Adiposity during Childhood and with Adipokines and Inflammatory Markers at 11 Years in Mexican Children

Pro-Inflammatory Diet Is Associated with Adiposity during Childhood and with Adipokines and Inflammatory Markers at 11 Years in Mexican Children

Meta-Analysis of Heifer Traits Identified Reproductive Pathways in Bos indicus Cattle

Adipose Tissue Development and Expansion from the Womb to Adolescence: An Overview

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