Testicular fat deposition attenuates reproductive performance via decreased follicle-stimulating hormone level and sperm meiosis and testosterone synthesis in mouse
2
조회
0
다운로드
0
인용
0
참고문헌
키워드
초록
Objective: Testicular fat deposition has been reported to affect animal reproduction. However, the underlying mechanism remains poorly understood. The present study explored whether sperm meiosis and testosterone synthesis contribute to mouse testicular fat depositioninduced reproductive performance.Methods: High fat diet (HFD)-induced obesity CD1 mice (DIO) were used as a testicular fat deposition model. The serum hormone test was performed by agent kit. The quality of sperm was assessed using a Sperm Class Analyzer. Testicular tissue morphology was analyzed by histochemical methods. The expression of spermatocyte marker molecules was monitored by an immuno-fluorescence microscope during meiosis. Analysis of the synthesis of testosterone was performed by real-time polymerase chain reaction and reagent kit.Results: It was found that there was a significant increase in body weight among DIO mice, however, the food intake showed no difference compared to control mice fed a normal diet (CTR). The number of offspring in DIO mice decreased, but there was no significant difference from the CTR group. The levels of follicle-stimulating hormone were lower in DIO mice and their luteinizing hormone levels were similar. The results showed a remarkable decrease in sperm density and motility among DIO mice. We also found that fat accumulation affected the meiosis process, mainly reflected in the cross-exchange of homologous chromosomes. In addition, overweight increased fat deposition in the testis and reduced the expression of testosterone synthesis-related enzymes, thereby affecting the synthesis and secretion of testosterone by testicular Leydig cells.Conclusion: Fat accumulation in the testes causes testicular cell dysfunction, which affects testosterone hormone synthesis and ultimately affects sperm formation.
Abstract
Objective: Testicular fat deposition has been reported to affect animal reproduction. However, the underlying mechanism remains poorly understood. The present study explored whether sperm meiosis and testosterone synthesis contribute to mouse testicular fat depositioninduced reproductive performance. Methods: High fat diet (HFD)-induced obesity CD1 mice (DIO) were used as a testicular fat deposition model. The serum hormone test was performed by agent kit. The quality of sperm was assessed using a Sperm Class Analyzer. Testicular tissue morphology was analyzed by histochemical methods. The expression of spermatocyte marker molecules was monitored by an immuno-fluorescence microscope during meiosis. Analysis of the synthesis of testosterone was performed by real-time polymerase chain reaction and reagent kit. Results: It was found that there was a significant increase in body weight among DIO mice, however, the food intake showed no difference compared to control mice fed a normal diet (CTR). The number of offspring in DIO mice decreased, but there was no significant difference from the CTR group. The levels of follicle-stimulating hormone were lower in DIO mice and their luteinizing hormone levels were similar. The results showed a remarkable decrease in sperm density and motility among DIO mice. We also found that fat accumulation affected the meiosis process, mainly reflected in the cross-exchange of homologous chromosomes. In addition, overweight increased fat deposition in the testis and reduced the expression of testosterone synthesis-related enzymes, thereby affecting the synthesis and secretion of testosterone by testicular Leydig cells. Conclusion: Fat accumulation in the testes causes testicular cell dysfunction, which affects testosterone hormone synthesis and ultimately affects sperm formation.
참고문헌 (37)
- Pini T, "Obesity and male reproduction; placing the western diet in context", Front Endocrinol(Lausanne), 12, pp.622292~ (2021)[DOI]
- Schwander B, "Replication of published health economic obesity models : assessment of facilitators, hurdles and reproduction success", Pharmacoeconomics, 39, pp.433~446 (2021)[DOI]
- Piche ME, "Obesity phenotypes, diabetes, and cardiovascular diseases", Circ Res, 126, pp.1477~1500 (2020)[DOI]
- Luo R, "Possible role of GnIH as a novel link between hyperphagia-induced obesity-related metabolic derangements and hypogonadism in male mice", Int J Mol Sci, 23, pp.8066~ (2022)[DOI]
- Yi X, "Effects of obesity and exercise on testicular leptin signal transduction and testosterone biosynthesis in male mice", Am J Physiol Regul Integr Comp Physiol, 312, pp.R501~R510 (2017)[DOI]
- Deshpande SS, "Genetically inherited obesity and high-fat diet–induced obesity differentially alter spermatogenesis in adult male rats", Endocrinology, 160, pp.220~234 (2019)[DOI]
- Ye L, "Inhibitors of testosterone biosynthetic and metabolic activation enzymes", Molecules, 16, pp.9983~10001 (2011)[DOI]
- Khodamoradi K, "The role of leptin and low testosterone in obesity", Int J Impot Res, 34, pp.704~713 (2022)[DOI]
- Krause BR, "Adipose tissue and cholesterol metabolism", J Lipid Res, 25, pp.97~110 (1984)
- Du FM, "Effects of thyroid hormone and depression on common components of central obesity", J Int Med Res, 47, pp.3040~3049 (2019)[DOI]
- Akpovi CD, "The predominance of one of the SR-BI isoforms is associated with increased esterified cholesterol levels not apoptosis in mink testis", J Lipid Res, 47, pp.2233~2247 (2006)[DOI]
- Ghanayem BI, "Dietinduced obesity in male mice is associated with reduced fertility and potentiation of acrylamide-induced reproductive toxicity", Biol Reprod, 82, pp.96~104 (2010)[DOI]
- Craig JR, "Obesity, male infertility, and the sperm epigenome", Fertil Steril, 107, pp.848~859 (2017)[DOI]
- Katib A, "Mechanisms linking obesity to male infertility", Cent European J Urol, 68, pp.79~85 (2015)[DOI]
- Khodamoradi K, "The role of leptin and obesity on male infertility", Curr Opin Urol, 30, pp.334~339 (2020)[DOI]
- Staub C, "Review : Spermatogenesis in the bull", Animal, 12(s1), pp.s27~s35 (2018)[DOI]
- Hess RA, "Spermatogenesis and cycle of the seminiferous epithelium", Adv Exp Med Biol, 636, pp.1~15 (2008)[DOI]
- Bhalla N, "Meiosis : Is spermatogenesis stress an opportunity for evolutionary innovation?", Curr Biol, 30, pp.R1471~R1473 (2020)[DOI]
- Nishimura H, "Spermatogenesis", Curr Biol, 27, pp.R988~R994 (2017)[DOI]
- O'Donnell L, "Testosterone promotes the conversion of round spermatids between stages VII and VIII of the rat spermatogenic cycle", Endocrinology, 135, pp.2608~2614 (1994)[DOI]
- Baker SM, "Involvement of mouse Mlh1 in DNA mismatch repair and meiotic crossing over", Nat Genet, 13, pp.336~342 (1996)[DOI]
- Liu YJ, "Degradation of the separasecleaved Rec8, a meiotic cohesin subunit, by the N-end rule pathway", J Biol Chem, 291, pp.7426~7438 (2016)[DOI]
- Song Y, "Loss of circSRY reduces gammaH2AX level in germ cells and impairs mouse spermatogenesis", Life Sci Alliance, 6, pp.e202201617~ (2023)[DOI]
- Liang H, "Homeostatic control of pololike kinase-1 engenders non-genetic heterogeneity in G2checkpoint fidelity and timing", Nat Commun, 5, pp.4048~ (2014)[DOI]
- Teerds KJ, "Functional relationship between obesity and male reproduction : from humans to animal models", Hum Reprod Update, 17, pp.667~683 (2011)[DOI]
- Carvalho MG, "Effects of obesity and diabetes on sperm cell proteomics in rats", J Proteome Res, 20, pp.2628~2642 (2021)[DOI]
- Li QL, "Quantification of testicular fat deposition in the evaluation of middle-aged overweight male infertility", MAGMA, 33, pp.377~384 (2020)[DOI]
- Amiri M, "Potential adverse effects of female and male obesity on fertility : a narrative review", Int J Endocrinol Metab, 18, pp.e101776~ (2020)[DOI]
- Martini AC, "Obesity and male fertility", Rev Fac Cien Med Univ Nac Cordoba, 69, pp.102~110 (2012)
- Tortoriello DV, "Dietary-induced obesity and hypothalamic infertility in female DBA", 2J mice, 2004, pp.145, 1238~1247
- Jedrzejczak P, "Prediction of spontaneous conception based on semen parameters", Int J Androl, 31, pp.499~507 (2008)[DOI]
- Wang S, "LncRNA Tug1 maintains blood–testis barrier integrity by modulating Ccl2 expression in high-fat diet mice", Cell Mol Life Sci, 79, pp.114~ (2022)[DOI]
- Chu DS, "Spermatogenesis", Adv Exp Med Biol, 757, pp.171~203 (2013)[DOI]
- Kostic TS, "Pharmacological doses of testosterone upregulated androgen receptor and 3-Beta-hydroxysteroid dehydrogenase", delta-5-delta-4 isomerase and impaired leydig cells steroidogenesis in adult rats, 2011, pp.121, 397~407
- Motohashi M, "In utero-exposed di(n-butyl)phthalate induce dose dependent, age-related changes of morphology and testosterone-biosynthesis enzymes", associated proteins of Leydig cell mitochondria in rats, 2016, pp.41, 195~206
- Choi Y, "Amodiaquine promotes testosterone production and de novo synthesis of cholesterol and triglycerides in Leydig cells", J Lipid Res, 62, pp.100152~ (2021)[DOI]
- Wang X, "HIF 1 inhibits StAR transcription and testosterone synthesis in murine Leydig cells", J Mol Endocrinol, 62, pp.1~13 (2018)[DOI]
