Association of adiponectin, leptin and resistin with inflammatory markers and obesity in dementia

Bednarska-Makaruk, Małgorzata; Graban, Ałła; Wiśniewska, Anna; Łojkowska, Wanda; Bochyńska, Anna; Gugała-Iwaniuk, Magdalena; Sławińska, Ksenia; Ługowska, Agnieszka; Ryglewicz, Danuta; Wehr, H

doi:10.1007/s10522-017-9701-0

Cited by 64 publications

(44 citation statements)

References 65 publications

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“…Another finding in the current study that supports the therapeutic effect of β-OHB in both AD and atherosclerosis is that β-OHB reduced the serum level of resistin, a hormone that plays important roles in, and is associated with, both AD [35] and atherosclerosis [36]. Evidence in multicohort studies also indicates it as a biomarker as well as a risk factor for AD [37][38][39]. Higher levels of resistin in both serum and cerebrospinal fluid were observed in AD patients.…”

Section: Discussionsupporting

confidence: 79%

β-hydroxybutyrate Impedes the Progression of Alzheimer’s Disease and Atherosclerosis in ApoE-Deficient Mice

et al. 2020

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β-hydroxybutyrate (β-OHB) has been shown to exert an anti-inflammatory activity. Apolipoprotein-E (ApoE) is strongly associated with atherosclerosis and Alzheimer’s disease (AD). This study aimed to explore the therapeutic effect of β-OHB in the brain and the aorta of high-fat diet (HFD)-fed ApoE-deficient mice. We found in Apo-E deficient mice that β-OHB attenuated lipid deposition in the choroid plexus (ChP) and decreased amyloid plaque in the substantia nigra pars compacta. We also found decreased CD68-positive macroglia infiltration of the ChP in β-OHB-treated ApoE-deficient mice. β-OHB treatment ameliorated IgG extravasation into the hippocampal region of the brain. In vitro study using ChP mice cell line revealed that β-OHB attenuated oxidized low-density lipoprotein-induced ApoE-specific differentially expressed inflammatory ChP genes. Treatment with β-OHB reduced aortic plaque formation without affecting blood lipid profiles and decreased serum production of resistin, a well-established risk factor for both AD and atherosclerosis. Thus, the current study suggests and describes the therapeutic potential of β-OHB for the treatment of AD and atherosclerosis.

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Section: Discussionsupporting

confidence: 79%

β-hydroxybutyrate Impedes the Progression of Alzheimer’s Disease and Atherosclerosis in ApoE-Deficient Mice

et al. 2020

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“…Furthermore, a study on general population showed a negative correlation between serum levels of HDL-C and resistin [57]. A negative correlation between the levels of resistin with HDL-cholesterol was stated in patients with all-cause dementia [62]. Also, in another general population based study, it has been shown that resistin level was correlated inversely with HDL cholesterol [63] (see ▶ table 3).…”

Section: Resistin and Hdl Cholesterolmentioning

confidence: 94%

Correlation Between Resistin Level and Metabolic Syndrome Component: A Review

et al. 2018

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Metabolic syndrome (MetS) has a collection of some abnormal and pathological conditions that cause many critical diseases. Resistin is one of the possible candidates for these pathologies but there are not enough data to prove if resistin has positive, neutral, or negative effects on one or some components of MetS. This review summarizes data about comparing the effects and contribution of resistin in initiation and progression of MetS components and also its different actions between human and other mammalians. This summarized data about the relationship of resistin and MetS components have been obtained from clinical researches and in some cases even animal studies. To find the relevant studies, the search in PubMed, Science Direct, and Scopus were performed. Human and animal studies on relationships between resistin and MetS (initiation and progression of components) were included in our search. In experiments reported among different human genetic groups as well as the patients with various disease such as diabetes, no significant correlation is shown between FBG and resistin level. Furthermore, this review shows that the results of correlation between resistin and TG, HDL, and central or abdominal obesity were inconsistent. These inconsistencies can arise from different sample size or genetic groups, gender, and also from experimental studies. Therefore, to obtain precise results systematic review and meta-analyses are required.

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“…These mice also developed AD, displaying increased β-amyloid-42 fragments (Aβ42) levels in the hippocampus and frontal cortex, due to ADPN deficiency [28]. Bednarska-Makaruk [46] found that in the all-cause dementia group there are higher levels both of IL-6 and ADPN in AD and Mixed Dementia (MD).…”

Section: Adiponectin and Alzheimer Disease (Ad)mentioning

confidence: 99%

Adiponectin and Cognitive Decline

Rizzo

Fasano

Paolisso

2020

IJMS

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Adiponectin (ADPN) is a plasma protein secreted by adipose tissue showing pleiotropic effects with anti-diabetic, anti-atherogenic, and anti-inflammatory properties. Initially, it was thought that the main role was only the metabolism control. Later, ADPN receptors were also found in the central nervous system (CNS). In fact, the receptors AdipoR1 and AdipoR2 are expressed in various areas of the brain, including the hypothalamus, hippocampus, and cortex. While AdipoR1 regulates insulin sensitivity through the activation of the AMP-activated protein kinase (AMPK) pathway, AdipoR2 stimulates the neural plasticity through the activation of the peroxisome proliferator-activated receptor alpha (PPARα) pathway that inhibits inflammation and oxidative stress. Overall, based on its central and peripheral actions, ADPN appears to have neuroprotective effects by reducing inflammatory markers, such as C-reactive protein (PCR), interleukin 6 (IL6), and Tumor Necrosis Factor a (TNFa). Conversely, high levels of inflammatory cascade factors appear to inhibit the production of ADPN, suggesting bidirectional modulation. In addition, ADPN appears to have insulin-sensitizing action. It is known that a reduction in insulin signaling is associated with cognitive impairment. Based on this, it is of great interest to investigate the mechanism of restoration of the insulin signal in the brain as an action of ADPN, because it is useful for testing a possible pharmacological treatment for the improvement of cognitive decline. Anyway, if ADPN regulates neuronal functioning and cognitive performances by the glycemic metabolic system remains poorly explored. Moreover, although the mechanism is still unclear, women compared to men have a doubled risk of developing cognitive decline. Several studies have also supported that during the menopausal transition, the estrogen reduction can adversely affect the brain, in particular, verbal memory and verbal fluency. During the postmenopausal period, in obese and insulin-resistant individuals, ADPN serum levels are significantly reduced. Our recent study has evaluated the relationship between plasma ADPN levels and cognitive performances in menopausal women. Thus, the aim of this review is to summarize both the mechanisms and the effects of ADPN in the central nervous system and the relationship between plasma ADPN levels and cognitive performances, also in menopausal women.

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Association of adiponectin, leptin and resistin with inflammatory markers and obesity in dementia

Cited by 64 publications

References 65 publications

β-hydroxybutyrate Impedes the Progression of Alzheimer’s Disease and Atherosclerosis in ApoE-Deficient Mice

β-hydroxybutyrate Impedes the Progression of Alzheimer’s Disease and Atherosclerosis in ApoE-Deficient Mice

Correlation Between Resistin Level and Metabolic Syndrome Component: A Review

Adiponectin and Cognitive Decline

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