scholarly journals Late reproductive analysis in rat male offspring exposed to nicotine during pregnancy and lactation

Andrology ◽  
2016 ◽  
Vol 4 (2) ◽  
pp. 218-231 ◽  
Author(s):  
M. Miranda-Spooner ◽  
C. C. Paccola ◽  
F. M. O. Neves ◽  
S. U. de Oliva ◽  
S. M. Miraglia
Keyword(s):  
Male Offspring ◽  
Pregnancy And Lactation ◽  
Reproductive Analysis

scholarly journals Altered Gut Microbiota and Its Metabolites in Hypertension of Developmental Origins: Exploring Differences between Fructose and Antibiotics Exposure

2021 ◽  
Vol 22 (5) ◽  
pp. 2674
Author(s):  
Chien-Ning Hsu ◽  
Julie Y. H. Chan ◽  
Kay L. H. Wu ◽  
Hong-Ren Yu ◽  
Wei-Chia Lee ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Negative Impact ◽  
Short Chain Fatty Acids ◽  
Normal Diet ◽  
Male Offspring ◽  
Sprague Dawley ◽  
Minocycline Treatment ◽  
High Fructose ◽  
Induced Hypertension ◽  
Pregnancy And Lactation

Gut microbiota-derived metabolites, in particular short chain fatty acids (SCFAs) and their receptors, are linked to hypertension. Fructose and antibiotics are commonly used worldwide, and they have a negative impact on the gut microbiota. Our previous study revealed that maternal high-fructose (HF) diet-induced hypertension in adult offspring is relevant to altered gut microbiome and its metabolites. We, therefore, intended to examine whether minocycline administration during pregnancy and lactation may further affect blood pressure (BP) programmed by maternal HF intake via mediating gut microbiota and SCFAs. Pregnant Sprague-Dawley rats received a normal diet or diet containing 60% fructose throughout pregnancy and lactation periods. Additionally, pregnant dams received minocycline (50 mg/kg/day) via oral gavage or a vehicle during pregnancy and lactation periods. Four groups of male offspring were studied (n = 8 per group): normal diet (ND), high-fructose diet (HF), normal diet + minocycline (NDM), and HF + minocycline (HFM). Male offspring were killed at 12 weeks of age. We observed that the HF diet and minocycline administration, both individually and together, causes the elevation of BP in adult male offspring, while there is no synergistic effect between them. Four groups displayed distinct enterotypes. Minocycline treatment leads to an increase in the F/B ratio, but decreased abundance of genera Lactobacillus, Ruminococcus, and Odoribacter. Additionally, minocycline treatment decreases plasma acetic acid and butyric acid levels. Hypertension programmed by maternal HF diet plus minocycline exposure is related to the increased expression of several SCFA receptors. Moreover, minocycline- and HF-induced hypertension, individually or together, is associated with the aberrant activation of the renin–angiotensin system (RAS). Conclusively, our results provide a new insight into the support of gut microbiota and its metabolite SCAFs in the developmental programming of hypertension and cast new light on the role of RAS in this process, which will help prevent hypertension programmed by maternal high-fructose and antibiotic exposure.

scholarly journals Increased exposure to sodium during pregnancy and lactation changes basal and induced behavioral and neuroendocrine responses in adult male offspring

2017 ◽  
Vol 5 (6) ◽  
pp. e13210 ◽  
Author(s):  
Marcia S. Silva ◽  
Fabiana Lúcio-Oliveira ◽  
Andre Souza Mecawi ◽  
Lucas F. Almeida ◽  
Silvia G. Ruginsk ◽  
...  
Keyword(s):  
Adult Male ◽  
Male Offspring ◽  
Pregnancy And Lactation ◽  
Neuroendocrine Responses

scholarly journals Lactiplantibacillus plantarum WJL administration during pregnancy and lactation improves lipid profile, insulin sensitivity and gut microbiota diversity in dyslipidemic dams and protects male offspring against cardiovascular dysfunction in later life

2020 ◽  
Vol 11 (10) ◽  
pp. 8939-8950
Author(s):  
Keyth Sulamitta de Lima Guimarães ◽  
Valdir de Andrade Braga ◽  
Sylvana I. S. Rendeiro de Noronha ◽  
Whyara Karoline Almeida da Costa ◽  
Kassem Makki ◽  
...  
Keyword(s):  
Insulin Sensitivity ◽  
Gut Microbiota ◽  
Lipid Profile ◽  
Later Life ◽  
Male Offspring ◽  
Cardiovascular Dysfunction ◽  
Pregnancy And Lactation ◽  
Microbiota Diversity

Lactiplantibacillus plantarum WJL administration during pregnancy and lactation improves gut microbiota diversity.

Maternal undernutrition during pregnancy and lactation affects testicular morphology, the stages of spermatogenic cycle, and the testicular IGF-I system in adult offspring

2020 ◽  
Vol 11 (5) ◽  
pp. 473-483 ◽  
Author(s):  
Graciela Pedrana ◽  
Helen Viotti ◽  
Paula Lombide ◽  
Daniel Cavestany ◽  
Graeme B. Martin ◽  
...  
Keyword(s):  
Male Offspring ◽  
Standard Diet ◽  
Adult Offspring ◽  
Ki 67 ◽  
Maternal Undernutrition ◽  
Control Frequency ◽  
Igf I ◽  
Testicular Morphology ◽  
Pregnancy And Lactation ◽  
Diet Control

AbstractMaternal undernutrition decreases sperm production in male offspring, possibly through insulin-like growth factor (IGF-I). To test this hypothesis, we fed pregnant Wistar rats ad libitum with a standard diet (CONTROL) or fed 50% of CONTROL intake, either throughout pregnancy (UNP), lactation (UNL, or both (UNPL). After weaning, male offspring (n = 10 per treatment) were fed a standard diet until postnatal day 160, when testes process for histological and molecular analyses. IGF-I immunostaining area and intensity in the testis were greater (P = 0.003) in the UNPL group compared to CONTROL, but lower in the UNP group (P < 0.0001). Levels of IGF-I receptor transcript were lower in the UNPL and UNL groups, compared to CONTROL. There were more Ki-67-positive germ and Sertoli cells, in all underfed groups than in CONTROL. Compared to CONTROL, frequency of spermatogenic cycle stage VII was lower in all underfed groups, and seminiferous tubule diameter was smaller in UNP and UNPL. Plasma FSH concentrations were greater in UNP male offspring compared to all groups (P = 0.05), whereas inhibin B concentrations were greater in UNP (P = 0.01) and UNL (P = 0.003) than in CONTROL or UNPL. Thus, prenatal undernutrition leads to a decrease in testicular IGF-I levels, whereas of pre- and postnatal undernutrition increased testicular IGF-I levels and decreased amounts of IGF-I receptor mRNA in adult offspring. We conclude that maternal undernutrition during pregnancy and lactation leads to long-lasting effects on adult male offspring testicular morphology, spermatogenesis, and IGF-I testicular system.

Pre and postnatal exposure to endosulfan in Wistar rats

2003 ◽  
Vol 22 (4) ◽  
pp. 171-175 ◽  
Author(s):  
Paulo R Dalsenter ◽  
Samanta L deAraújo ◽  
Helena C da Silva de Assis ◽  
Anderson JM Andrade ◽  
Eliane Dallegrave
Keyword(s):  
Adverse Effects ◽  
Sexual Development ◽  
Wistar Rats ◽  
Outcome Data ◽  
Male Offspring ◽  
Postnatal Exposure ◽  
Pregnancy And Lactation ◽  
Testis Descent ◽  
Dose Levels ◽  
Daily Sperm Production

The possible reproductive adverse effects of the pesticide endosulfan on male offspring rats exposed in utero and during lactation were investigated. Dams were treated orally with 0, 0.5 or 1.5 mg of endosulfan/kg 21 days prior to mating, during the mating, pregnancy and lactation. Maternal and reproductive outcome data and male sexual development landmarks (testis descent and preputial separation) were assessed. Reproductive endpoints of the male offspring were examined at adulthood: sex organ weights, daily sperm production, spermatid number, sperm transit, sperm morphology and testosterone level. No signs of maternal toxicity were detected at the dose levels tested. Sexual development landmarks were also unaffected. Moreover, with the exception of a significant increase in the relative epididymis weight seen in the group treated with the lowest dose, we have not found any statistically significant adverse effect in the reproductive endpoints investigated at adulthood. The results of the present study indicate that pre and post-natal exposure to low doses of endosulfan (0.5 and 1.5 mg/kg) do not induce significant adverse effects in the reproductive system of male offspring Wistar rats at adulthood.

Altered regulation of hepatic glucose output in the male offspring of protein-malnourished rat dams

1996 ◽  
Vol 270 (4) ◽  
pp. E559-E564 ◽  
Author(s):  
S. E. Ozanne ◽  
G. D. Smith ◽  
J. Tikerpae ◽  
C. N. Hales
Keyword(s):  
Glucose Transporter ◽  
Insulin Binding ◽  
Hormonal Control ◽  
Male Offspring ◽  
Insulin Degradation ◽  
Hepatic Glucose Output ◽  
Low Protein ◽  
Hepatic Glucose ◽  
Pregnancy And Lactation ◽  
Glucose Output

Offspring of protein-malnourished rat dams have permanent alterations in hepatic enzyme activities associated with glucose homeostasis. Hormonal control of hepatic glucose output (HGO) was studied in male offspring of dams fed either a 20% (control) or 8% (low protein) protein diet during pregnancy and lactation. Glucagon (210 pM) stimulated HGO significantly more (P < 0.04) in controls (from 0.72 +/- 0.11 to 3.18 +/- 0.30 mumol.min-1.g liver-1) compared with low-protein animals (from 0.53 +/- 0.11 to 2.05 +/- 0.24 mumol.min-1.g liver-1). Insulin (1 nM) decreased (P < 0.001) HGO in controls to 2.39 +/- 0.37 mumol.min-1.g liver-1 after 10 min but increased HGO (to 2.82 +/- 0.40 mumol.min-1.g liver-1; P < 0.04) in low-protein rats. There were fivefold fewer (P = 0.01) glucagon receptors but a threefold increase (P < 0.05) in hepatic insulin receptor number in the low-protein rats, which was reflected by increased in insulin degradation (P < 0.001). The glucose transporter GLUT-2 was also raised threefold in the low-protein group (P < 0.001). The anomalous response to insulin indicates changes in its metabolic signaling, but normal insulin binding suggests that this alteration is a postreceptor event.

scholarly journals Maternal N-Acetylcysteine Therapy Prevents Hypertension in Spontaneously Hypertensive Rat Offspring: Implications of Hydrogen Sulfide-Generating Pathway and Gut Microbiota

Antioxidants ◽  
2020 ◽  
Vol 9 (9) ◽  
pp. 856 ◽  
Author(s):  
Chien-Ning Hsu ◽  
Chih-Yao Hou ◽  
Guo-Ping Chang-Chien ◽  
Sufan Lin ◽  
You-Lin Tain
Keyword(s):  
Drinking Water ◽  
Hydrogen Sulfide ◽  
Gut Microbiota ◽  
Spontaneously Hypertensive Rat ◽  
Later Life ◽  
Male Offspring ◽  
Protective Effects ◽  
Male Adult ◽  
Spontaneously Hypertensive ◽  
Pregnancy And Lactation

Hypertension can come from early life. N-acetylcysteine (NAC), a hydrogen sulfide (H2S) precursor as well as an antioxidant, has antihypertensive effect. We investigated whether maternal NAC therapy can protect spontaneously hypertensive rats (SHR) male offspring against hypertension. The pregnant rats were assigned to four groups: SHRs without treatment; Wistar Kyoto (WKY) without treatment; SHR+NAC, SHRs received 1% NAC in drinking water throughout pregnancy and lactation; and, WKY+NAC, WKY rats received 1% NAC in drinking water during pregnancy and lactation. Male offspring (n = 8/group) were killed at 12 weeks of age. Maternal NAC therapy prevented the rise in systolic blood pressure (BP) in male SHR offspring at 12 weeks of age. Renal cystathionine β-synthase (CBS) and 3-mercaptopyruvate sulphurtransferase (3MST) protein levels and H2S-releasing activity were increased in the SHR+NAC offspring. Maternal NAC therapy increased fecal H2S and thiosulfate levels in the SHR+NAC group. Additionally, maternal NAC therapy differentially shaped gut microbiota and caused a distinct enterotype in each group. The protective effect of maternal NAC therapy against hypertension in SHR offspring is related to increased phylum Actinobacteria and genera Bifidobacterium and Allobaculum, but decreased phylum Verrucomicrobia, genera Turicibacter, and Akkermansia. Several microbes were identified as microbial markers, including genera Bifidobacterium, Allobaculum, Holdemania, and Turicibacter. Our results indicated that antioxidant therapy by NAC in pregnant SHRs can prevent the developmental programming of hypertension in male adult offspring. Our findings highlight the interrelationships among H2S-generating pathway in the kidneys and gut, gut microbiota, and hypertension. The implications of maternal NAC therapy elicited long-term protective effects on hypertension in later life that still await further clinical translation.

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