Hippocampal apoptosis involved in learning deficits in the offspring exposed to maternal high sucrose diets

Kuang, Hanzhe; Sun, Miao; Lv, Jian; Li, Jiayue; Wu, Chonglong; Chen, Ningjing; Bo, Le; Wei, Xiaoguang; Gu, Xiuxia; Liu, Zhen; Mao, Caiping; Xu, Zhice

doi:10.1016/j.jnutbio.2014.04.012

Cited by 35 publications

(40 citation statements)

References 33 publications

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“…Alternatively, perinatal exposure to sugar may have a more detrimental effect on adult memory function than perinatal exposure to fat. Consistent with this notion, one study demonstrated that maternal consumption of a 20% sucrose sweetened solution from gestational day 1 to day 21 produced impairments in spatial learning performance of juvenile and adolescent offspring [27], however, the effects of perinatal sucrose exposure in adult offspring was not tested.…”

Section: Perinatal Period: Obesogenic Diets and Memory Functionmentioning

confidence: 99%

“…Impaired IR and/or IGF-1R signaling may be one mechanism through which early life consumption of obesogenic dietary factors leads to hippocampal dysfunction. For example, when confined only to the gestational period, maternal consumption of a 20% sucrose sweetened beverage impairs spatial learning concurrent with reduced expression of IGF-1, and downstream signaling molecules phosphoinositide 3 kinase (PI3K), and phosphorylated protein kinase B (pAKT) in the hippocampus of juvenile offspring [27]. Insulin receptor expression was reduced in the hippocampus of adult rats that were exposed to HFD (39% kcal from fat) prior to weaning, both in animals weaned on chow and on HFD.…”

Section: Neurobiological Mechanismsmentioning

confidence: 99%

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Early life exposure to obesogenic diets and learning and memory dysfunction

Noble

Kanoski

2016

Current Opinion in Behavioral Sciences

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Obesogenic dietary factors, such as simple sugars and saturated fatty acids, have been linked to memory impairments and hippocampal dysfunction. Recent evidence suggests that the brain may be particularly vulnerable to the effects of obesogenic diets during early life periods of rapid growth, maturation, and brain development. Investigations utilizing rodent models indicate that early life exposure to “high fat diets” (40-65% kcal derived from fat) or simple sugars (sucrose or high fructose corn syrup) can impair hippocampus-dependent learning and memory processes. In some cases, these deficits occur independent of obesity and metabolic derangement and can persist into adulthood despite dietary intervention. Various neurobiological mechanisms have been identified that may link early life consumption of obesogenic dietary factors with hippocampal dysfunction, including increased neuroinflammation and reduced neurotrophin mediated regulation of neurogenesis and synaptic plasticity. Age, duration of exposure, and dietary composition are key variables contributing to the interaction between early life diet and cognitive dysfunction, however, more research is needed to unravel the precise critical windows of development and causal dietary factors.

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Section: Perinatal Period: Obesogenic Diets and Memory Functionmentioning

confidence: 99%

Section: Neurobiological Mechanismsmentioning

confidence: 99%

Early life exposure to obesogenic diets and learning and memory dysfunction

Noble

Kanoski

2016

Current Opinion in Behavioral Sciences

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“…In the present study, 50 mg/kg body weight was used with the intention to alter gut microbiota and to study the effect of the induced overgrowth of PPA-related bacteria. The persistent elevation of glutamate in ampicillintreated rats fed a high-sucrose diet can be supported by the recent report by Kuang et al [22]. The study demonstrated that a maternal high-sucrose (HS) diet affects behavior and hippocampal neurons in the young offspring, leading to learning deficits through a significant increase in the expression of N-methyl-Daspartate (NMDA) receptors.…”

Section: Discussionmentioning

confidence: 66%

Elimination of high-refined-sugar diet as treatment strategy for autistic features induced in a rodent model

Al-Daihan¹,

Bhat²,

Dbass³

et al. 2017

Trop. J. Pharm Res

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“…In our previous study, maternal HS diets during pregnancy led to impaired learning and memory in the male offspring [13]. These findings indicated that similar to mater obesity and high fat diet [23–25], maternal HS diets during pregnancy could lead to altered fetal neuroendocrine development, subsequently resulting in potential cognitive dysfunction in the offspring.…”

Section: Discussionmentioning

confidence: 88%

“…Feeding mother rats with a diet high in sugar could cause adverse outcomes such as cardiovascular diseases and metabolic syndrome in the offspring [10,11]. Our previous study demonstrated that high sucrose (HS) diets during pregnancy not only altered microvessel tone via depressed BKCa channels in offspring’s mesenteric arteries [12], but also led to impaired learning and memory in the male offspring [13]. Since middle cerebral artery (MCA) is a critical blood vessel in supplying blood and oxygen to the brain, MCA dysfunction could be considered as major contributor to multiple brain problems, such as vascular dementia and cognitive dysfunction [14,15].…”

Section: Introductionmentioning

confidence: 99%

Regulation of cerebral arterial BKCa channels by angiotensin II signaling in adult offspring exposed to prenatal high sucrose diets

Fan

et al. 2017

Bioscience Reports

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Prenatal insults have been shown to affect vascular functions, leading to increased risks of cardiovascular diseases in offspring. The present study determined whether high sucrose (HS) intake in pregnancy affected central vascular functions in middle cerebral artery (MCA) of offspring. Sprague-Dawley rats were fed a standard food and tap water with normal or high (20%) sucrose content during pregnancy. Offspring were maintained with normal diets and tap water. Central vascular functions and related ion channels were assessed in male offspring at 5 months old. Compared with the control, angiotensin II (AII)-induced vasoconstrictions were significantly higher in the MCA of the offspring exposed to prenatal HS. In the MCA, large conductance Ca2+-activated K+ channels (BKCa) currents were decreased with a reduction of opening frequency, sensitivity to intracellular Ca2+/membrane voltage, and BKβ1 expression. mRNA levels of AT1α and AT2, as well as AT1/AT2 ratio, were significantly increased in the MCA of offspring following exposure to prenatal HS diets. The data suggested that prenatal HS diets could alter microvascular activities in the MCA, probably via changes of BKCa channels in the brain.

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Hippocampal apoptosis involved in learning deficits in the offspring exposed to maternal high sucrose diets

Cited by 35 publications

References 33 publications

Early life exposure to obesogenic diets and learning and memory dysfunction

Early life exposure to obesogenic diets and learning and memory dysfunction

Elimination of high-refined-sugar diet as treatment strategy for autistic features induced in a rodent model

Regulation of cerebral arterial BKCa channels by angiotensin II signaling in adult offspring exposed to prenatal high sucrose diets

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