Adiponectin-leptin ratio: A promising index to estimate adipose tissue dysfunction. Relation with obesity-associated cardiometabolic risk

Frühbeck, Gema; Catalán, Victoria; Rodrı́guez, Amaia; Gómez-Ambrosi, Javier

doi:10.1080/21623945.2017.1402151

Cited by 305 publications

(325 citation statements)

References 52 publications

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“…Adiponectin acts as an insulin-sensitizing hormone in muscle and liver, and lower levels of adiponectin further contribute to peripheral insulin resistance in obesity [75,76]. The adiponectin/leptin ratio is a functional biomarker of adipose tissue inflammation [77] and a good indicator of a dysfunctional adipose tissue, which may be a useful estimator of obesity and metabolic syndrome [77]. This emerging biomarker correlates with insulin resistance better than adiponectin or leptin alone [77], while insulin resistance correlates with cognitive dysfunction [78][79][80].…”

Section: Molecular Biomarkers and Correlations With Neurocognitive Pementioning

confidence: 99%

“…The adiponectin/leptin ratio is a functional biomarker of adipose tissue inflammation [77] and a good indicator of a dysfunctional adipose tissue, which may be a useful estimator of obesity and metabolic syndrome [77]. This emerging biomarker correlates with insulin resistance better than adiponectin or leptin alone [77], while insulin resistance correlates with cognitive dysfunction [78][79][80]. Since individuals with type 2 diabetes suffer from severe cognitive deficits [79] and deficits in hippocampal function may appear due to peripheral insulin resistance and hyperlipidemia caused by a high-calorie diet, which declines hippocampal synaptic plasticity and impairs cognitive function [80], this is a plausible reason for the significant correlation between the adiponectin/leptin ratio and the neurophysiological performance observed in the present study.…”

Section: Molecular Biomarkers and Correlations With Neurocognitive Pementioning

confidence: 99%

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Neurocognitive Inhibitory Control Ability Performance and Correlations with Biochemical Markers in Obese Women

Wen

Tsai

2020

IJERPH

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Inhibitory control, the ability to suppress prepotent responses and resist irrelevant stimuli, is thought to play a critical role in the maintenance of obesity. However, electrophysiological performance related to different inhibitory control processes and their relationship with motor response inhibition and cognitive interference and potential biochemical mechanisms in middle-aged, obese women are as yet unclear. This work thus compared different neurocognitive Go/Nogo and Stroop task performance in healthy sedentary normal-weight and obese women, as well as their correlation with biochemical markers. Twenty-six healthy, sedentary obese women (obese group) and 26 age-matched (21-45 years old) normal-weight women (control group) were the participants, categorized by body mass index and percentage fat, as measured with dual-energy X-ray absorptiometry. They provided a fasting blood sample and performed two cognitive tasks (i.e., Go/Nogo and Stroop tasks) with concomitant electrophysiological recording. The N2 and P3 waveforms of event-related potential (ERP) were recorded. Although the between-group behavioral performance was comparable, the obese group relative to the control group showed significantly longer N2 latency and smaller P3 amplitude in the Stroop task and smaller N2 and P3 amplitudes in the Go/Nogo task. Significant inflammation response indices (e.g., CRP, leptin, adiponectin/leptin ratio) were observed in the obese group. The Nogo P3 amplitude was significantly correlated with the adiponectin/leptin ratio. These findings indicate that healthy obese women still exhibit deviant neurophysiological performance when performing Go/Nogo and Stroop tasks, where the adiponectin/leptin ratio could be one of the influencing factors for the deficit in neural processes of motor response inhibition.healthy individuals since individuals with obesity feel that they have failed to resist food (overeating behavior) [3,4].Inhibitory control, as a subcomponent of executive functions, refers to an individual's capacity to suppress a prepotent but ineffective behavior provoked by an external cue to stop an ongoing response and to resist distracting stimuli [5]. Such cognitive processing capabilities have been associated with many different aspects of life, being positively related to general success in health and the accumulation of wealth [6] and negatively related to addictions [7] and obesity [8]. The inhibitory control functions regulated and supported by multiple top-down neural connections [9] could be impaired in obese individuals. Indeed, obese individuals demonstrate characteristics of weak inhibitory control, which is considered to play a critical role in difficulties related to resisting external cues that suggest delicious food [10,11]. These behavioral characteristics may be associated with dopamine-modulated mesolimbic circuits and the dorsolateral regions of the prefrontal cortex [10]. In comparison with normal-weight controls, obese adults have also exhibited lower dopamine D2 receptor density in the str...

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Section: Molecular Biomarkers and Correlations With Neurocognitive Pementioning

confidence: 99%

Section: Molecular Biomarkers and Correlations With Neurocognitive Pementioning

confidence: 99%

Neurocognitive Inhibitory Control Ability Performance and Correlations with Biochemical Markers in Obese Women

Wen

Tsai

2020

IJERPH

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“…Moreover, low adiponectin levels are often found in individuals with insulin resistance as well as in patients with Type 2 diabetes mellitus (Yatagai et al, ) and are now considered as an independent risk factor for diabetes and insulin resistance as well as for cardiovascular disease (Kumada et al, ). Also, the adiponectin/leptin ratio has been proposed as a valuable index to estimate WAT dysfunction and obesity‐associated cardiometabolic risk (Frühbeck, Catalán, Rodríguez, & Gómez‐Ambrosi, ). Mechanisms regulating adiponectin production continue to be a matter of debate (Fang & Judd, ).…”

Section: Introductionmentioning

confidence: 99%

The cholecystokinin receptor agonist, CCK‐8, induces adiponectin production in rat white adipose tissue

Plaza

Merino

Olmo

et al. 2019

British J Pharmacology

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Background and Purpose:A cholecystokinin (CCK) system has been identified in white adipose tissue (WAT). Nevertheless, the endocrine actions of CCK on WAT remain unknown. Our goal was to investigate the role of CCK in regulating the production of adiponectin, an adipokine expressed in WAT, which is pivotal in preserving energy homeostasis. Experimental Approach:The effect of the bioactive CCK fragment CCK-8 on adiponectin production was studied both in vivo and in vitro. CCK-8 effects were characterized in rats treated with selective CCK 1 and CCK 2 receptor antagonists as well as in pre-adipocytes carrying the selective silencing of either CCK 1 or CCK 2 receptors. The influence of insulin on CCK-8 responses was also analysed. Key Results: In WAT, CCK-8 increased plasma adiponectin levels and the expression of the adiponectin gene (Adipoq). In pre-adipocytes, CCK-8 up-regulated adiponectin production. CCK-8 effects were abolished by L-365,260, a selective CCK 2 receptor antagonist. CCK 2 receptor knockdown also abolished the effects of CCK-8 in pre-adipocytes. Moreover, in vitro CCK-8 effects were blocked by triciribine, a specific inhibitor of protein kinase B (Akt) and by the PPARγ antagonist T0070907. Silencing the expression of the insulin receptor inhibited CCK-8-induced Adipoq expression in pre-adipocytes. Furthermore, insulin potentiated the effect of CCK-8. Conclusion and Implications: CCK-8 stimulates adiponectin production in WAT by acting on CCK 2 receptors, through a mechanism involving both Akt and PPARγ. Moreover, CCK-8 actions are only observed in the presence of insulin. Our results could have translational value in the design of new insulin-sensitizing therapies.

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“…The precise mechanisms underpinning these interaction effects require future studies into the role of a number of metabolic pathways related to lipids, immunity, and vascular function, as well as glucose and insulin resistance. Here, we explored the potential moderating effects of systolic and diastolic BP, of plasma markers of inflammation with CRP and IL8, and of adipose tissue dysfunction with the Leptin/Adiponectin Ratio, that may reflect insulin resistance and/or low-grade inflammation 89 . Differences in BP had an impact on WBWM MPF and right PHC ICSF but controlling for these variables did not fully account for the observed interaction in microstructure.…”

Section: Discussionmentioning

confidence: 99%

“…Finally, we tested whether differences in blood pressure, plasma markers of inflammation (C-Reactive Protein, Interleukin 8), and adipose tissue dysfunction (leptin/adiponection ratio) 89 accounted for any effects of risk factors on white matter microstructure and cognition to explore potential contributing mechanisms.…”

Section: Insert Table 1 and Figure 1 Herementioning

confidence: 99%

Genetic risk of dementia modifies the impact of obesity on limbic white matter and spatial navigation behavior in cognitively healthy adults

Mole

Fasano

Evans

et al. 2019

Preprint

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A family history (FH) of dementia, APOE-e4 genotype, and obesity are major risk factors for developing Alzheimer's disease but their combined effects on the brain and cognition remain elusive. We tested the hypothesis that these risk factors affect apparent white matter (WM) myelin and cognition including spatial navigation and processing speed in 166 asymptomatic individuals (38-71 years). Microstructure in temporal [fornix, parahippocampal cingulum, uncinate fasciculus], motor and whole-brain WM was assessed with myelin-sensitive indices from quantitative magnetization transfer [macromolecular proton fraction (MPF)] and axon density from diffusion imaging. Individuals with the highest genetic risk compared to those with FH+ alone showed obesity-related reductions in MPF and axon density in the right parahippocampal cingulum. No effects were present for those without FH.Furthermore, FH modulated obesity-related effects on spatial navigation behaviour. In summary, an individual's genetic dementia risk influenced the impact of obesity on WM myelin and cognition. quantitative magnetization transfer, NODDI, white matter, myelin, parahippocampal cingulum 7 ResultsInsert Table 2 and Figures 2 and 3 here 2.1 Multivariate covariance analysis (MANCOVA) of white matter microstructural indices MANCOVA tested for the effects of APOE genotype (e4+, e4-), family history (FH+, FH-) and central obesity (WHR+, WHR-) on all microstructural indices (MPF, kf, R1, ISOSF, ICSF, ODI) in all white matter pathways (left PHC, right PHC, left UF, right UF, left CST, right CST and fornix) and WBWM regions whilst controlling for age, sex, and years of education. Omnibus effects: Main effects were observed for age [F(48,60) = 2.64, p < 0.001, hp 2 = 0.68] and sex [F(48,60) = 2.61, p < 0.001, hp 2 = 0.67]. Interaction effects were present between APOE and WHR [F(48,60) = 1.6, p = 0.04, hp 2 = 0.56] and between APOE, FH and WHR [F(48,60) = 1.7, p = 0.02, hp 2 = 0.58].Post-hoc effects: Ageing was associated with reductions in MPF, kf, and R1 in WBWM, fornix and right UF (Table 2). MPF and kf reductions were also present in the left UF and bilateral CST respectively. In addition, age-related increases in ISOSF were observed in WBWM and fornix and increases in ODI in the fornix (Table 2, Figure 2A).Women relative to men showed lower kf, ISOSF and ODI in WBWM and the fornix and larger fornix MPF (Table 2, Figure 2B). Two-way interaction effects between APOE and WHR were present for right PHC ( Figure 3A) and bilateral CST but additional post-hoc group comparisons to assess the directions of these effects were non-significant. Three-way interaction effects between FH, APOE and WHR were observed for MPF in WBWM, bilateral CST, bilateral UF and right PHC ( Figure 3B). For right PHC there was also an effect on ICSF. These three-way interaction effects were followed up by testing for APOE and WHR interactions in FH+ and FH-individuals separately ( Figure 3C). FH-individuals did not show any interaction effects B from the Alzheimer's Society and the BR...

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Adiponectin-leptin ratio: A promising index to estimate adipose tissue dysfunction. Relation with obesity-associated cardiometabolic risk

Cited by 305 publications

References 52 publications

Neurocognitive Inhibitory Control Ability Performance and Correlations with Biochemical Markers in Obese Women

Neurocognitive Inhibitory Control Ability Performance and Correlations with Biochemical Markers in Obese Women

The cholecystokinin receptor agonist, CCK‐8, induces adiponectin production in rat white adipose tissue

Genetic risk of dementia modifies the impact of obesity on limbic white matter and spatial navigation behavior in cognitively healthy adults

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