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1.
J Dev Orig Health Dis ; 12(2): 286-292, 2021 04.
Article in English | MEDLINE | ID: mdl-32345396

ABSTRACT

Alterations in the maternal environment may impact on the fetal development. The objective of this study was to investigate the gastrointestinal consequences of maternal hypothyroidism for the male offspring from Wistar rats. The pregnant rats were divided into three groups: control (C - received water), experimental 1 [E1 - received methimazole (MMI) solution] during gestation and lactation, and experimental 2 (E2 - received MMI solution) during gestation. Maternal parameters evaluated: free T3 and T4, bodyweight variation, and water/food intake. Offspring parameters evaluated: litter size, number of male/female, free T3 and T4, stomach area, gastric ulcer susceptibility, small intestine length and weight, small intestine and distal colon motility, the stomach and intestinal weight-body weight ratio (SW/BW-IW/BW), and the accumulation of intestinal fluid. Maternal T3 and T4 from E1 were decreased when compared to the other groups. There were no differences for maternal water/food intake and weight gain, litter size, and number of males and females. Regarding to offspring, free T3, SW/BW, IW/BW, and intestinal fluid accumulation were not different between the groups, but T4 was decreased in E1. However, 30-day-old pups from E1 and E2 were smaller with lower stomach and small intestine. Even more, E1 presented a lower ulcer index when compared to the C, while E2 had a higher distal colon transit. It can be concluded that maternal hypothyroidism impaired the total body development, as well as gastric and intestinal development, besides interfering with the susceptibility to the ulcer and intestinal transit of male offspring from Wistar rats.


Subject(s)
Gastrointestinal Motility , Hypothyroidism/complications , Maternal Exposure/adverse effects , Stomach Ulcer/pathology , Animals , Animals, Newborn , Female , Male , Pregnancy , Rats , Rats, Wistar , Stomach Ulcer/etiology
2.
Cell Biol Int ; 43(4): 373-383, 2019 Apr.
Article in English | MEDLINE | ID: mdl-30353973

ABSTRACT

Recent studies have been trying to find out how diet and metabolic changes such as dyslipidaemia, hyperglycaemia, and hyperinsulinaemia can stimulate cancer progression. This investigation aimed to evaluate the effect of high concentrations of fatty acids and/or glucose in tumour prostate cells, focusing on the proliferation/migration profile and oxidative stress. PC3 cells were treated with high concentration of saturated fatty acid (palmitate, 100 µM), glucose (220 mg/dL), or both for 24 or 48 h. Results demonstrated that PC3 cells showed a significant increase in proliferation after 48 h of treatment with glucose and palmitate+glucose. Cell proliferation was associated with reduced levels of AMPK phosphorylation in glucose group at 24 and 48 h of treatment, while palmitate group presented this result only after 48 h of treatment. Also, there was a significant increase in cell migration between time 0 and 48 h after all treatments, except in the control. Catalase activity was increased by palmitate in the beginning of treatment, while glucose presented a later effect. Also, nitrite production was increased by glucose only after 48 h, and the total antioxidant activity was enhanced by palmitate in the initial hours. Thus, we conclude that the high concentration of the saturated fatty acid palmitate and glucose in vitro influences PC3 cells and stimulates cellular activities related to carcinogenesis such as cell proliferation, migration, and oxidative stress in different ways. Palmitate presents a rapid and initial effect, while a glucose environment stimulates cells later on, maintaining high levels of cell proliferation.


Subject(s)
Glucose/metabolism , Palmitates/metabolism , Prostatic Neoplasms/metabolism , Cell Movement/drug effects , Cell Proliferation/drug effects , Fatty Acids/metabolism , Glucose/adverse effects , Glucose/physiology , Humans , Hyperinsulinism/metabolism , Insulin/metabolism , Male , PC-3 Cells/drug effects , Palmitates/pharmacology , Phosphorylation , Prostate/metabolism
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