Central <scp>IGF</scp>‐I Receptors in the Brain are Instrumental to Neuroprotection by Systemically Injected <scp>IGF</scp>‐I in a Rat Model for Ischemic Stroke

Geyter, Deborah De; Smedt, Ann De; Stoop, Wendy; Keyser, Jacques De; Kooijman, Ron

doi:10.1111/cns.12550

Cited by 27 publications

(20 citation statements)

References 39 publications

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“…Pro-opiomelanocortin (Pomc) Rn00595020_m1 (2,17) = 126.5, p < 0.001], with an interaction between these factors [F (2, 17) = 4.9, p < 0.05]. As expected, HFD rats consumed more kcal from fat compared to chow and LFD animals (p < 0.001).…”

Section: Gene Referencementioning

confidence: 69%

“…On a chow diet males had higher levels of IGF2 than females on the same diet [F (1, 9) = 6.2, p < 0.05; Figure 1C]. In males, IGF2 levels were lower on the HFD compared to chow [F (2,15) a, overall sex effect; b, overall diet effect; # different compared to chow rats of the same sex; @ different between sexes on the same diet. ns, non-significant.…”

Section: Serum Levels Of Metabolic Factors and Igf Family Membersmentioning

confidence: 99%

“…Insulin-like growth factor (IGF) 1 is involved in a wide range of functions ( 1 , 2 ) including promotion of systemic growth through actions exerted directly on bone ( 3 ), anabolic effects promoting protein synthesis and glucose uptake in muscle ( 4 ) and stimulation of lipogenesis ( 5 ). Because of their structural similarity, IGF1 shares metabolic functions with insulin ( 6 ) and elevated levels of this growth factor reduce glycemia ( 7 ).…”

Section: Introductionmentioning

confidence: 99%

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Short-Term Diet Induced Changes in the Central and Circulating IGF Systems Are Sex Specific

et al. 2020

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Insulin-like growth factor (IGF) 1 exerts a wide range of functions in mammalians participating not only in the control of growth and metabolism, but also in other actions such as neuroprotection. Nutritional status modifies the IGF system, although little is known regarding how diet affects the newest members of this system including pregnancy-associated plasma protein-A (PAPP-A) and PAPP-A2, proteases that liberate IGF from the IGF-binding proteins (IGFBPs), and stanniocalcins (STCs) that inhibit PAPP-A and PAPP-A2 activity. Here we explored if a 1-week dietary change to either a high-fat diet (HFD) or a low-fat diet (LFD) modifies the central and peripheral IGF systems in both male and female Wistar rats. The circulating IGF system showed sex differences in most of its members at baseline. Males had higher levels of both free (p < 0.001) and total IGF1 (p < 0.001), as well as IGFBP3 (p < 0.001), IGFBP5 (p < 0.001), and insulin (p < 0.01). In contrast, females had higher serum levels of PAPP-A2 (p < 0.05) and IGFBP2 (p < 0.001). The responses to a short-term dietary change were both diet and sex specific. Circulating levels of IGF2 increased in response to LFD intake in females (p < 0.001) and decreased in response to HFD intake in males (p < 0.001). In females, LFD intake also decreased circulating IGFBP2 levels (p < 0.001). In the hypothalamus LFD intake increased IGF2 (p < 0.01) and IGFBP2 mRNA (p < 0.001) levels, as well as the expression of NPY (p < 0.001) and AgRP (p < 0.01), but only in males. In conclusion, short-term LFD intake induced more changes in the peripheral and central IGF system than did short-term HFD intake. Moreover, these changes were sex-specific, with IGF2 and IGFBP2 being more highly affected than the other members of the IGF system. One of the main differences between the commercial LFD employed and the HFD or normal rodent chow is that the LFD has a significantly higher sucrose content, suggesting that this nutrient could be involved in the observed responses.

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Section: Gene Referencementioning

confidence: 69%

Section: Serum Levels Of Metabolic Factors and Igf Family Membersmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Short-Term Diet Induced Changes in the Central and Circulating IGF Systems Are Sex Specific

et al. 2020

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“…Factors that are known to modulate vascular and endothelial growth and thus vascular rarefaction included vascular endothelial growth factor (VEGF), growth hormone (GH), and insulin-like growth factor-1 (IGF-1). With regard to endothelial cell function and hypertension, IGF-1 has been shown to promote EC cell function and capillary density [ 151 ], [ 36 ••], and an age-related decline in IGF-1 is significantly associated with an increased risk for hypertension [ 146 , 152 ].…”

Section: Introductionmentioning

confidence: 99%

Hypertension and Age-Related Cognitive Impairment: Common Risk Factors and a Role for Precision Aging

et al. 2020

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Purpose of Review Precision Aging® is a novel concept that we have recently employed to describe how the model of precision medicine can be used to understand and define the multivariate risks that drive age-related cognitive impairment (ARCI). Hypertension and cardiovascular disease are key risk factors for both brain function and cognitive aging. In this review, we will discuss the common mechanisms underlying the risk factors for both hypertension and ARCI and how the convergence of these mechanisms may be amplified in an individual to drive changes in brain health and accelerate cognitive decline. Recent Findings Currently, our cognitive health span does not match our life span. Age-related cognitive impairment and preventing and treating ARCI will require an in-depth understanding of the interrelated risk factors, including individual genetic profiles, that affect brain health and brain aging. Hypertension and cardiovascular disease are important risk factors for ARCI. And, many of the risk factors for developing hypertension, such as diabetes, smoking, stress, viral infection, and age, are shared with the development of ARCI. We must first understand the mechanisms common to the converging risk factors in hypertension and ARCI and then design person-specific therapies to optimize individual brain health. Summary The understanding of the convergence of shared risk factors between hypertension and ARCI is required to develop individualized interventions to optimize brain health across the life span. We will conclude with a discussion of possible steps that may be taken to decrease ARCI and optimize an individual's cognitive life span.

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“…Neurogenesis is thereby influenced through the milieu of secreted factors . Microglia can secrete pro‐inflammatory factors such as tumor necrosis factors‐α (TNF‐α) and neurotrophic factors such as insulin growth factors (IGF) and brain‐derived neurotrophic factor (BDNF), both of which can reduce inflammation and exert neuroprotective effects . The complex role of microglia in neurogenesis is also due to its modulatory nature .…”

Section: The Role Of Neuroinflammation In Multiple Brain Repair Mechamentioning

confidence: 99%

The evolving role of neuro‐immune interaction in brain repair after cerebral ischemic stroke

et al. 2018

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Stroke is the world's leading cause of disability with limited brain repair treatments which effectively improve long-term neurological deficits. The neuroinflammatory responses persist into the late repair phase of stroke and participate in all brain repair elements, including neurogenesis, angiogenesis, synaptogenesis, remyelination and axonal sprouting, shedding new light on post-stroke brain recovery. Resident brain glial cells, such as astrocytes not only contribute to neuroinflammation after stroke, but also secrete a wide range of trophic factors that can promote post-stroke brain repair. Alternatively, activated microglia, monocytes, and neutrophils in the innate immune system, traditionally considered as major damaging factors after stroke, have been suggested to be extensively involved in brain repair after stroke. The adaptive immune system may also have its bright side during the late regenerative phase, affecting the immune suppressive regulatory T cells and B cells. This review summarizes the recent findings in the evolving role of neuroinflammation in multiple post-stroke brain repair mechanisms and poses unanswered questions that may generate new directions for future research and give rise to novel therapeutic targets to improve stroke recovery.

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Central IGF‐I Receptors in the Brain are Instrumental to Neuroprotection by Systemically Injected IGF‐I in a Rat Model for Ischemic Stroke

Abstract: Systemically injected rhIGF-I passes the blood-brain barrier and protects neurons via IGF-I receptors in the brain in rats with an ischemic stroke.

Cited by 27 publications

References 39 publications

Short-Term Diet Induced Changes in the Central and Circulating IGF Systems Are Sex Specific

Short-Term Diet Induced Changes in the Central and Circulating IGF Systems Are Sex Specific

Hypertension and Age-Related Cognitive Impairment: Common Risk Factors and a Role for Precision Aging

The evolving role of neuro‐immune interaction in brain repair after cerebral ischemic stroke

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