Seminal Levels of Omentin-1/ITLN1 in Inflammatory Conditions Related to Male Infertility and Localization in Spermatozoa and Tissues of Male Reproductive System

Moretti, Elena; Signorini, Cinzia; Noto, Daria; Tripodi, Sergio; Menchiari, Andrea; Sorrentino, Ester; Collodel, Giulia

doi:10.2147/jir.s339515

Cited by 4 publications

(1 citation statement)

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“…It modulates insulin resistance by increasing the expression of uncoupling proteins in adipose tissue and decreasing the levels of adiponectin [ 62 , 63 ]. Omentin-1 seems to have an anti-inflammatory and antioxidative action [ 64 ]. Levels of omentin-1/intelectin, like adiponectin, decrease with insulin resistance, BMI, and adiposity [ 62 , 65 ].…”

Section: Endocrine Changesmentioning

confidence: 99%

The Molecular Basis of Male Infertility in Obesity: A Literature Review

George,

Jhancy,

Dube

et al. 2023

IJMS

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The rising incidence of obesity has coincided with rising levels of poor reproductive outcomes. The molecular basis for the association of infertility in obese males is now being explained through various mechanisms. Insulin resistance, hyperglycemia, and changes in serum and gonadal concentrations of adipokines, like leptin, adiponectin, resistin, and ghrelin have been implicated as causes of male infertility in obese males. The effects of obesity and hypogonadism form a vicious cycle whereby dysregulation of the hypothalamic–pituitary–testicular axis—due to the effect of the release of multiple mediators, thus decreasing GnRH release from the hypothalamus—causes decreases in LH and FSH levels. This leads to lower levels of testosterone, which further increases adiposity because of increased lipogenesis. Cytokines such as TNF-α and interleukins, sirtuins, and other inflammatory mediators like reactive oxygen species are known to affect fertility in obese male adults. There is evidence that parental obesity can be transferred through subsequent generations to offspring through epigenetic marks. Thus, negative expressions like obesity and infertility have been linked to epigenetic marks being altered in previous generations. The interesting aspect is that these epigenetic expressions can be reverted by removing the triggering factors. These positive modifications are also transmitted to subsequent generations.

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Section: Endocrine Changesmentioning

confidence: 99%

The Molecular Basis of Male Infertility in Obesity: A Literature Review

George,

Jhancy,

Dube

et al. 2023

IJMS

View full text Add to dashboard Cite

show abstract

Genes and Pathways Underpinning Klinefelter Syndrome at Bulk and Single-Cell Levels

Tian,

Yu,

Mao

et al. 2024

Biochem Genet

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Klinefelter syndrome (KS) is the most frequent genetic anomaly in infertile males. Despite this, the molecular mechanisms involved in KS are poorly de ned. Based on bulk transcriptome and single-cell RNA sequencing datasets with peripheral blood monocyte (PBMC) sample(s) from healthy and KS men, this study was designed to address critical genes and pathways correlated with the occurrence of KS.Through a comparison between control and KS samples, we obtained 5 hub genes, including two upregulated genes (XG and ITLN1) and three downregulated genes (DEFA4, BPI and MPO). Without exception, these ve genes yielded an excellent discriminatory capacity for KS with an area under the receiver-operator-characteristic curve over 0.75. We also assessed between-group differences of immune cell in ltration using ssGSEA. In ltrated degree of some immune cells such as CD56 bright NK cell was found to be positively associated with the expression of ITLN1 and XG. Through Kyoto Encyclopedia of Genes and Genomes enrichment, we identi ed PI3K/AKT pathway and neuroactive ligand-receptor interaction as upregulated pathways for KS. Gene set enrichment analysis together with gene set variation analysis con rmed upregulation of G2M checkpoint, mitotic spindle, and heme metabolism for KS. Furthermore, scRNA-seq data analysis was conducted to detect intercellular communication between different immune cell types, and a strong correlation was detected for macrophages, dendritic cells or NK cells with the other cell types. Collectively, we provided hub genes, pathways, immune cell in ltration degree, and cell-cell communication interactions for KS, warranting novel insights into the mechanisms of KS.

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