Rats with prenatal dexamethasone exposure and postnatal high-fat diet exhibited insulin resistance, and spatial learning and memory impairment

Chronic exposures to high-fat diets are linked to neuropathological changes that culminate in obesity-related cognitive dysfunction and brain alteration. Learning, memory performance, and executive function are the main domains affected by an obesogenic diet. There are limited effective therapies for addressing cognitive deficits. Thus, it is important to identify additional and alternative therapies. In African traditional medicine, Gnidia glauca has putative efficacy in the management of obesity and associated complications. The use of Gnidia glauca is largely based on its long-term traditional use. Its therapeutic application has not been accompanied by sufficient scientific evaluation to validate its use. Therefore, the current study sought to explore the modulatory effects of dichloromethane leaf extracts of Gnidia glauca on cognitive function in the high-fat diet- (HFD-) induced obese rats. Obesity was induced by feeding the rats with prepared HFD and water ad libitum for 6 weeks. The in vivo antiobesity effects were determined by oral administration of G. glauca at dosage levels of 200, 250, and 300 mg/kg body weight in HFD-induced obese rats from the 6th to the 12th weeks. The Lee obesity index was used as a diagnostic criterion of obesity. The Morris water maze was employed to test spatial learning and memory retention in rats. The results indicated that Gnidia glauca showed potent antiobesity effects as indicated in the reduction of body weight and obesity index in extract-treated rats. Moreover, Gnidia glauca exhibited cognitive-enhancing effects in obese rats. The positive influences on cognitive functions might be attributed to the extracts’ phytochemicals that have been suggested to confer protection against obesity-induced oxidative damage, reduction of central inflammation, and increased neurogenesis. The therapeutic effects observed suggest that Gnidia glauca might be an alternative to current medications for the symptomatic complications of obesity, such as learning and memory loss. Further studies are therefore needed to establish its toxicity profiles.

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A maternal high-fat diet during pregnancy and lactation, in addition to a postnatal high-fat diet, leads to metabolic syndrome with spatial learning and memory deficits: beneficial effects of resveratrol

Oncotarget ◽

10.18632/oncotarget.22960 ◽

2017 ◽

Vol 8 (67) ◽

pp. 111998-112013 ◽

Cited By ~ 11

Author(s):

Shih-Wen Li ◽

Hong-Ren Yu ◽

Jiunn-Ming Sheen ◽

Mao-Meng Tiao ◽

You-Lin Tain ◽

...

Keyword(s):

Metabolic Syndrome ◽

Learning And Memory ◽

Spatial Learning ◽

High Fat Diet ◽

Memory Deficits ◽

Spatial Learning And Memory ◽

High Fat ◽

Beneficial Effects ◽

Pregnancy And Lactation ◽

Learning And Memory Deficits

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A Long-Term Enriched Environment Ameliorates the Accelerated Age-Related Memory Impairment Induced by Gestational Administration of Lipopolysaccharide: Role of Plastic Mitochondrial Quality Control

Frontiers in Cellular Neuroscience ◽

10.3389/fncel.2020.559182 ◽

2021 ◽

Vol 14 ◽

Author(s):

Zhan-Qiang Zhuang ◽

Zhe-Zhe Zhang ◽

Yue-Ming Zhang ◽

He-Hua Ge ◽

Shi-Yu Sun ◽

...

Keyword(s):

Learning And Memory ◽

Spatial Learning ◽

Memory Impairment ◽

Spatial Learning And Memory ◽

Mitochondrial Quality Control ◽

Protein Levels ◽

Age Related ◽

Old Mice ◽

Lps Treatment

Studies have shown that gestational inflammation accelerates age-related memory impairment in mother mice. An enriched environment (EE) can improve age-related memory impairment, whereas mitochondrial dysfunction has been implicated in the pathogenesis of brain aging. However, it is unclear whether an EE can counteract the accelerated age-related memory impairment induced by gestational inflammation and whether this process is associated with the disruption of mitochondrial quality control (MQC) processes. In this study, CD-1 mice received daily intraperitoneal injections of lipopolysaccharide (LPS, 50 μg/kg) or normal saline (CON group) during gestational days 15–17 and were separated from their offspring at the end of normal lactation. The mothers that received LPS were divided into LPS group and LPS plus EE (LPS-E) treatment groups based on whether the mice were exposed to an EE until the end of the experiment. At 6 and 18 months of age, the Morris water maze test was used to evaluate spatial learning and memory abilities. Quantitative reverse transcription polymerase chain reaction and Western blot were used to measure the messenber RNA (mRNA) and protein levels of MQC-related genes in the hippocampus, respectively. The results showed that all the aged (18 months old) mice underwent a striking decline in spatial learning and memory performances and decreased mRNA/protein levels related to mitochondrial dynamics (Mfn1/Mfn2, OPA1, and Drp1), biogenesis (PGC-1α), and mitophagy (PINK1/parkin) in the hippocampi compared with the young (6 months old) mice. LPS treatment exacerbated the decline in age-related spatial learning and memory and enhanced the reduction in the mRNA and protein levels of MQC-related genes but increased the levels of PGC-1α in young mice. Exposure to an EE could alleviate the accelerated decline in age-related spatial learning and memory abilities and the accelerated changes in MQC-related mRNA or protein levels resulting from LPS treatment, especially in aged mice. In conclusion, long-term exposure to an EE can counteract the accelerated age-related spatial cognition impairment modulated by MQC in CD-1 mother mice that experience inflammation during pregnancy.

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