Testosterone Levels and Development of the Penile Spines and Testicular Tissue during the Postnatal Growth in Wistar Rats

Aim of Study: Gonadal hormones exert a profound influence on the development, structure and function of the sexual organs. The testosterone is one of the androgens that plays an essential role in the development of sexual organs in male mammals. Therefore, the present study was undertaken to evaluate the testosterone levels and developmental pattern of the penile spines and seminiferous tubules during early postnatal life of Wistar rats. Methods and Materials: At 7, 14, 21, 28, 35, 42, 49, 56, 63 and 70 days after birth, penile and testicular tissues of male rats were dissected out and fixed for histological study and plasma testosterone levels were determined using high resolution chromatography. Results: An increase in the number of penile follicles, primarily in the distal region of the penis, was observed from postnatal days 14 to 42, followed by a gradual decrease. Penile spines were absent from birth until the first growth peak, which was observed at 42 postnatal days. Both testicular weight and the area of seminiferous tubules showed gradual increases before achieving their highest values at 42 postnatal days. Similarly, a gradual increase in testosterone levels was detected from day 28, with a peak at 42 postnatal days. Conclusions: These data show a temporal association between the development of the penile spines and testicular tissue with gradual increases in testosterone levels. These results may contribute to a better understanding of the behavioral, hormonal and morphological changes underlying sexual maturation in male rats.

Abnormal adipose tissue-derived microbes drive metabolic disorder and exacerbate postnatal growth retardation in piglet

Postnatal growth retardation(PGR)frequently occurs during early postnatal development of piglets and induces high mortality.To date,the mechanism of PGR remains poorly understood.Adipose tissue-derived microbes have been documented to be associated with several disorders of metabolism and body growth.However,the connection between microbial disturbance of adipose tissue and pig PGR remains unclear.Here,we investigated piglets with PGR and found that the adipose tissue of PGR piglets was charac-terized by metabolism impairment,adipose abnormality,and specific enrichment of culturable bacteria from Proteobacteria.Gavage of Sphingomonas paucimobilis,a species of Sphingomonas genus from the alphaproteobacteria,induced PGR in piglets.Moreover,this bacterium could also lead to metabolic disorders and susceptibility to acute stress,resulting in weight loss in mice.Mechanistically,multi-omics analysis indicated the changes in lipid metabolism as a response of adipose tissue to abnormal microbial composition.Further experimental tests proved that one of the altered lipids phosphatidylethanolamines could rescue the metabolism disorder and growth retardation,thereby suppressing the amount of Sphingomonas in the adipose tissue.Together,these results highlight that the microbe–host crosstalk may regulate the metabolic function of adipose tissue in response to PGR.

The Effect of Electromagnetic Fields with the Mg2+ Cyclotron Frequency on Mouse Reproductive Performance

The present study is aimed to test whether exposure to electromagnetic fields of very weak intensity (≤1 mT) and low frequency (≤100 Hz) may influence reproductive performance and induce teratogenesis in mice. We speculate that a resonant effect occur when the applied frequency matches the cyclotron frequency of Mg2+ (≈60 Hz) involved in the cell duplication. Four groups of mice (four dams and one male each) were exposed to ?50 μT electromagnetic field continuous irradiation of for 100 days. A control group (four dams and one male) was also examined. The exposed dams exhibited a significantly lower number of offspring per birth than the control ones (11.0 vs. 11.6;P = 0.006). A significantly lower average daily gain of body weight per mouse was observed (0.74 vs. 0.77 g/d;P = 0.002), resulting in a reduction of the average body weight per nest at 11 days of age (404 vs. 463 g;P = 0.048). Post mortem examinations revealed a significant increase in mild chronic hepatic inflammatory findings (28 vs. 0%;P = 0.001) in the offspring and myocardial hypertrophy (25 vs. 0%;P = 0.023) in the dams. The exposure of mice to an electromagnetic field with the cyclotron frequency of Mg2+ during pregnancy caused a measurable effect on the reproductive performance in terms of offspring per birth. This finding may be considered as a warning about the environmental effects of the electromagnetic fields on the stability of individual species and ecosystems.

LRP6 Bidirectionally Regulates Insulin Sensitivity through Insulin Receptor and S6K Signaling in Rats with CG-IUGR

Objective Intrauterine growth restriction followed by postnatal catch-up growth(CG-IUGR)increases the risk of insulin resistance-related diseases.Low-density lipoprotein receptor-related protein 6(LRP6)plays a substantial role in glucose metabolism.However,whether LRP6 is involved in the insulin resistance of CG-IUGR is unclear.This study aimed to explore the role of LRP6 in insulin signaling in response to CG-IUGR.Methods The CG-IUGR rat model was established via a maternal gestational nutritional restriction followed by postnatal litter size reduction.The mRNA and protein expression of the components in the insulin pathway,LRP6/β-catenin and mammalian target of rapamycin(mTOR)/S6 kinase(S6K)signaling,was determined.Liver tissues were immunostained for the expression of LRP6 andβ-catenin.LRP6 was overexpressed or silenced in primary hepatocytes to explore its role in insulin signaling.Results Compared with the control rats,CG-IUGR rats showed higher homeostasis model assessment for insulin resistance(HOMA-IR)index and fasting insulin level,decreased insulin signaling,reduced mTOR/S6K/insulin receptor substrate-1(IRS-1)serine307 activity,and decreased LRP6/β-catenin in the liver tissue.The knockdown of LRP6 in hepatocytes from appropriate-for-gestational-age(AGA)rats led to reductions in insulin receptor(IR)signaling and mTOR/S6K/IRS-1 serine307 activity.In contrast,LRP6 overexpression in hepatocytes of CG-IUGR rats resulted in elevated IR signaling and mTOR/S6K/IRS-1 serine307 activity.Conclusion LRP6 regulated the insulin signaling in the CG-IUGR rats via two distinct pathways,IR and mTOR-S6K signaling.LRP6 may be a potential therapeutic target for insulin resistance in CG-IUGR individuals.