β-Amyloid-induced cognitive dysfunction impairs glucose homeostasis by increasing insulin resistance and decreasing β-cell mass in non-diabetic and diabetic rats

Park, Sunmin; Kim, Da Sol; Kang, Suna; Moon, Na Rang

doi:10.1016/j.metabol.2013.08.007

Cited by 38 publications

(54 citation statements)

References 46 publications

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“…Transient high glucose stimulates insulin secretion to enhance glucose utilization, which maintains glucostasis under physical conditions (Le Roith and Zick, 2001). Conversely, persistent hyperglycemia damages beta cells and diminishes insulin secretion (Park et al, 2013). GDM is characterized by hyperglycemia and insulin deficiency, which adversely affects mothers and fetuses.…”

Section: Methodsmentioning

confidence: 99%

Retardation of fetal dendritic development induced by gestational hyperglycemia is associated with brain insulin/IGF‐I signals

Jing

Song

Yao

et al. 2014

Intl J of Devlp Neuroscience

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Hyperglycemia is an essential risk factor for mothers and fetuses in gestational diabetes. Clinical observation has indicated that the offspring of mothers with diabetes shows impaired somatosensory function and IQ. However, only a few studies have explored the effects of hyperglycemia on fetal brain development. Neurodevelopment is susceptible to environmental conditions. Thus, this study aims to investigate the effects of maternal hyperglycemia on fetal brain development and to evaluate insulin and insulin-like growth factor-I (IGF-I) signals in fetal brain under hyperglycemia or controlled hyperglycemia. At day 1 of pregnancy, gestational rats were intraperitoneally injected with streptozocin (60 mg/kg). Some of the hyperglycemic gestational rats were injected with insulin (20 IU, two times a day) to control hyperglycemia; the others were injected with saline of equal volume. The gestational rats were sacrificed at days 14, 16, and 18 of embryo development. The dendritic spines of subplate cortex neurons in the fetal brain were detected by Golgi-Cox staining. The mRNA levels of insulin receptors (IRs) and IGF-IR in the fetal brain were measured using qRT-PCR. The protein levels of synaptophysin, IR, and IGF-IR in the fetal brain were detected by western blot. No significant difference in fetal brain formation was observed between the maternal hyperglycemic group and insulin-treated group. By contrast, obvious retardation of dendritic development in the fetus was observed in the maternal hyperglycemic group. Similarly, synaptophysin expression was lower in the fetus of the maternal hyperglycemic group than in that of the insulin-treated group. The mRNA and protein expression levels of IRs in the fetal brain were higher in the hyperglycemic group than in the insulin-treated group. By contrast, the levels of IGF-IR in the brain were lower in the fetus of the maternal hyperglycemic group than in that of the insulin-treated group. These results suggested that maternal hyperglycemia can retard dendritic development in the fetal brain and that these changes partially resulted from abnormal insulin/IGF-I signaling in the fetal brain.

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Section: Methodsmentioning

confidence: 99%

Retardation of fetal dendritic development induced by gestational hyperglycemia is associated with brain insulin/IGF‐I signals

Jing

Song

Yao

et al. 2014

Intl J of Devlp Neuroscience

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“…The infusion of β-amyloid (25)(26)(27)(28)(29)(30)(31)(32)(33)(34)(35) into the LV causes the accumulation of β-amyloid whereas the infusion of β-amyloid , the reverse sequence of β-amyloid (25)(26)(27)(28)(29)(30)(31)(32)(33)(34)(35), does not accumulate in the brain, as confirmed by immunohistochemistry using β-amyloid antibody [4,21]. Each β-amyloid solution was infused via an osmotic pump (Alzet Osmotic Pump Company, Cupertino, CA) at the rate of 16.8 nmol/day for 3 days.…”

Section: Animal Care and Surgical Proceduresmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

“…In Alzheimer's disease the β-amyloid accumulation in the hippocampus is also reported to impair glucose utilization in both the brain and peripheral tissues and to dysregulate energy homeostasis through hippocampal insulin signaling [4]. Alzheimer's disease also impairs hepatic insulin sensitivity and β-cell function and vice versa [3,4]. The hypothalamus is known to have both orexigenic and anorexigenic neurons where neuropeptides, adipokines and gut hormones regulate food intake and modulate peripheral glucose homeostasis [5].…”

Section: Introductionmentioning

confidence: 99%

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Central acylated ghrelin improves memory function and hippocampal AMPK activation and partly reverses the impairment of energy and glucose metabolism in rats infused with β-amyloid

et al. 2015

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“…22). Further, recent evidence indicates β-cell dysfunction in AD rodent models 23,24 and that Aβ and Tau have been shown to accumulate in human post-mortem pancreatic tissue in T2D 25 , possibly contributing to β-cell dysfunction. Despite this evidence, there is a lack of literature investigating pancreatic β-cell activity (HOMA-B) on cognition and AD related pathology.…”

Section: Growing Evidence Supports the Hypothesis That Type 2 Diabetementioning

confidence: 99%

[P4–134]: Insulin Resistance Is Associated With Reductions in Specific Cognitive Domains and Increases in CSF Tau in Cognitively Normal Adults

Laws

Gaskin

Woodfield

et al. 2017

Alzheimer's & Dementia

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Growing evidence supports the hypothesis that type 2 diabetes (T2D) increases the risk of developing dementia. Experimental evidence from mouse models demonstratesEpidemiological studies indicate that Type 2 diabetes (T2D) is associated with an increased risk of dementia [1][2][3][4][5] . Clinical studies using cross-sectional designs support this association by showing that cognition is worse in patients with T2D as compared to matched controls without T2D 6,7 . Furthermore, studies of structural magnetic resonance imaging (MRI) show that in T2D cognitive impairment is associated with greater levels of vascular

show abstract

β-Amyloid-induced cognitive dysfunction impairs glucose homeostasis by increasing insulin resistance and decreasing β-cell mass in non-diabetic and diabetic rats

Cited by 38 publications

References 46 publications

Retardation of fetal dendritic development induced by gestational hyperglycemia is associated with brain insulin/IGF‐I signals

Retardation of fetal dendritic development induced by gestational hyperglycemia is associated with brain insulin/IGF‐I signals

Central acylated ghrelin improves memory function and hippocampal AMPK activation and partly reverses the impairment of energy and glucose metabolism in rats infused with β-amyloid

[P4–134]: Insulin Resistance Is Associated With Reductions in Specific Cognitive Domains and Increases in CSF Tau in Cognitively Normal Adults

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