scholarly journals Effects of Gestational Diabetes in Cognitive Behavior, Oxidative Stress and Metabolism on the Second-Generation Off-Spring of Rats

Nutrients ◽  
2021 ◽  
Vol 13 (5) ◽  
pp. 1575
Author(s):  
Maribel Huerta-Cervantes ◽  
Donovan J. Peña-Montes ◽  
Miguel Ángel López-Vázquez ◽  
Rocío Montoya-Pérez ◽  
Christian Cortés-Rojo ◽  
...  

Gestational diabetes (GD) has a negative impact on neurodevelopment, resulting in cognitive and neurological deficiencies. Oxidative stress (OS) has been reported in the brain of the first-generation offspring of GD rats. OS has been strongly associated with neurodegenerative diseases. In this work, we determined the effect of GD on the cognitive behavior, oxidative stress and metabolism of second-generation offspring. GD was induced with streptozotocin (STZ) in pregnant rats to obtain first-generation offspring (F1), next female F1 rats were mated with control males to obtain second-generation offspring (F2). Two and six-month-old F2 males and females were employed. Anxious-type behavior, spatial learning and spatial working memory were evaluated. In cerebral cortex and hippocampus, the oxidative stress and serum biochemical parameters were measured. Male F2 GD offspring presented the highest level of anxiety-type behavior, whilst females had the lowest level of anxiety-type behavior at juvenile age. In short-term memory, adult females presented deficiencies. The offspring F2 GD females presented modifications in oxidative stress biomarkers in the cerebral cortex as lipid-peroxidation, oxidized glutathione and catalase activity. We also observed metabolic disturbances, particularly in the lipid and insulin levels of male and female F2 GD offspring. Our results suggest a transgenerational effect of GD on metabolism, anxiety-like behavior, and spatial working memory.

2020 ◽  
Vol 34 (S1) ◽  
pp. 1-1
Author(s):  
Maribel Huerta-Cervantes ◽  
Donovan J. Peña-Montes ◽  
Salvador Manzo-Avalos ◽  
Rafael Salgado-Garciglia ◽  
Christian Cortés-Rojo ◽  
...  

Nutrients ◽  
2020 ◽  
Vol 12 (2) ◽  
pp. 376
Author(s):  
Maribel Huerta-Cervantes ◽  
Donovan J. Peña-Montes ◽  
Rocío Montoya-Pérez ◽  
Xóchitl Trujillo ◽  
Miguel Huerta ◽  
...  

Gestational diabetes (GD) has been linked with an increased risk of developing metabolic disorders and behavioral abnormalities in the offspring. Oxidative stress is strongly associated with neurodegeneration and cognitive disruption. In the offspring brains in a GD experimental rat model, increased oxidative stress in the prenatal and postnatal stages was reported. However, long-term alterations to offspring behavior and oxidative stress, caused by changes in the cerebral cortex and hippocampus, remain unclear. In this study, we evaluated the effect of GD on young and adult male and female rat offspring in metabolic parameters, cognitive behavior, and oxidative stress. GD was induced using streptozotocin in dams. Next, the offspring were evaluated at two and six months of age. Anxiety-like behavior was evaluated using the elevated plus maze and open field maze; spatial learning and short-term memory were evaluated using the Morris water maze and radial maze, respectively. We determined oxidative stress biomarkers (reactive oxygen species (ROS), lipid peroxidation and glutathione status) and antioxidant enzymes (superoxide dismutase and catalase) in the brain of offspring. We observed that male GD offspring showed a reduced level of anxiety at both ages as they spent less time in the closed arms of the elevated plus maze at adult age ((P = 0.019, d = 1.083 ( size effect)) and spent more time in the open area of an open field (P = 0.0412, d = 0.743) when young and adult age (P = 0.018, d = 0.65). Adult female GD offspring showed a reduced level of anxiety (P = 0.036; d = 0.966), and young female GD offspring showed a deficiency in spatial learning (P = 0.0291 vs. control, d = 3.207). Adult male GD offspring showed a deficiency in short-term memory (P = 0.017, d = 1.795). We found an increase in ROS and lipid peroxidation, a disruption in the glutathione status, and decreased activity of catalase and superoxide dismutase (P < 0.05 vs. control, d > 1.0), in the cerebral cortex and hippocampus of male and female GD offspring. GD altered metabolism; male offspring of both ages and adult females showed a high level of triglycerides and a lower level of high-density lipoprotein-cholesterol (P < 0.05 vs. control, d > 1.0). Young and adult female offspring displayed higher insulin levels (P < 0.05, d > 1.0). These results suggest that gestational diabetes modifies oxidative stress and cognitive behavior in an age- and sex-dependent manner.


2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Sachie Sasaki-Hamada ◽  
Masaatsu Ikeda ◽  
Jun-Ichiro Oka

Abstract Glucagon-like peptide 2 (GLP-2) is derived from the proglucagon gene expressed in the intestines, pancreas and brain. Our previous study showed that GLP-2 improved lipopolysaccharide-induced memory impairments. The current study was designed to further investigated the potential of GLP-2 in memory impairment induced by intracerebroventricular administration of streptozotocin (ICV-STZ) in mice, which have been used as an animal model of sporadic Alzheimer’s disease (AD). STZ was administered on alternate days (Day-1 and Day-3) in order to induce dementia in male ddY mice. ICV-STZ-treated mice were administered GLP-2 (0.6 μg/mouse, ICV) for 5 days from 14 days after the first ICV administration of STZ. In these mice, we examined spatial working memory, the biochemical parameters of oxidative stress, or neurogenesis. The GLP-2 treatment restored spatial working memory in ICV-STZ-treated mice. ICV-STZ-treated mice showed markedly increased thiobarbituric acid reactive species (TBARS) and decreased glutathione (GSH) levels, and GLP-2 significantly restored these ICV-STZ-induced changes. GLP-2 also significantly restored neurogenesis in the subgranular zone of the dentate gyrus in ICV-STZ-treated mice. We herein demonstrated that GLP-2 significantly restored ICV-STZ-induced memory impairments as well as biochemical and histopathological alterations, and accordingly, propose that the memory restorative ability of GLP-2 is due to its potential to reduce oxidative stress.


2007 ◽  
Vol 92 (3) ◽  
pp. 583-589 ◽  
Author(s):  
James A. Armitage ◽  
Asuka Ishibashi ◽  
Aswini A. Balachandran ◽  
Runa I. Jensen ◽  
Lucilla Poston ◽  
...  

2016 ◽  
Vol 33 (S1) ◽  
pp. s286-s286
Author(s):  
A. Sevastre-Berghian ◽  
V. Făgărăşăn ◽  
N. Decea ◽  
R. Moldovan ◽  
B. Sevastre ◽  
...  

IntroductionCurcumin (CUR), a polyphenolic compound, extracted from Curcuma longa, is known for its neuroprotective, antioxidant and anti-inflammatory effects.ObjectivesTo evaluate the effect of CUR on ambulatory activity, spatial working memory and on oxidative stress in rats induced by Diazepam (DZP) administration.AimsTo analyze whether CUR may improve the cognitive performance and offer systemic protection from oxidative stress.MethodsThe effect of CUR on DZP-induced memory impairment and oxidative stress was studied on Wistar rats. Group I received a vehicle, group II – vehicle and CUR, group III – vehicle and DZP, group IV – vehicle, CUR and DZP. CUR (150 mg/kg bw) and vehicle were orally administered for five weeks long. DZP (2 mg/kg bw) was administered i.p. 20 minutes before the behavioral tests. Behavioral tests, i.e. Open Field and Y Maze Test, were performed. Malondialdehyde and reduced glutathione/oxidized glutathione ratio were determined in the serum and brain tissue homogenate. Hippocampal sections were histologically assessed. The data were statistically analyzed by one-way ANOVA, followed by Dunns post-test.ResultsDZP decreased (P < 0.01) the number of spontaneous alternations, as compared to control group, thus suggesting an impairment of spatial working memory. Behavioral tests revealed no enhancing effect of CUR on spontaneous alternation behaviors in Y Maze. CUR reversed (P < 0.01) the inhibitory effect of diazepam (P < 0.05) on the ambulatory activity in OFT and decreased the lipid peroxidation in the serum (P < 0.05).ConclusionsThe results show that CUR may offer systemic protection from oxidative stress, thus improving the cognitive performance.Disclosure of interestThe authors have not supplied their declaration of competing interest.


2016 ◽  
Author(s):  
Aviva M Stein ◽  
Melanie J. Young ◽  
John Darby ◽  
Philip John Seddon ◽  
Yolanda van Heezik

Longitudinal studies focusing on lifetime reproductive success (LRS) have been used to measure individual breeding performance and identify commonalities among successful breeders. By extending the focus to subsequent generations we identify a proportion of high-quality individuals that contribute disproportionately to the population over multiple generations. We used 23 years of yellow-eyed penguin (Megadyptes antipodes) breeding data from one breeding area to identify the proportion of individual birds that raised successful breeders, which in turn raised offspring that bred successfully. We explored which life-history components influenced lifetime reproductive success, as this knowledge would enable conservation resources to be focused on high-performing individuals in this endangered population. From 2147 birds marked as chicks, 370 (17.2%) survived to adulthood and recruited to their natal location, of which 219 (10.2%) fledged offspring: 124 (56.6%) of the 219 birds produced offspring that recruited as breeders. Only 102 birds (4.8% of 2147) fledged first-generation offspring that in turn fledged offspring (second-generation offspring, or grand-offspring). We found that c. 26% of the birds that survived to breed had above-average LRS as well as above-average numbers of grand-offspring, and were more likely to have produced first-generation chicks that recruited and also produced above-average numbers of second-generation chicks. Our findings suggest that there is a core of “super-breeders” that contribute disproportionately to the population over successive generations. Lifespan and age-at-first-breeding were correlated with LRS. We suggest that traits of birds relating to longevity, health (e.g. immunocompetence) and fitness could be examined to identify potential links with high LRS and inter-generational fecundity. “Super-breeders” appear to consistently balance high LRS with long- life-span in a stochastic environment, demonstrating greater resilience in the face of extreme events.


2019 ◽  
Vol 359 ◽  
pp. 910-917 ◽  
Author(s):  
Ingryd Fortes Souza Lipaus ◽  
Elisa Fraga Gomes ◽  
Cleciane Waldetário Martins ◽  
Cristina Martins e Silva ◽  
Rita Gomes Wanderley Pires ◽  
...  

2020 ◽  
Vol 13 (12) ◽  
pp. 457
Author(s):  
Giuseppe Caruso ◽  
Margherita Grasso ◽  
Annamaria Fidilio ◽  
Fabio Tascedda ◽  
Filippo Drago ◽  
...  

Recent studies suggest a primary role of oxidative stress in an early phase of the pathogenesis of schizophrenia and a strong neurobiological link has been found between dopaminergic system dysfunction, microglia overactivation, and oxidative stress. Different risk factors for schizophrenia increase oxidative stress phenomena raising the risk of developing psychosis. Oxidative stress induced by first-generation antipsychotics such as haloperidol significantly contributes to the development of extrapyramidal side effects. Haloperidol also exerts neurotoxic effects by decreasing antioxidant enzyme levels then worsening pro-oxidant events. Opposite to haloperidol, second-generation antipsychotics (or atypical antipsychotics) such as risperidone, clozapine, and olanzapine exert a strong antioxidant activity in experimental models of schizophrenia by rescuing the antioxidant system, with an increase in superoxide dismutase and glutathione (GSH) serum levels. Second-generation antipsychotics also improve the antioxidant status and reduce lipid peroxidation in schizophrenic patients. Interestingly, second-generation antipsychotics, such as risperidone, paliperidone, and in particular clozapine, reduce oxidative stress induced by microglia overactivation, decreasing the production of microglia-derived free radicals, finally protecting neurons against microglia-induced oxidative stress. Further, long-term clinical studies are needed to better understand the link between oxidative stress and the clinical response to antipsychotic drugs and the therapeutic potential of antioxidants to increase the response to antipsychotics.


Antioxidants ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 1710
Author(s):  
Dhondup Namgyal ◽  
Sher Ali ◽  
Muhammad Delwar Hussain ◽  
Mohsin Kazi ◽  
Ajaz Ahmad ◽  
...  

Age-related neurodegenerative diseases and vascular dementia are major challenges to the modern health care system. Most neurodegenerative diseases are associated with impaired spatial working memory and anxiety-like behavior. Thus, it is important to understand the underlying cellular mechanisms of neurodegenerative diseases in different regions of the brain to develop an effective therapeutic approach. In our previous research paper, we have reported the ameliorative effect of curcumin in Cd-induced hippocampal neurodegeneration. However, recently many researchers had reported the important role of the prefrontal cortex in higher cognitive functions. Therefore, to look into the cellular mechanism of curcumin protection against Cd-induced prefrontal cortex neurotoxicity, we investigated spatial working memory, anxiety-like behavior and analyzed prefrontal cortex inflammatory markers (IL-6, IL-10, and TNFα), antioxidant enzymes (SOD, GSH, and CAT), and pro-oxidant MDA level. Further, we conducted histological studies of the prefrontal cortex in Swiss albino mice exposed to cadmium (2.5 mg/kg). We observed that curcumin treatment improved the spatial working memory and anxiety-like behavior of mice through reduction of prefrontal cortex neuroinflammation and oxidative stress as well as increasing the number of viable prefrontal cortex neuronal cells. Our result suggests that environmental heavy metal cadmium can induce behavioral impairment in mice through prefrontal cortex cellular inflammation and oxidative stress. We found that curcumin has a potential therapeutic property to mitigate these behavioral and biochemical impairments induced by cadmium.


Sign in / Sign up

Export Citation Format

Share Document