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

ABSTRACT: The aim of the study was to determine the role of adiponectin, leptin and resistin in various types of dementia and to investigate their association with inflammatory markers, insulin resistance and abdominal obesity. In 205 patients with dementia [89 with Alzheimer's disease (AD), 47 with vascular dementia (VaD), 69 with mixed dementia (MD)], 113 persons with mild cognitive impairment and in 107 controls serum adiponectin, leptin and resistin levels, pro-inflammatory [interleukin-6 (IL-6), C-reactive protein (hsCRP) and chitotriosidase] and anti-inflammatory (25-OH vitamin D, HDL-cholesterol and paraoxonase 1) markers, as well as glucose metabolism parameters (glucose, insulin and HOMA-IR) were determined. In all-cause dementia adiponectin and resistin levels were significantly higher as compared to the controls; leptin levels did not show differences. Higher adiponectin levels concerned AD and MD, whereas higher resistin-VaD and MD. After stratification by abdominal obesity the differences in adiponectin levels remained significant in subjects without obesity. In all-cause dementia negative correlation of adiponectin with obesity, glucose metabolism parameters, IL-6 and hsCRP and positive correlation with HDL-cholesterol were found. Positive correlation of resistin with age, IL-6, hsCRP and chitotriosidase and negative correlation with HDL-cholesterol and paraoxonase 1 were stated. We conclude that dementia of neurodegenerative origin is characterized by elevated adiponectin levels, whereas dementia with vascular changes by increase of resistin. Association with inflammatory indicators may suggest the pro-inflammatory role of resistin in the development of dementia, especially in dementia of vascular mechanism. Identification of this novel biomarker may be important in preventing dementia.

SUBMITTER: Bednarska-Makaruk M

PROVIDER: S-EPMC5514216 | biostudies-literature | 2017 Aug

REPOSITORIES: biostudies-literature

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

Bednarska-Makaruk Małgorzata M Graban Ałła A Wiśniewska Anna A Łojkowska Wanda W Bochyńska Anna A Gugała-Iwaniuk Magdalena M Sławińska Ksenia K Ługowska Agnieszka A Ryglewicz Danuta D Wehr Hanna H

Biogerontology 20170418 4

The aim of the study was to determine the role of adiponectin, leptin and resistin in various types of dementia and to investigate their association with inflammatory markers, insulin resistance and abdominal obesity. In 205 patients with dementia [89 with Alzheimer's disease (AD), 47 with vascular dementia (VaD), 69 with mixed dementia (MD)], 113 persons with mild cognitive impairment and in 107 controls serum adiponectin, leptin and resistin levels, pro-inflammatory [interleukin-6 (IL-6), C-re ...[more]

PMID: 28421328

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Project description:The imbalanced network of adipokines may contribute to the development of systemic low-grade inflammation, metabolic diseases and coronary artery disease (CAD). In the last decade, three classic adipokines-adiponectin, leptin and resistin-have been of particular interest in studies of patients with CAD due to their numerous properties in relation to the cardiovascular system. This has directed our attention to the association of adipokines with cardiac structure and function and the development of heart failure (HF), a common end effect of CAD. Thus, the purpose of this study was to analyse the associations of plasma concentrations of adiponectin, leptin and resistin with parameters assessed in the echocardiographic examinations of CAD patients. The presented study enrolled 167 Caucasian patients (133 male; 34 female) with CAD. Anthropometric, echocardiographic and basic biochemical measurements, together with plasma concentrations of adiponectin, leptin and resistin assays, were performed in each patient. Adiponectin concentrations were negatively associated with left ventricular ejection fraction (LVEF) and shortening fraction (LVSF), and positively associated with mitral valve E/A ratio (E/A), left ventricular end-diastolic volume (LVEDV), left ventricular end-diastolic diameter (LVEDD), left ventricular end-systolic diameter LVESD, and left atrium diameter (LAD). Resistin concentrations were negatively associated with E/A. Leptin concentrations, although correlated with HF severity assessed by the New York Heart Association (NYHA) Functional Classification, were not independently associated with the echocardiographic parameters of cardiac structure or function. In conclusion, adiponectin and resistin, but not leptin, are associated with the echocardiographic parameters of cardiac remodelling and dysfunction. These associations suggest that adiponectin and resistin might be involved in mechanisms of cardiac remodelling or compensative response. We also suggest the possible benefits of adiponectin and resistin level measurements in the monitoring of patients with CAD.

Project description:The present meta-analysis was performed to examine the association between circulating blood adipokine levels and Kawasaki disease (KD). Studies were identified by searching various databases, including Web of Science, EMBASE, PubMed, Wanfang and China National Knowledge Infrastructure. After the studies were pooled, the mean difference (MD) and corresponding 95% CI were calculated. Subgroup analyses and publication bias detection were also performed. The Cochrane Q test and I2 statistics were performed using Review Manager software (version 5.3) to test for heterogeneity. A Begg's test was used to assess publication bias and STATA software (version 12.0) was used for statistical analysis. The results revealed that the KD group exhibited higher levels of resistin compared with those in the healthy controls or disease controls (non-KD; MD=20.76, 95% CI=16.16-25.36, P<0.001; MD=21.27, 95% CI=14.24-28.29, P<0.001, respectively). In addition, when compared with those in patients exhibiting non-coronary artery lesions (NCAL), those with coronary artery lesions (CAL) had higher levels of adiponectin and resistin (MD=1.00, 95% CI=0.06-1.96, P=0.04; MD=2.77, 95% CI=1.32-4.22, P<0.001). Furthermore, compared with those in the inactive-phase group, patients in the active-phase group exhibited higher levels of resistin (MD=17.73, 95% CI=12.82-22.65, P<0.001). In conclusion, the present meta-analysis indicated that resistin levels were elevated in patients with KD. It was also revealed that circulating resistin and adiponectin levels in the CAL group were significantly increased compared with those in patients with NCAL. Furthermore, the active group had higher levels of resistin than the inactive group. The results of these meta-analyses indicated that resistin may serve an important role in the pathogenesis of KD and may therefore be used as biomarkers for the diagnosis of KD, whereas adiponectin may only serve an important role in the pathogenesis of CAL and may therefore be used as a biomarker to distinguish CAL from NCAL.

Project description:Adiponectin exerts beneficial effects by reducing inflammation and improving lipid metabolism and insulin sensitivity. Although the adiponectin level is lower in obese individuals, whether weight gain reduces adiponectin expression in humans is controversial. We sought to investigate the role of weight gain, and consequent changes in leptin, on altering adiponectin expression in humans.Forty-four normal-weight healthy subjects were recruited (mean age 29 years; 14 women) and randomized to either gain 5% of body weight by 8 weeks of overfeeding (n=34) or maintain weight (n=10). Modest weight gain of 3.8±1.2?kg resulted in increased adiponectin level (P=0.03), whereas weight maintenance resulted in no changes in adiponectin. Further, changes in adiponectin correlated positively with changes in leptin (P=0.0085). In-vitro experiments using differentiated human white preadipocytes showed that leptin increased adiponectin mRNA and protein expression, whereas a leptin antagonist had opposite effects. To understand the role of leptin in established obesity, we compared adipose tissue samples obtained from normal-weight versus obese subjects. We noted, first, that leptin activated cellular signaling pathways and increased adiponectin mRNA in the adipose tissue from normal-weight participants, but did not do so in the adipose tissue from obese participants. Second, we noted that obese subjects had increased caveolin-1 expression, which attenuates leptin-dependent increases in adiponectin.Modest weight gain in healthy individuals is associated with increases in adiponectin levels, which correlate positively with changes in leptin. In vitro, leptin induces adiponectin expression, which is attenuated by increased caveolin-1 expression. In addition, the adipose tissue from obese subjects shows increased caveolin-1 expression and impaired leptin signaling. This leptin signal impairment may prevent concordant increases in adiponectin levels in obese subjects despite their high levels of leptin. Therefore, impaired leptin signaling may contribute to low adiponectin expression in obesity and may provide a target for increasing adiponectin expression, hence improving insulin sensitivity and cardio-metabolic profile in obesity.

Dataset Information

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

Publications

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

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